ATAR Notes: Forum
VCE Stuff => VCE Science => VCE Mathematics/Science/Technology => VCE Subjects + Help => VCE Biology => Topic started by: Yacoubb on January 18, 2013, 02:55:39 am
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Hey :) I'd like to share some definitions I have + please tell me how my expression is :)
Homeostasis: the homeostatic maintenance of a relatively stable internal environment maintained within narrow ranges despite fluctuating conditions of an organism's external environment.
I'll be posting more + I'd appreciate it if you could tell me how good the definitions are :)
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Does the definition have to be that long?
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Regarding your definition:
Pros: Mentions 'narrow limits', partial independence from the external environment.
Cons: Uses the word that's being defined in the definition; 'fluctuating conditions' bit could be worded better.
If I were to rewrite this definition:
"Homeostasis: the maintenance of a stable internal environment of an organism, maintained within narrow ranges regardless of changes in the external environment in which the organism exists".
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I would shorten the definition as much as possible to eliminate room for assessors owning you. Ideal answer would be:
Homeostasis: The maintenance of a stable internal environment within narrow limits despite the effect of various stimuli.
Google definition was also very simple: "The tendency toward a relatively stable equilibrium between interdependent elements"
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One thing to note everyone doing biology:
When writing down definitions NEVER ever use and repeat any derivative of the word in the definition. This shows the examiner that one you don't really understand the word or a different word that can describe it and two you aren't really describing the word.
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One thing to note everyone doing biology:
When writing down definitions NEVER ever use and repeat any derivative of the word in the definition. This shows the examiner that one you don't really understand the word or a different word that can describe it and two you aren't really describing the word.
Hey that was a bit dumb because I initially wrote down 3 definitions for you guys to check and I must have done it wrong because I did this at 3 in the morning lol
New definition:
Enzyme: a protein catalyst that increases the speed of chemical reactions by lowering the activation energy required; they are not consumed by reactions they catalyse.
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That definition seems acceptable - you may want to include this though:
- "Lock-and-key" aspect: a particular enzyme only acts as a catalyst for one specific molecule.
- The reaction occurs on the surface of the active site of the enzyme.
I'm not sure if this is necessary; I think I'm just being picky. :P
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Enzyme: a protein catalyst that increases the speed of chemical reactions by lowering the activation energy required; they are not consumed by reactions they catalyse.
I wouldn't say 'the speed of chemical reactions' - rather say 'the rate of chemical reactions'. Assessors strongly consider the use of proper scientific language when marking.
Also, consider mentioning that each enzyme is specific to only one substrate (assessors love it if you use the word 'specificity' correctly). :)
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I wouldn't say 'the speed of chemical reactions' - rather say 'the rate of chemical reactions'. Assessors strongly consider the use of proper scientific language when marking.
Also, consider mentioning that each enzyme is specific to only one substrate (assessors love it if you use the word 'specificity' correctly). :)
I think the depth of my answer will ultimaty depend on the bumber of lines on an exam/SAC. The thing is, I'd mention my definition for a 2line answer whereas a 4 line question (i.e. 4 lines to write on), I would mention the following
* an organic, protein catalyst
* increases rate of chemical reactions by lowering activation energy
* the tertiary structure of the enzyme is critical to its specific function as the shape of the active site is specifically complementary to its substrate!
^ I think that would be satisfactory for an in depth answer they may very-well ask.
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That definition seems acceptable - you may want to include this though:
- "Lock-and-key" aspect: a particular enzyme only acts as a catalyst for one specific molecule.
- The reaction occurs on the surface of the active site of the enzyme.
I'm not sure if this is necessary; I think I'm just being picky. :P
I was just mentioning that the depth of my answer would be dependent upon the space provided by VCAA on the exam paper.
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I think the depth of my answer will ultimaty depend on the bumber of lines on an exam/SAC. The thing is, I'd mention my definition for a 2line answer whereas a 4 line question (i.e. 4 lines to write on), I would mention the following
* an organic, protein catalyst
* increases rate of chemical reactions by lowering activation energy
* the tertiary structure of the enzyme is critical to its specific function as the shape of the active site is specifically complementary to its substrate!
^ I think that would be satisfactory for an in depth answer they may very-well ask.
More importantly, look at the number of marks!
But I think that definition is good.
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More importantly, look at the number of marks!
But I think that definition is good.
My strategy of how deep to delve into an answer is determined by number of lines in addition to the allocation of marks. Thank you for the tip though :)
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Hey that was a bit dumb because I initially wrote down 3 definitions for you guys to check and I must have done it wrong because I did this at 3 in the morning lol
New definition:
Enzyme: a protein catalyst that increases the speed of chemical reactions by lowering the activation energy required; they are not consumed by reactions they catalyse.
Just trying to help bud.
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Enzymes don't have to be proteins...
I would say "macromolecules" instead of proteins in my definition.
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Just trying to help bud.
Hey just want to mention that I was saying what I did was dumb; not you!! Sorry for the misunderstanding!
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Carbohydrate: C H O
Proteins: C H O N (sometimes Sulfur)
Lipids: C H O
Nucleic Acids: C H O Phosphorus :)
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That isn't entirely correct. Some proteins contain phosphorus and the bases of nucleic acids contain nitrogen. :)
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That isn't entirely correct. Some proteins contain phosphorus and the bases of nucleic acids contain nitrogen. :)
But that is basically what is 100% required for proteins to be deemed proteins. And I forgot nitrogen in the N-containing bases
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But that is basically what is 100% required for proteins to be deemed proteins. And I forgot nitrogen in the N-containing bases
Hmm... All proteins contain carbon, hydrogen, oxygen and nitrogen, some contain phosphorus, but you can distinguish a protein from another type of biomacromolecule with the presence of sulfur.
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Proteins must contain Nitrogen, Carbon, Hydrogen and Oxygen. However, they can also contain Sulfur/Phosphorus. Nucleic Acids contain Carbon, Hydrogen, Oxygen, Phosphorus and Nitrogen.
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Proteins must contain Nitrogen, Carbon, Hydrogen and Oxygen. However, they can also contain Sulfur/Phosphorus.
Rather than just remembering it like that, it's important to know why.
Whether a protein contains Sulfur/Phosphorus is ultimately dependent on what sort of amino acids are present in the protein's primary structure.
Due to the carboxyl (-COOH) and amine (NH2) groups, which comprise a part of every amino acid, you definitely have to have nitrogen, carbon, hydrogen and oxygen in proteins.
Amino acids have different R-variable groups, and some will have Sulfur/Phosphorus in these groups (i.e Cysteine) whereas other amino acids don't (i.e Valine). If you have an amino acid which has sulfur/phorphorus in the R-variable group, inevitably you will get a protein molecule which has these elements in it. If you don't have such an amino acid, then you'll just have carbon, nitrogen, oxygen and hydrogen.
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Just a quick question.
Why can't you work out how much of a protein will be present by measuring the amount of mRNA that codes for that particular protein?
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There's no amino acid that contains phosphorus in its R group. Phosphorus can later be added to a protein but doesn't make up any amino acids :P
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Just a quick question.
Why can't you work out how much of a protein will be present by measuring the amount of mRNA that codes for that particular protein?
Because the entire mRNA sequence doesn't necessarily code. In unit 4, you'll learn about a process called RNA splicing.
Basically, the DNA template strand isn't copied straight to the mRNA that is read in translation. In a gene, within the coding region, there are 'sub-regions' known as introns and exons. Introns do not code for anything, while exons are coding sequences. The mRNA that is transcribed from the DNA template is known as pre-mRNA, and it contains both intron and exon sequences. However, the process of RNA splicing occurs and the intron regions are removed, and the resulting mRNA strand (which consists only of exon sequences) is capped by a Poly-A (as in AAA repeating) tail. This is the mRNA sequence used in translation.
tl;dr: Technically, not all of the mRNA codes for something. Furthermore, certain codons code for a stop sequence, which is not an amino acid. Hence it would be inefficient to both count the mRNA codons and factor in conditions to account for stop codons.
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There's no amino acid that contains phosphorus in its R group. Phosphorus can later be added to a protein but doesn't make up any amino acids :P
So would that be post translational modification? (Thanks by the way for answering.)
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Because the entire mRNA sequence doesn't necessarily code. In unit 4, you'll learn about a process called RNA splicing.
Basically, the DNA template strand isn't copied straight to the mRNA that is read in translation. In a gene, within the coding region, there are 'sub-regions' known as introns and exons. Introns do not code for anything, while exons are coding sequences. The mRNA that is transcribed from the DNA template is known as pre-mRNA, and it contains both intron and exon sequences. However, the process of RNA splicing occurs and the intron regions are removed, and the resulting mRNA strand (which consists only of exon sequences) is capped by a Poly-A (as in AAA repeating) tail. This is the mRNA sequence used in translation.
tl;dr: Technically, not all of the mRNA codes for something. Furthermore, certain codons code for a stop sequence, which is not an amino acid. Hence it would be inefficient to both count the mRNA codons and factor in conditions to account for stop codons.
Okay don't know about any of that but thanks for answering. I should come back to this next time.
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Okay don't know about any of that but thanks for answering. I should come back to this next time.
You do more on mRNA and all the jazz in Unit 4, so don't be worried :)
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Just a quick question.
Why can't you work out how much of a protein will be present by measuring the amount of mRNA that codes for that particular protein?
Also because some mRNA are reused; recycled if you like.
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So would that be post translational modification? (Thanks by the way for answering.)
Yeah, that would be considered a post-translational modification. You don't really have to know anything about that though
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Can anyone please help me with these questions from chapter 2 review (Nature of biology book two, fourth edition).
Q5-The folded internal membranes of mitochondria have many stalked particles on their innermost surfaces (figure 2.31). Given the function of mitochondria and where most of the reactions occur, of what advantage might the presence of these particles be for the production of ATP in the organelle?
Q6 In figure 2.31, you may have noted the holes in the folds of the inner membrane of mitochondria. Explain a possible function of these holes
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figure- for above question
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Can anyone please help me with these questions from chapter 2 review (Nature of biology book two, fourth edition).
Q5-The folded internal membranes of mitochondria have many stalked particles on their innermost surfaces (figure 2.31). Given the function of mitochondria and where most of the reactions occur, of what advantage might the presence of these particles be for the production of ATP in the organelle?
Q6 In figure 2.31, you may have noted the holes in the folds of the inner membrane of mitochondria. Explain a possible function of these holes
For question 5, the stalked particles increase the surface area of the internal membrane. The greater surface area increases the rate of ATP production in the organelle. I think.
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Can anyone please help me with these questions from chapter 2 review (Nature of biology book two, fourth edition).
Q5-The folded internal membranes of mitochondria have many stalked particles on their innermost surfaces (figure 2.31). Given the function of mitochondria and where most of the reactions occur, of what advantage might the presence of these particles be for the production of ATP in the organelle?
The stalked particles increase SA:V ratio, allowing reactant molecules to diffuse across mitochondria more quickly. Therefore, the rate of ATP production in mitochondria will be higher.
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What't the difference between polymerisation and condensation reaction?
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What't the difference between polymerisation and condensation reaction?
arent they the same ?
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A condensation reaction is one type of polymerisation reaction.
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arent they the same ?
Thought so too. But my bio teacher told me that there are differences. Not clear on that.
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A condensation reaction is one type of polymerisation reaction.
oh ok.
Could you please explain a little more
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oh ok.
Could you please explain a little more
A polymerisation reaction is a reaction where monomers are bonded together to form a polymer.
In a condensation polymerisation reaction, a small molecule such as water is created when two monomers bond to each other.
If you've done chemistry, you may have heard of another type of polymerisation reaction called an addition polymerisation reaction.
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A polymerisation reaction is a reaction where monomers are bonded together to form a polymer.
In a condensation polymerisation reaction, a small molecule such as water is created when two monomers bond to each other.
If you've done chemistry, you may have heard of another type of polymerisation reaction called an addition polymerisation reaction.
thanks :)
how important do you think this is for the exam?
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thanks :)
how important do you think this is for the exam?
I'd say it's quite important; you want to understand quite well how biomacromolecules are formed from their subunits.
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I'd say it's quite important; you want to understand quite well how biomacromolecules are formed from their subunits.
ok thanks do we need to know the difference between polymerisation and condensation reaction?
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Yes
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Yes
ok
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The difference between polymerisation and condensation is that polymerisation is the process by which monomers join together to form a long chain of monomers (polymer), wheras condensation involves the release of a H2O molecule before a bond can actually form between the monomers.
@fushandchups: Sub-units are important to understand and it is also beneficial to know the type of bonds that exist because you'll impress the examiners if you know that during the condensation reaction of glycogen synthesis, glucose monosaccharide sub-units are joined by glycosidic bonds.. or the enzyme maltase is made up of amino acids joined by peptide bonds.. It's just additional knowledge that can maximise your understanding of Biomacromolecules :)
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can someone please tell me why the pancreas has more rough endoplasmic reticulum and the liver more smooth endoplasmic reticulum? thanks in advance. :)
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Pancreas is where the insulin is made? Therefore more RoughER more proteins are made, more insulin to regulate blood (I assume)
And Liver needs SmoothER to package alcohol and stuff (i assume)
These are just guesses from organelle functions and organ functions
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Pancreas is where the insulin is made? Therefore more RoughER more proteins are made, more insulin to regulate blood (I assume)
And Liver needs SmoothER to package alcohol and stuff (i assume)
These are just guesses from organelle functions and organ functions
You're almost dead on!
Pancreatic cells are involved in the production of a number of hormones, such as insulin and glucagon - both of which are peptide hormones. Rough Endoplasmic Reticuli are 'dotted' with fixed ribosomes, which are involved in protein synthesis. Because pancreatic cells produce a greater range and amount of peptide-based molecules, more ribosomes (ergo more RERs) are required.
In liver cells, the Smooth Endoplasmic Reticuli contains enzymes that are essential to the detoxification of harmful drugs and metabolic by-products. For example, liver cells of an alcoholic would have a larger number of SERs so as to cope with the larger-than-normal intake of alcohol, which is a poison and needs to be detoxified and metabolised by the body.
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Haha yea! I'm surprised I can still do some of these questions!
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thanks haters gonna hate and alondouek. ;D
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My first SAC is next week and I'd really appreciate if someone could please check if this aim, hypothesis and observations are valid and any possible changes I can make in order to achieve the best I possibly can.
Aim:
What you will be investigating – the aim of the experiment was to investigate Osmosis in a plant cell when placed in solutions with different solute concentrations.
Hypothesis:
The educated guess as to what will happen –
* When the cell is placed in the hypertonic solution, water will move out of the cell by osmosis and the cells will plazmolyse.
* When the cell is placed in the hypotonic solution, water will move into the cell by osmosis and it will become turgid.
* When the cell is placed in the isotonic solution, there is no net movement of water molecules and so the plant cell becomes flaccid.
Observations:
* The plant cell mass decreased when it was placed in the hypertonic solution because water moved from an area of low solute concentration to high solute concentration, out of the cell, causing it to plazmolyse.
* The plant cell placed in the hypotonic solution had an increased mass as water moved in from an area of low solute concentration to high solute concentration, into the cell, causing it to become turgid.
* There was no mass change in the plant cell placed in the isotonic solution because there was no net movement of water, and so the plant cell remained flaccid.
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My first SAC is next week and I'd really appreciate if someone could please check if this aim, hypothesis and observations are valid and any possible changes I can make in order to achieve the best I possibly can.
Aim:
What you will be investigating – the aim of the experiment was to investigate Osmosis in a plant cell when placed in solutions with different solute concentrations.
Hypothesis:
The educated guess as to what will happen –
* When the cell is placed in the hypertonic solution, remember to point out the fact that its net movement water will move out of the cell by osmosis and the cells will plazmolyse.
* When the cell is placed in the hypotonic solution, water will move into the cell by osmosis and it will become the cell remains turgid- I think you said this yourself in one of the other threads turgid.
* When the cell is placed in the isotonic solution, there is no net movement of water molecules and so the plant cell becomes flaccid.
Observations:
* The plant cell mass decreased when it was placed in the hypertonic solution because water moved from an area of low solute concentration to high solute concentration, out of the cell, causing it to plazmolyse.
* The plant cell placed in the hypotonic solution had an increased mass as water moved in from an area of low solute concentration to high solute concentration, into the cell, causing it to become turgid.
* There was no mass change in the plant cell placed in the isotonic solution because there was no net movement of water, and so the plant cell remained flaccid.
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In you hypothesis, state what the tonicity is relative to.
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In you hypothesis, state what the tonicity is relative to.
Could you please elaborate on that?
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Thank you Bad Student - but are all the other aspects and the things I've written good, or do you think they're not so good. I just want to perfect them haha!
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Could you please elaborate on that?
When you write that the cell is placed in the hypertonic solution, you should say that the concentration of solute in the solution is greater than the concentration of solute in the cell.
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Thank you Bad Student - but are all the other aspects and the things I've written good, or do you think they're not so good. I just want to perfect them haha!
Everything else seems fine to me, but I'm not exactly the authority when it comes to prac reports.
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Could you please elaborate on that?
If you're moving a cell from a hypotonic solution to an isotonic solution, is that isotonic solution relative to the cell now or before you started?
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But wouldn't that be too much information for the hypothesis? I mean, I think the hypothesis should be an outline of what happens, and I'll elaborate on net movement of water molecules in the observation. :) Would that be sufficient?!
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You just need to state "relative to the intracellular fluid present in the plant cell." I wrote that down all the time in my SAC. :)
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I know salt or ions cannot pass the plasma membrane by themselves. But can salt pass through the cell wall?
Can someone quickly run me through the cell wall and sodium chloride?
thanks
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You just need to state "relative to the intracellular fluid present in the plant cell." I wrote that down all the time in my SAC. :)
This.
Detail to make it non-ambiguous is important.
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I know salt or ions cannot pass the plasma membrane by themselves. But can salt pass through the cell wall?
Can someone quickly run me through the cell wall and sodium chloride?
thanks
The cell wall isn't semi-permeable, its pretty much permeable to everything.
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Hey guys :)
Just a quick question. I was doing a LisaChem diagnostic test and I was stumped by these questions.
- Name the two major organic components that make up a molecule of ATP.
*I wrote Carbohydrates and Nucleic Acids, but I'm pretty sure that's wrong.
- Which particular group of molecules within ATP is considered biologically important of ATP? Explain.
I really didn't know how to approach these questions. Help would be really appreciated. Thank you :)
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Hey guys :)
Just a quick question. I was doing a LisaChem diagnostic test and I was stumped by these questions.
- Name the two major organic components that make up a molecule of ATP.
*I wrote Carbohydrates and Nucleic Acids, but I'm pretty sure that's wrong.
- Which particular group of molecules within ATP is considered biologically important of ATP? Explain.
I really didn't know how to approach these questions. Help would be really appreciated. Thank you :)
Organic components...? All I can really think of is the sugar component (in this case the purine) and the nitrogenous base.
The second one is the phosphate group, because when removed causes the release of energy that is able to drive metabolism and is also involved in pathways involving phosphorylation (for example, many signal transduction pathways)
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Organic components...? All I can really think of is the sugar component (in this case the purine) and the nitrogenous base.
The second one is the phosphate group, because when removed causes the release of energy that is able to drive metabolism and is also involved in pathways involving phosphorylation (for example, many signal transduction pathways)
Yeah thats what I thought :)
Hydrolysis of the terminal phosphate group of the ATP molecule releases ample energy, which is then used by endergonic reactions that require this energy input. Its that energy rich bond between the second + third (terminal) phosphate group that makes ATP such a high-energy molecule.
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I've begun Chapter 7 of Nature of Biology 2, and I don't know if its me or the study design says very little about what types of pathogens we need to know.
I've learnt about Prions, Viruses, Viroids, Bacteria and very generally about eukaryotic pathogens, and how pathogens can be classified as cellular or non-cellular. Would that be sufficient? I mean how much do we need to delve into pathogenic agents for the VCE Biology course??
Thanks for your help.
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I've begun Chapter 7 of Nature of Biology 2, and I don't know if its me or the study design says very little about what types of pathogens we need to know.
I've learnt about Prions, Viruses, Viroids, Bacteria and very generally about eukaryotic pathogens, and how pathogens can be classified as cellular or non-cellular. Would that be sufficient? I mean how much do we need to delve into pathogenic agents for the VCE Biology course??
Thanks for your help.
I think its enough to know generally about prions, viruses, etc. (in as much detail as there is in the book) but in more detail about cellular and eukaryotic pathogens (in my opinion) because when I was doing Unit 3 exams I saw more questions about eukaryotic pathogens (e.g. there was a question about hyphae of fungi). Usually when they're asking about pathogens though theres a passage beforehand about the specific organism/pathogenic agent.
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I was doing Unit 3 exams I saw more questions about eukaryotic pathogens (e.g. there was a question about hyphae of fungi).
Came across this question as well,
Q. Histoplasmosis is an infectious disease of the lungs caused by the soil-based fungus Histoplasma capsulatum The H. capsulatum is most likely to be
A. Killed by antibiotics
B. A prokaryotic organism
C. Only able to grow in a dry, cool environment
D. Made of thread-like filaments known as hyphae
Although you can eliminate A and B straight off, you can't derive the answer from the sentence provided. I'm assuming we need to have little knowledge of the structure of fungi.
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Came across this question as well,
Q. Histoplasmosis is an infectious disease of the lungs caused by the soil-based fungus Histoplasma capsulatum The H. capsulatum is most likely to be
A. Killed by antibiotics
B. A prokaryotic organism
C. Only able to grow in a dry, cool environment
D. Made of thread-like filaments known as hyphae
Although you can eliminate A and B straight off, you can't derive the answer from the sentence provided. I'm assuming we need to have little knowledge of the structure of fungi.
YEAH! that's the exact one.. I was confused as to C or D but then I realised that fungi would most likely grow in damp environments not dry ones so I picked D. But knowledge of fungi would have definitely helped...
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D is correct!
C can be eliminated by logic - if the fungus is 'soil-based', it's unlikely that it will be in a dry environment. So, AbominableMowman, your reasoning was correct.
Moreover, D is certainly correct as hyphae are the main mode of vegetative growth of a fungus, and they're pretty much universal in the fungi kingdom. (Side note: yeasts do not grow as hyphae, even though they are fungal in nature)
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Is this an appropriate definition for a target cell:
A target cell is a specific type of cell that has appropriate receptors, enabling these cells to be identified by specific signalling molecules and thus respond to these signalling molecules.
I'm really hesitant about using 'hormone' because neurotransmitters are also signalling molecules and their target cells would be either the next neuron (dendrites of the next neuron) or the effector muscle/gland.
Help would be appreciated :)
Thanks!
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Signalling molecule is definitely a good word to use. I think your definition is good, although I must admit I got a little confused about the 'identified by' which might just be because I have been studying cell markers for the last 24 hours or maybe because you're personifying the signalling molecule.
My VCE Biology definition probably went a little like this:
A specific type of cell that possesses a particular receptor allowing it to bind and respond to specific signalling molecules.
A bit shorter and a little more concise but feel free to keep yours if you wish!
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Signalling molecule is definitely a good word to use. I think your definition is good, although I must admit I got a little confused about the 'identified by' which might just be because I have been studying cell markers for the last 24 hours or maybe because you're personifying the signalling molecule.
My VCE Biology definition probably went a little like this:
A specific type of cell that possesses a particular receptor allowing it to bind and respond to specific signalling molecules.
A bit shorter and a little more concise but feel free to keep yours if you wish!
This is perfect. Thank you so much!!
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Would it be accurate to say that natural killer cells induce apoptosis in viral-infected cells??
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Would it be accurate to say that natural killer cells induce apoptosis in viral-infected cells??
I'm not sure if that's all they can do (I doubt it), but they definitely are able to induce apoptosis.
https://en.wikipedia.org/wiki/Granzyme
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I'm doing some revision of the plasma membrane, and movement across the plasma membrane, and I'd just like to see if my expression for the functions of the components of the plasma membrane are accurate.
Phospholipid Bi-layer:
- The hydrophilic phosphate heads and the hydrophobic fatty acid tails allow the movement of selectively small, uncharged and/or lipid-soluble substances into and out of the cell.
Protein Channel:
- Allow the movement of selective, non-lipid soluble substances into and out of a cell.
Cholestrol - found only in animal plasma membranes:
- Provides more stability and flexibility to the plasma membrane
- Reduces the fluidity of the plasma membrane at normal range temperatures to provide stability to the plasma membrane.
- Increases the fluidity of the plasma membrane
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I'm doing some revision of the plasma membrane, and movement across the plasma membrane, and I'd just like to see if my expression for the functions of the components of the plasma membrane are accurate.
Phospholipid Bi-layer:
- The hydrophilic phosphate heads and the hydrophobic fatty acid tails selectively allow the movement of small, uncharged and/or lipid-soluble substances into and out of the cell (I believe the nuclear membrane and vacuolar membrane and some other organelles also have phospholipid bilayer membranes..
Protein Channel:
- Selectively allow the movement of non-lipid soluble substances into and out of a cell.
I think it sounds slightly better if you put the "selectively" in those places.
Cholestrol - found only in animal plasma membranes:
- Provides more stability and flexibility to the plasma membrane more stability and flexibility than what?
- Reduces the fluidity of the plasma membrane at normal range temperatures to provide stability to the plasma membrane.
- Increases the fluidity of the plasma membrane
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I'm doing some revision of the plasma membrane, and movement across the plasma membrane, and I'd just like to see if my expression for the functions of the components of the plasma membrane are accurate.
Phospholipid Bi-layer:
- The hydrophilic phosphate heads and the hydrophobic fatty acid tails selectively allow the movement of small, uncharged and/or lipid-soluble substances into and out of the cell (I believe the nuclear membrane and vacuolar membrane and some other organelles also have phospholipid bilayer membranes.. [Good point]~!!
Protein Channel:
- Selectively allow the movement of non-lipid soluble substances into and out of a cell.
I think it sounds slightly better if you put the "selectively" in those places.
Cholestrol - found only in animal plasma membranes:
- Provides more stability and flexibility to the plasma membrane more stability and flexibility than what? (It just provides MORE flexbility and stability... not more than anything else).
- Reduces the fluidity of the plasma membrane at normal range temperatures to provide stability to the plasma membrane.
- Increases the fluidity of the plasma membrane
Thanks!
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It provides more stability and flexibility than a plasma membrane without cholesterol but phrasing it in this way sounds clumsy.
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It provides more stability and flexibility than a plasma membrane without cholesterol but phrasing it in this way sounds clumsy.
The assessment report has written that one of the functions of cholestrol is to provide more stability and flexibility!
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Then I guess that's good enough. I'm just really careful about this stuff because my school marks the SACs very harshly.
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Then I guess that's good enough. I'm just really careful about this stuff because my school marks the SACs very harshly.
Haha yeah same! I lost a mark because I said 'Test Tube A and B will have similar enzymatic activity rates', but I wasn't test tube specific and thus lost the mark. I learnt my lesson haha!
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HI :)
I was doing a practice paper and came across this question:
A series of experiments was carried out with rattlesnakes to determine the major receptors involved in their rapid accurate strikes to catch their food (mice, rats, etc). The following results were obtained.
- Experiment 1 - snake in bright light with dead mouse - no strike
- Experiment 2 - snake in dark with dead mouse pulled quickly along - no strike
- Experiment 3 - blindfolded snake in dark with live mouse - rapid, accurate strike
The results suggest rattlesnakes detect their prey using:
a) chemoreceptors
b) mechanoreceptors
c) photoreceptors
d) thermoreceptors
The answer was in fact D, however I chose B. Could someone explain this question to me and how the answer is in fact D?
Thanks![/list]
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can you please explain to me how you got your answer?:)
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if the answer is B, why didn't the snake strike in scenario 2?
Go down the list and eliminate each option as it becomes impossible. A is plausible. B would mean the snake would strike at any movement, not just a live mouse moving. C would mean the snake would not strike in scenario 3. D is plausible.
Comparing A and D, I prefer D since it has a rationale that seems based in science (live mouse is warm and snake can detect this) rather than conjecture (somehow the snake can detect chemicals from a live mouse that are not present on a dead mouse)
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We can rule out photoreceptors because the snake was blindfolded and in the dark so it would not have been able to see.
We can rule out chemoreceptors because both the dead mouse and the live mouse would have had a scent.
We can also rule out mechanoreceptors because the snake didn't strike the dead mouse which was being pulled along.
The only other difference between each each of the experimental groups is whether the mouse is alive or dead. Since mice are mammals, they will emit body heat when they are alive. Therefore, thermoreceptors is the best option.
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HI :)
I was doing a practice paper and came across this question:
A series of experiments was carried out with rattlesnakes to determine the major receptors involved in their rapid accurate strikes to catch their food (mice, rats, etc). The following results were obtained.
- Experiment 1 - snake in bright light with dead mouse - no strike
- Experiment 2 - snake in dark with dead mouse pulled quickly along - no strike
- Experiment 3 - blindfolded snake in dark with live mouse - rapid, accurate strike
The results suggest rattlesnakes detect their prey using:
a) chemoreceptors
b) mechanoreceptors
c) photoreceptors
d) thermoreceptors
The answer was in fact D, however I chose B. Could someone explain this question to me and how the answer is in fact D?
Thanks!
Right, lets start off by eliminating what we can. The changes to stimuli don't seem to have any relation to chemoreceptors, so we can get rid of A. Mechanoreceptors respond to pressure or physical distortion, so we can eliminate B as the stimuli don't relate to 'touch'.
C can be eliminated as experiments 1 and 2 demonstrate that light is not a factor in striking.
D is correct as the strike occurs when the mouse is living (i.e. producing thermal energy).
These sort of questions are easy marks in the exam, because it's really just comprehension![/list]
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Right, lets start off by eliminating what we can. The changes to stimuli don't seem to have any relation to chemoreceptors, so we can get rid of A. Mechanoreceptors respond to pressure or physical distortion, so we can eliminate B as the stimuli don't relate to 'touch'.
C can be eliminated as experiments 1 and 2 demonstrate that light is not a factor in striking.
D is correct as the strike occurs when the mouse is living (i.e. producing thermal energy).
These sort of questions are easy marks in the exam, because it's really just comprehension![/list]
Thanks. Are we required to know about any specialised receptors for the VCAA exam? (i.e. about mechano/chem/thermo/photoreceptors)? I know them basically in terms of their functions, but not a LOT about them...
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Doubt it. Generally, if they ask a question about a specific receptor, they'll give a couple of paragraphs background first (and the questions will likely be quite straightforward or more comprehension based).
You could certainly do some light wider reading if you wanted; maybe start with the wiki pages and follow some links?
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Doubt it. Generally, if they ask a question about a specific receptor, they'll give a couple of paragraphs background first (and the questions will likely be quite straightforward or more comprehension based).
You could certainly do some light wider reading if you wanted; maybe start with the wiki pages and follow some links?
Thanks :)
Quick question - after attending a headstart lecture for unit 4 and being a bit exposed to its content, I've realised that my approach will differ from Unit 3. For instance, there'll be more time dedicated to actually doing monohybrid/dihybrid crossing opposed to sitting and reading notes about it. Completing questions about evolution, DNA manipulation techniques, etc. Is Unit 4 the easier unit? Unit 3 I find relatively straightforward, but unit 4 seems more appealing to me..
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Thanks :)
Quick question - after attending a headstart lecture for unit 4 and being a bit exposed to its content, I've realised that my approach will differ from Unit 3. For instance, there'll be more time dedicated to actually doing monohybrid/dihybrid crossing opposed to sitting and reading notes about it. Completing questions about evolution, DNA manipulation techniques, etc. Is Unit 4 the easier unit? Unit 3 I find relatively straightforward, but unit 4 seems more appealing to me..
I guess that's up to you, really! Some people (like myself) somewhat prefer the cell and molecular biology in the unit 3 content - but unit 4 is still brilliant, and very interesting to learn. I wouldn't say unit 4 is easier, but some people might find that to be the case; just as with unit 3, there's a lot of knowledge that you'll need to process (just wait till pedigrees haha).
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I've gone through a couple of papers and I've seen a few qs come up on describing what happens at a particular stage of aerobic cellular respiration. Could someone please check if these are sufficient
Glycolysis:
- In the cytosol of the cell, a glucose molecule is broken down into two 3-C pyruvic acid molecules.
- H+ ions from the glucose molecule are collected by NAD+ to form NADH.
- 2 ATP molecules are produced.
Krebs Citric Acid Cycle:
- At the matrix of mitochondria, the pyruvate molecules are converted to acetyl coA, where 1 CO2 molecule is released per pyruvate molecule.
- The acetyl coA then enters the Krebs Cycle, further releasing CO2. Altogether, 6 CO2 molecules are released in the Krebs Cycle.
- FADH2 and NADH are formed in Krebs Cycle.
- 2 ATP molecules are produced per glucose molecule.
Electron Transport Chain:
- Electrons in FADH2 and NADH are carried by cytochromes through the electron transport chain.
- The energy that is released is used to drive the formation of 32-34 ATP molecules.
- The cytochromes deliver the electrons to oxygen, which then picks up two H+ ions to form H2O, a by-product.
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I've gone through a couple of papers and I've seen a few qs come up on describing what happens at a particular stage of aerobic cellular respiration. Could someone please check if these are sufficient
Glycolysis:
- In the cytosol of the cell, a glucose molecule is broken down into two 3-C pyruvic acid molecules.
- H+ ions from the glucose molecule are collected by NAD+ to form NADH.
- 2 ATP molecules are produced.
Krebs Citric Acid Cycle:
- At the matrix of mitochondria, the pyruvate molecules are converted to acetyl coA, where 1 CO2 molecule is released per pyruvate molecule.
- The acetyl coA then enters the Krebs Cycle, further releasing CO2. Altogether, 6 CO2 molecules are released in the Krebs Cycle.
- FADH2 and NADH are formed in Krebs Cycle.
- 2 ATP molecules are produced per glucose molecule.
Electron Transport Chain:
- Electrons in FADH2 and NADH are carried by cytochromes through the electron transport chain.
- The energy that is released is used to drive the formation of 32-34 ATP molecules.
- The cytochromes deliver the electrons to oxygen, which then picks up two H+ ions to form H2O, a by-product.
Just a few things...
Glycolysis
- Electrons are also accepted by NAD+
- 4 ATP molecules are produced by the pay-off phase and 2 are consumed by the preparatory phase. Therefore a net production of 2 ATP molecules
Krebs cycle
- At VCE level, pyruvate decarboxylation (reactions by which pyruvate is converted to acetyl Co-A) is considered part of the Krebs cycle
- 3 CO2 per pyruvate molecule - two from the cycle itself and one from pyruvate decarboxylation
Electron transport chain and oxidative phosphorylation
- Not all of the proteins in the electron transport chain are cytochromes. I don't think you'd be penalised for what you wrote though
- The electron transport chain doesn't really "deliver" the electrons to O2 - they just hang around the end of the chain and are accepted by O2
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Just a few things...
Glycolysis
- Electrons are also accepted by NAD+
- 4 ATP molecules are produced by the pay-off phase and 2 are consumed by the preparatory phase. Therefore a net production of 2 ATP molecules
Would you be penalised for not saying 2 "net" ATPs though? I've never seen any instance yet where such information is really necessary.
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If they ask "how many ATP molecules are produced", the answer 2 is strictly wrong and indicates a misunderstanding of the process, which is why I will always mark it as wrong. If the question is along the lines of "how many ATP molecules are there after glycolysis" then 2 is fine.
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Would you be penalised for not saying 2 "net" ATPs though? I've never seen any instance yet where such information is really necessary.
I doubt you'd get pulled up for it. It's something they might take a mark off for if the exam's on the easy side and they need a better spread
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Are we required to know the historical aspect behind Mendel and his discoveries for the Unit 4 exam? I mean, chapter 10 of Nature of Biology 2 has a large segment devoted to Mendel's findings and all these other scientists. Would it just be best to know about their discoveries. For instance, DNA being double stranded, monohybrid/dihybrid crossing, genes, etc?
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Are we required to know the historical aspect behind Mendel and his discoveries for the Unit 4 exam? I mean, chapter 10 of Nature of Biology 2 has a large segment devoted to Mendel's findings and all these other scientists. Would it just be best to know about their discoveries. For instance, DNA being double stranded, monohybrid/dihybrid crossing, genes, etc?
NOB has a lot of irrelevant stuff. There's nothing on history on the study design and I doubt it's necessary to know.
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NOB has a lot of irrelevant stuff. There's nothing on history on the study design and I doubt it's necessary to know.
Yeah true :) Thanks for that!
How about the Human Genome Project?
And do we only have to know about Genomics & Proteomics for VCE biology?
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Yeah true :) Thanks for that!
How about the Human Genome Project?
And do we only have to know about Genomics & Proteomics for VCE biology?
You don't need to know about the details of the Human Genome project. Distinguishing between genomics and proteomics is about all you'll need to know for this area, I daresay. The study design is very specific about what you need to know, so that'll definitely give you an idea.
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Could someone please check that this is sufficient for an exam question asking us to outline the steps of Transcription and Translation:
Transcription:
- The DNA template strand is copied by RNA polymerase in the nucleus.
- A pre-mRNA molecule is formed and then undergoes post-transcription modification.
- The introns (non-coding regions) are removed by splicing, a poly-A tail is added to the 3' end of the mRNA molecule and a methyl-cap is added to the 5'end of the mRNA molecule.
- The mRNA molecule leaves the nucleus via the nuclear pores, entering the cytoplasm.
Translation:
- The mRNA molecule attaches to the ribosomes, where it is translated.
- tRNA (carrying amino acids) anti-codons attach to complementary mRNA molecules.
- The amino acids are assembled into a particular sequence based upon the pre-defined mRNA codon sequence, synthesising the desired polypeptide.
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VCAA actually asked the transcription last year. I've attached their marking scheme for it.
The translation answer looks good, though you need to emphasise the fact that the mRNA is read at the ribosomes. I think you'd probably have lost a mark on your answer because you haven't clearly started that mRNA's involvement in translation is that it is read at the ribosome. It's not really good enough to say that mRNA is translated at the ribosome if you get what I mean, despite being completely true.
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I doubt you'd get pulled up for it. It's something they might take a mark off for if the exam's on the easy side and they need a better spread
I wouldn't put it past them. These kind of questions are common in Biology. They like the trick question a bit!
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VCAA actually asked the transcription last year. I've attached their marking scheme for it.
The translation answer looks good, though you need to emphasise the fact that the mRNA is read at the ribosomes. I think you'd probably have lost a mark on your answer because you haven't clearly started that mRNA's involvement in translation is that it is read at the ribosome. It's not really good enough to say that mRNA is translated at the ribosome if you get what I mean, despite being completely true.
Okay so would this be better:
Translation:
- mRNA attaches to the ribosome, where it is read and translated.
- tRNA anti-codons attach to the mRNA codons; the tRNA molecules carry amino acids to the ribosomes.
- The amino acids are assembled into a pre-defined sequence to form a desired polypeptide.
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- The ribosomes are assembled into a pre-defined sequence to form a desired polypeptide.
wat
Also tRNA triplets are anticodons
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wat
Also tRNA triplets are anticodons
Err lol I know that I need to learn to check over my responses - I was in the middle of answering a text & writing the response.
I meant the 'amino acids are assembled into a pre-defined sequence to form a desired polypeptide'.
3 concurrent tRNA bases = anti-codon.
3 concurrent mRNA bases = codon
3 concurrent DNA bases = triplet.
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Okay so would this be better:
Translation:
- mRNA attaches to the ribosome, where it is read and translated.
- tRNA codons attach to the mRNA codons; the tRNA molecules carry amino acids to the ribosomes.
- The ribosomes are assembled into a pre-defined sequence to form a desired polypeptide.
As psyxwar has alluded to, you'd probably get in a little bit of trouble with some of the specifics there.
mRNA goes to the ribosome, this is true.
tRNA anticodons are complimentary to the mRNA codons. The tRNA molecule with the complimentary anticodon brings the amino acid it's bound to to the ribosome.
The way the sequence is actually created is by constant repetition of this process. The bond between the amino acid and the tRNA molecule is broken, whilst enzymes make a bond between it and the previous amino acid. The mRNA moves along, and the next codon is (let's say but not technically right) "shown". The tRNA molecule comes along, and we all know what happens there. Keeps on keeping on until the mRNA molecule is done.
It's really, really crappy to describe. But the key points are the mRNA gives the sequence, it's read at the ribosome, tRNA brings the amino acids and has a complimentary anticodon to the mRNA. These are the really key points. The actual mechanism for building the protein isn't well covered in the course.
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As psyxwar has alluded to, you'd probably get in a little bit of trouble with some of the specifics there.
mRNA goes to the ribosome, this is true.
tRNA anticodons are complimentary to the mRNA codons. The tRNA molecule with the complimentary anticodon brings the amino acid it's bound to to the ribosome.
The way the sequence is actually created is by constant repetition of this process. The bond between the amino acid and the tRNA molecule is broken, whilst enzymes make a bond between it and the previous amino acid. The mRNA moves along, and the next codon is (let's say but not technically right) "shown". The tRNA molecule comes along, and we all know what happens there. Keeps on keeping on until the mRNA molecule is done.
It's really, really crappy to describe. But the key points are the mRNA gives the sequence, it's read at the ribosome, tRNA brings the amino acids and has a complimentary anticodon to the mRNA. These are the really key points. The actual mechanism for building the protein isn't well covered in the course.
The assessment report says this from VCAA 2010:
- mRNA is read by the ribosomes.
- tRNA anti-codons attach to mRNA codons.
- A polypeptide is synthesised.
That gained the full marks ^^ I'm going to go with that. Is my transcription summary good though?
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The assessment report says this from VCAA 2010:
- mRNA is read by the ribosomes.
- tRNA anti-codons attach to mRNA codons.
- A polypeptide is synthesised.
That gained the full marks ^^ I'm going to go with that. Is my transcription summary good though?
Good pick-up on that one. That would suffice obviously.
For your transcription answer, looking at the marking scheme you'd have lost a mark for failing to mention complimentary base pairing. It's important to note that the RNA strand is based on the DNA strand, as it really is the underpinning of gene expression. Otherwise, it's fine.
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Good pick-up on that one. That would suffice obviously.
For your transcription answer, looking at the marking scheme you'd have lost a mark for failing to mention complimentary base pairing. It's important to note that the RNA strand is based on the DNA strand, as it really is the underpinning of gene expression. Otherwise, it's fine.
But the marking scheme based upon the 2012 VCAA exam 2 said 'three' of the below and I had mentioned:
- DNA template strand being copied by RNA polymerase.
- pre-mRNA being produced that undergoes post-transcription modification.
- the introns are removed from the mRNA molecule, a poly-A tail is added at the 3'end of the mRNA molecule and a methyl cap is added at the 5'end of the mRNA molecule.
- the mRNA molecule leaves the nucleus.
^Surely my answer has 3 of the parts of the marking scheme?
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But the marking scheme based upon the 2012 VCAA exam 2 said 'three' of the below and I had mentioned:
- DNA template strand being copied by RNA polymerase.
- pre-mRNA being produced that undergoes post-transcription modification.
- the introns are removed from the mRNA molecule, a poly-A tail is added at the 3'end of the mRNA molecule and a methyl cap is added at the 5'end of the mRNA molecule.
- the mRNA molecule leaves the nucleus.
^Surely my answer has 3 of the parts of the marking scheme?
It probably does, but the VCAA marking schemes aren't the full marking schemes. They're a fairly rough guide. I daresay that it being based on the complimentary strand of DNA is a fairly important thing, and it may cost you a mark. Having said that, it may not. I think there's probably reasonable doubt (there is in my mind), so I guess it can be improved!
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It probably does, but the VCAA marking schemes aren't the full marking schemes. They're a fairly rough guide. I daresay that it being based on the complimentary strand of DNA is a fairly important thing, and it may cost you a mark. Having said that, it may not. I think there's probably reasonable doubt (there is in my mind), so I guess it can be improved!
Oh okay then fair enough. I'll mentioned that the pre-mRNA molecule is formed by complementary base pairing. Would I need to add anything to that or would the bolded sentence be sufficient?
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Oh okay then fair enough. I'll mentioned that the pre-mRNA molecule is formed by complementary base pairing. Would I need to add anything to that or would the bolded sentence be sufficient?
That'd be great. It really is nitpicking but it seems as though that's where you're at! :)
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That'd be great. It really is nitpicking but it seems as though that's where you're at! :)
Thanks t-rav. I need the nit-picking. Its those small things that could cost valuable marks! So I'll quickly list transcription and translation again and this is taking everything into consideration.
Transcription:
- The DNA template strand is copied by RNA polymerase.
- The pre-mRNA molecule is formed by complementary base pairing.
- The pre-mRNA molecule undergoes post-transcription modification, where introns are removed, a poly-A tail is added at the 3' end of the mRNA molecule and a methyl cap is added at the 5' end of the mRNA molecule.
- The mRNA molecule leaves the nucleus via the nuclear pores, entering the cytoplasm.
Translation:
- The mRNA molecule is read and translated by the ribosome.
- tRNA anti-codons attach to mRNA codons.
- tRNA molecules carry specific amino acids to the ribosome, where a polypeptide is then synthesised.
Question:
Would it be sufficient to say that the function of RNA polymerase is to copy the template strand of DNA to produce a pre-mRNA molecule, and that it is involved in transcription as an enzyme?
And would these be sufficient:
mRNA:
Carries the genetic code from the nucleus to the ribosomes.
tRNA:
Carries a specific amino acid to the ribosome.
Why is pre-mRNA longer than mRNA?
* pre-mRNA contains both introns and exons.
* Following post-transcription modification, the introns are removed, making the mRNA strand shorter.
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Thanks t-rav. I need the nit-picking. Its those small things that could cost valuable marks! So I'll quickly list transcription and translation again and this is taking everything into consideration.
Transcription:
- The DNA template strand is copied by RNA polymerase.
- The pre-mRNA molecule is formed by complementary base pairing.
- The pre-mRNA molecule undergoes post-transcription modification, where introns are removed, a poly-A tail is added at the 3' end of the mRNA molecule and a methyl cap is added at the 5' end of the mRNA molecule.
- The mRNA molecule leaves the nucleus via the nuclear pores, entering the cytoplasm.
Translation:
- The mRNA molecule is read and translated by the ribosome.
- tRNA anti-codons attach to mRNA codons.
- tRNA molecules carry specific amino acids to the ribosome, where a polypeptide is then synthesised.
Question:
Would it be sufficient to say that the function of RNA polymerase is to copy the template strand of DNA to produce a pre-mRNA molecule, and that it is involved in transcription as an enzyme?
And would these be sufficient:
mRNA:
Carries the genetic code from the nucleus to the ribosomes.
tRNA:
Carries a specific amino acid to the ribosome.
Why is pre-mRNA longer than mRNA?
* pre-mRNA contains both introns and exons.
* Following post-transcription modification, the introns are removed, making the mRNA strand shorter.
That all looks fine. Though you don't need to say the last bit about RNA polymerase. Just that it synthesises pre-mRNA from DNA :)
The remarks about pre-mRNA and mRNA are completely correct too, and I think your definitions of the different RNAs are sufficient as well!
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That all looks fine. Though you don't need to say the last bit about RNA polymerase. Just that it synthesises pre-mRNA from DNA :)
The remarks about pre-mRNA and mRNA are completely correct too, and I think your definitions of the different RNAs are sufficient as well!
Okay fair enough :) Thanks so much!
How much do we need to know in regards to linked genes? Would it be sufficient to know about how the chances of recombinant gametes decreasing the closer the loci of two particular genes?
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Okay fair enough :) Thanks so much!
How much do we need to know in regards to linked genes? Would it be sufficient to know about how the chances of recombinant gametes decreasing the closer the loci of two particular genes?
Hmm I'm not really sure! I can't remember much about linked genes to be honest. I think you'd need to just appreciate how they affect probabilities of certain phenotypes. I'm not entirely sure what you mean by recombinant gametes though?
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How much do we need to know in regards to linked genes? Would it be sufficient to know about how the chances of recombinant gametes decreasing the closer the loci of two particular genes?
You should be familiar with the technique of performing a dihybrid cross with linked genes (as opposed to the more conventional unlinked gene dihybrid cross, which you've likely already covered!).
I don't know if it is still part of the course, but if it is then learn the basic techniques behind gene mapping with linked genes (e.g. distance between two loci relating to probability of recombination).
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You should be familiar with the technique of performing a dihybrid cross with linked genes (as opposed to the more conventional unlinked gene dihybrid cross, which you've likely already covered!).
I don't know if it is still part of the course, but if it is then learn the basic techniques behind gene mapping with linked genes (e.g. distance between two loci relating to probability of recombination).
The first part of what you've said is definitely it. It's all coming back to me now haha
I don't think the second part is relevant though. I never learned it, that's for sure.
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Really? Have a quick read through this, maybe it might be familiar. Though my teacher did teach some content outside of the course for context's sake, luckily :P
http://www.life.illinois.edu/ib/201/lectures/Mapping.pdf
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Really? Have a quick read through this, maybe it might be familiar. Though my teacher did teach some content outside of the course for context's sake, luckily :P
http://www.life.illinois.edu/ib/201/lectures/Mapping.pdf
Yeah, my school wasn't one to teach the whole course let alone stuff outside of it! haha
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I remember I did that once when I was bored in class but I don't think it was relevant to the exam in my day.
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I remember I did that once when I was bored in class but I don't think it was relevant to the exam in my day.
You took the same course as me. And the new course that they've started this year has just been cut down, so I think it's fair to say it's not part of it! :)
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Hey :)
Homologous chromosomes are matching pairs of chromosomes of the same size that carry the same genes. One set is inherited paternally, whilst the other set of the homologous pair is inherited maternally.
^ Is that right? Should I add/remove anything?
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Hey :)
Homologous chromosomes are matching pairs of chromosomes of the same size that carry the same genes. One set is inherited paternally, whilst the other set of the homologous pair is inherited maternally.
^ Is that right? Should I add/remove anything?
Homologous chromosomes:
- carry the same gene loci
- are of the same length
- have the same banding pattern when stained
- have the same centromere position
although I'd say the first one is the most imperative when given such a question. Homologous chromosomes are not necessarily in pairs either (eg. trisomy 21/ DS).
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Homologous chromosomes:
- carry the same gene loci
- are of the same length
- have the same banding pattern when stained
- have the same centromere position
although I'd say the first one is the most imperative when given such a question. Homologous chromosomes are not necessarily in pairs either (eg. trisomy 21/ DS).
Thank you :) But couldn't we say they are normally paired. I mean, trisomy is a genetic mutation, where there is an additional number 21 chromosome, so it isn't normal. Dunno..
So:
Homologous chromosomes are matching pairs of chromosomes of relatively the same length that carry the same gene loci, have the same chromosome banding pattern when stained and have their centromeres located at the same position.
^^ Would that be a fine written explanation?
Thanks!
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Thank you :) But couldn't we say they are normally paired. I mean, trisomy is a genetic mutation, where there is an additional number 21 chromosome, so it isn't normal. Dunno..
So:
Homologous chromosomes are matching pairs of chromosomes of relatively the same length that carry the same gene loci, have the same chromosome banding pattern when stained and have their centromeres located at the same position.
^^ Would that be a fine written explanation?
Thanks!
I'd say it's probably fine to talk about them being matching pairs, but I'm not sure if it's necessary to put it in. I'll need someone who's actually done Unit 4 to clarify that though.
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I'd say it's probably fine to talk about them being matching pairs, but I'm not sure if it's necessary to put it in. I'll need someone who's actually done Unit 4 to clarify that though.
I'd avoid matching pairs too because it isn't correct.
Homologous=same. Homologous chromosomes describes chromosomes that contain the same gene loci, in the same order...though not necessarily the same alleles. Pretty simple way to put it, though sufficient I'd say.
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I'd avoid matching pairs too because it isn't correct.
Homologous=same. Homologous chromosomes describes chromosomes that contain the same gene loci, in the same order...though not necessarily the same alleles. Pretty simple way to put it, though sufficient I'd say.
Okay so homologous chromosomes are chromosomes of roughly the same size that carry identical gene loci, have the same banding when stained and have centromere constrictions at roughly the same locations.
^^ would that be fine - I think thats avoiding the 'matching pairs'..
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Okay so homologous chromosomes are chromosomes of roughly the same size that carry identical gene loci, have the same banding when stained and have centromere constrictions at roughly the same locations.
^^ would that be fine - I think thats avoiding the 'matching pairs'..
It's fine, just take away the roughly :)
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so i have this question from the Melbourne University Drosophila Experiment. It was on my SAC yesterday but i dont know if what i wrote was right or wrong.
Q1.State two limitation that you encountered during the Prac and suggest how these could be overcome in the future.
My answers: - Some flies had escaped during the anesthetizing process which would affect the results giving inaccurate readings. In the
future we should anesthetize the flies in the tube they inhabited.
- Only one person in each group counted the flies which made up our results. This increased the chances of counting errors,
thus possibly leading to inaccurate results. In the future all members of the group should count to ensure correct reading.
Furthermore, results of all schools should have been combined to account for such errors and give an even more accurate
reading as the sample size would have increased.
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so i have this question from the Melbourne University Drosophila Experiment. It was on my SAC yesterday but i dont know if what i wrote was right or wrong.
Q1.State two limitation that you encountered during the Prac and suggest how these could be overcome in the future.
My answers: - Some flies had escaped during the anesthetizing process which would affect the results giving inaccurate readings. In the
future we should anesthetize the flies in the tube they inhabited.
- Only one person in each group counted the flies which made up our results. This increased the chances of counting errors,
thus possibly leading to inaccurate results. In the future all members of the group should count to ensure correct reading.
Furthermore, results of all schools should have been combined to account for such errors and give an even more accurate
reading as the sample size would have increased.
You perhaps should have elaborated on why the missing flies would be a problem. Otherwise though it should be fine I think.
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Could someone please kindly check my stages of mitosis and fix up anything that is necessary. :)
Mitosis refers to the nuclear division of somatic cells which involves the replication of one nucleus into two identical nuclei with identical genetic material and the same number of chromosomes. The purposes of mitosis:
--> The development of an embryo from a zygote, to an embryo and then to a fetus.
--> The repair of damaged or diseased tissue.
--> The replacement of cells that have been killed by apopotosis.
Interphase:
- Interphase is made up of three phases:
* G1 Phase
- Involves the growth of the cell and increase in the number of cell organelles.
- The cell undergoes normal metabolic processes.
* S- Phase:
- DNA replication occurs here.
- This allows for the formation of sister chromatids that join to their identical chromatids at the centromere.
* G2 Phase:
- The second growth phase involves the condensation and supercoiling of the chromatin (DNA + proteins found in the nucleoplasm) into condensed structures called chromosomes.
- The coiling of the DNA molecule into condensed structures called chromosomes is facilitated by histone proteins. (Is it accurate to say that histone proteins facilitate the super-coiling and condensation of DNA into chromosomes?)
- The cell then prepares for mitotic division; chromosomes are now visible using a light microscope.
Prophase:
- The chromosomes continue to thicken and shorten; the chromatids become distinct. Here, the chromosomes are made up of 2 sister chromatids joined at the centromere.
- Nuclear envelope disintegreates.
- In animal cells, centrioles move to opposite poles of the cells are form the spindle fibres. As the spindle fibres form, they attach to the kinetochore proteins found at the centromere of the chromosomes.
Metaphase:
- The chromosomes line up along the equator of the cell; each chromosome is attach to the spindle fibres at the centromere.
Anaphase:
- As the spindle fibre contracts, the sister chromatids are pulled apart at the centromere. One chromatid moves to one pole of the cell, whilst the other chromatid migrates to the opposite pole of the cell. This is called disjunction.
- The spindle fibres then begin to disapppear.
Telophase:
- Two new nuclei are formed, each containing identical genetic material with an equal number of chromosomes ( a diploid set of chromosomes).
- The chromosomes are no longer visible as they uncoil to form the chromatin found in the nucleoplasm.
Cytokinesis:
- Cytokinesis is the division of the cytoplasm; this involves the replication of the organelles and other contents of the cytoplasm.
- In animal cells, a cleavage furrow forms around the cell to separate the two nuclei. In plant cells, a cell plate forms to create the cellulose cell wall deposited over the plasma membrane.
- Two separate somatic cells with a diploid set of chromosomes (i.e. identical diploid set) are formed.
Thanks :)
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Could someone please check my meiosis for accuracy? Thanks!
Interphase:
- G1, S and G2 phase as per mitosis
Prophase I:
- Sister chromatids join up at the centromere, as the chromosomes continue to shorten and thicken.
- Homologous chromosomes pair up and the nuclear membrane begins to disintegrate.
- The spindle fibres form and attach to the chromosomes at the kinetochore structures found at the centromeres.
- Homologous chromosomes form a synapsis; that is, there is an exchange of genetic material that results from part of one chromosome being spliced and exchanged with part of its partner homologoue. The part at which this occurs is called the chiasma.
Metaphase I:
- The formation of the spindle fibres is complete.
- The homologous chromosomes line up along the equator of the cell; independent assortment occurs here. That is, maternal and paternal chromosomes line up independent of other homologous chromosomes.
Anaphase I:
- The spindle fibres contract, pulling apart homologous pairs of chromosomes. That is, one member of the homologous pair moves to one pole of the cell, while the other member moves to the opposite pole of the cell.
- The spindle fibres begin to disappear.
Telophase I:
- Two new nuclei are formed; each nucleus contains a haploid (n) set of chromosomes; however, each chromosome is double stranded (made up of 2 chromatids joined together at the centromere).
- Each nucleus becomes enveloped in a nuclear envelope (double membrane).
- Chromosomes are no longer visible using a light microscope.
Cytokinesis (cytoplasmic division) occurs.
Prophase II:
- The chromosomes begin to thicken, condense and shorten; each chromatid joins up with its sister chromatid at the centromere.
- The nuclear membrane begins to disintegrate and the spindle fibres begin to form.
- The chromosomes attach to the spindle fibres at the kinetochores, located on the centromeres of the chromosomes.
Metaphase II:
- The spindle fibre forms completely.
- The chromosomes line up along the equator of the cell.
Anaphase II:
- The disjunction of sister chromatids at the centromere occurs as a result of the spindle fibres contracting.
- The spindle fibres begin to disappear.
- Each chromatid moves to respective poles of the cell.
Telophase II:
- 4 new nuclei are formed - each nucleus contains a haploid (n) number of chromosomes made up of one chromatid.
- A nuclear envelope forms around each nucleus; that is, a double-membrane forms around each nucleus.
- The chromosomes are no longer visible under a light microscope.
Cytokinesis occurs
- Spermatogenesis - 4 haploid daughter cells (4 sperm cells) are produced.
- Oogenesis - 1 haploid daughter cell (1 ovum) is produced along with 3 polar bodies.
* Sources of variation in meiosis:
- Recombination of DNA
- Independent assortment of chromosomes into 4 nuclei to provide genetic variability in offspring.
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Does transcription start when RNA polymerase binds to the promotor in the upstream (flanking region) of a gene? I mean, is it that once RNA polymerase forms a complex with the promotor, transcription of the DNA template strand occurs?
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Does transcription start when RNA polymerase binds to the promotor in the upstream (flanking region) of a gene? I mean, is it that once RNA polymerase forms a complex with the promotor, transcription of the DNA template strand occurs?
In the traditional sense, yes. Though it's outside of the course.
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I've taken a look at the 2012 assessment report on what they listed as the steps for PCR (Polymerase Chain Reaction). I've added a few things of my own to my explanation. Could someone please check if it is good enough? I've ensured I've covered the points mentioned by VCAA but added a few of my own for a bit more detail. Thanks!
1. The DNA is heated to approximately 95oC; the DNA molecule denatures, and the two complementary polynucleotide strands separate as the hydrogen bonds between the two strands are broken.
2. The DNA is cooled to approximately 50oC; the primer (short, single stranded DNA or RNA molecule made up of 10-20 nucleotides) anneals to the 3' end of the target DNA sequence.
3. The DNA is heated to approximately 72oC; TAQ/DNA polymerase begins to construct the complementary DNA strands indicated by the primer in a 3' to 5' direction.
4. The cycle is repeated to further amplify the quantity of DNA.
Thank you!
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I've taken a look at the 2012 assessment report on what they listed as the steps for PCR (Polymerase Chain Reaction). I've added a few things of my own to my explanation. Could someone please check if it is good enough? I've ensured I've covered the points mentioned by VCAA but added a few of my own for a bit more detail. Thanks!
1. The DNA is heated to approximately 95oC; the DNA molecule denatures, and the two complementary polynucleotide strands separate as the hydrogen bonds between the two strands are broken.
2. The DNA is cooled to approximately 50oC; the primer (short, single stranded DNA or RNA molecule made up of 10-20 nucleotides) anneals to the 3' end of the target DNA sequence.
3. The DNA is heated to approximately 72oC; TAQ/DNA polymerase begins to construct the complementary DNA strands indicated by the primer in a 3' to 5' direction.
4. The cycle is repeated to further amplify the quantity of DNA.
Thank you!
Nothing wrong with it. Remember that PCR does it to both strands. Yours seems to suggest that there's one target strand, but really, that's not particularly important! :)
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Is it accurate to say that male mammals are hemizygous for the X chromosome? Would it be accurate to state that only females can be carriers for autosomal recessive traits because a carrier must be heterozygous (thus have two X chromosomes), and males only have one X chromosomes (hence hemizygous for the X chromosome), rendering them unable to be carriers and instead either affected or not affected by the trait under investigation.
Also, would we need to ever state the genotypic ratio for a dihybrid cross involving two heterozygote parents (for each of the traits - e.g. TtBb). Because there are literally 9 different possible genotypes. The phenotypic ratio for such a cross is much simpler to write.
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Is it accurate to say that male mammals are hemizygous for the X chromosome? Would it be accurate to state that only females can be carriers for autosomal recessive traits because a carrier must be heterozygous (thus have two X chromosomes), and males only have one X chromosomes (hence hemizygous for the X chromosome), rendering them unable to be carriers and instead either affected or not affected by the trait under investigation.
Also, would we need to ever state the genotypic ratio for a dihybrid cross involving two heterozygote parents (for each of the traits - e.g. TtBb). Because there are literally 9 different possible genotypes. The phenotypic ratio for such a cross is much simpler to write.
Hemizygous refers to genotype when it's an X-linked gene and you're talking about a male afaik (rather than homo or hetero as you only have one chromosome actually carrying the gene). I don't think you use it to reference chromosomes, eg. You don't say that females are homozygous for the X
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Also, would we need to ever state the genotypic ratio for a dihybrid cross involving two heterozygote parents (for each of the traits - e.g. TtBb). Because there are literally 9 different possible genotypes. The phenotypic ratio for such a cross is much simpler to write.
Potentially, but it would probably come as a part of drawing a cross. So they would be right in front of them and you would just reiterate them at the bottom. If you mean 'am I expected to know there are x number of this genotype and x number of that genotype off by heart without doing a cross' the answer is no. Just the kind of phenotypic ratio you would have off by heart, if they ask you for the genotypic ratio I'm sure drawing the cross would also be worth some kind of marks and there would be space for that on the page.
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Hemizygous refers to genotype when it's an X-linked gene and you're talking about a male afaik (rather than homo or hetero as you only have one chromosome actually carrying the gene). I don't think you use it to reference chromosomes, eg. You don't say that females are homozygous for the X
Okay I forgot to mention that the trait under investigation was X-linked. So what other way could I say that males are unable to be carriers because in this case, the trait is autosomal recessive, and so females whom are heterozgous (e.g. XHXh) can be carriers, but because males have only one X chromosome, they can either be affected with the trait (XhY) or unaffected (XHY).
Note: h is the allele for the recessive trait and H is the allele for the dominant trait.
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Okay I forgot to mention that the trait under investigation was X-linked. So what other way could I say that males are unable to be carriers because in this case, the trait is autosomal recessive, and so females whom are heterozgous (e.g. XHXh) can be carriers, but because males have only one X chromosome, they can either be affected with the trait (XhY) or unaffected (XHY).
Note: h is the allele for the recessive trait and H is the allele for the dominant trait.
I'm not sure why a male couldn't be a carrier for an autosomal recessive trait? Autosomes are your non-sex chromosomes and both males and females have a homologous pair.
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I'm not sure why a male couldn't be a carrier for an autosomal recessive trait? Autosomes are your non-sex chromosomes and both males and females have a homologous pair.
Edit: X-linked recessive! Sorry I'm so out of it today LOL!
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Does progeny mean offspring?
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Does progeny mean offspring?
yup
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That all looks fine. Though you don't need to say the last bit about RNA polymerase. Just that it synthesises pre-mRNA from DNA :)
The remarks about pre-mRNA and mRNA are completely correct too, and I think your definitions of the different RNAs are sufficient as well!
ok this is going to sound really stupid but i keep getting confused on transcription and translation and dna replication because i keep seeing different notes on it
does anyone have any clear notes pleases
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ok this is going to sound really stupid but i keep getting confused on transcription and translation and dna replication because i keep seeing different notes on it
does anyone have any clear notes pleases
Remember DNA replication as being part of the cell cycle (S-phase of Interphase), and then remember Transcription and Translation as gene expression!
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Remember DNA replication as being part of the cell cycle (S-phase of Interphase), and then remember Transcription and Translation as gene expression!
whats gene expresssion?
and does dna replication come first?
where do all the enzymes come in ?
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Gene expression is exactly what it sounds like: transcribing a gene to give an mRNA and translating the mRNA to give a protein is gene expression. To remember the difference, remember that translation comes later than transcription.
DNA replication does not come 'first' because it's not related to gene expression. DNA replication exists to make a copy of the genome right before a cell divides. Most cells in your body don't replicate (much) anymore but for as long as they live they need to keep expressing genes because proteins are the functional components of the cell that allow it to carry out its role in the body. So think of DNA replication and transcription/translation as separate entities even though the processes are somewhat similar.
Which enzymes are you talking about? DNA replication involves a DNA polymerase (ie, something that makes DNA) while transcription involves an RNA polymerase (ie, something that makes RNA). The only protein you should need to know about for translation is RNA polymerase (and potentially activators or repressors since you were asking about those in another thread). Most all other enzymes you will discuss (primase, ligase, helicase, topoisomerases) are involved in replication.
RNA polymerase does not require a helicase to open DNA, it can do this itself. RNA polymerase also doesn't require a primer so there would be no primase involved in transcription.
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whats gene expresssion?
and does dna replication come first?
where do all the enzymes come in ?
Genes are units of DNA that encode the set of genetic instructions to synthesise particular polypeptides. It is through these polypeptides (e.g. Enzymes) that a particular gene, for instance, eye colour, is expressed in appropriate regions of the body (in this case, the eyes). It's really alluding to protein synthesis, which involes the 2 stages:
1.) Transcription - where the template (antisense) strand of DNA is tramscribed to form mRNA.
2.) Translation - the mRNA is translated to synthesise a particular polypeptide.
DNA replication is part of the cell cycle - during the S-phase of interphase, the genetic material duplicates so that the genetic material can be divided into two diploid somatic cells in mitosis or recombined and assorted into 4 nuclei during meiosis.
The function of an enzyme is to increase the rate of a reaction by lowering its activation energy. So, the enzymes you should know about for DNA replication are:
* DNA helicase (unravels the double-helix DNA molecule and separates the two polynucleotide strands by breaking the weak hydrogen bonds between them).
* DNA polymerase which collects free DNA nucleotides and builds the complementary DNA strands according to the complementary base pairing rule.
The enzymes in Transcription:
* RNA polymerase that builds the pre-mRNA molecule using the DNA template strand, funnily enough, as a template, and building that pre-mRNA using collected RNA nucleotides which attach to complementary base pairs.
* Ligase - during post transcriptional modification, once introns and sometimes exons are removed, the remaining exons are joined by ligase enzymes to form a continuous mRNA strand.
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thanks both of you
I feel like an idiot but I get it now
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thanks both of you
I feel like an idiot but I get it now
You're not an idiot :) You're smart for asking a question you need an answer to and therefore consolidating it! Don't be hard on yourself!
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thanks both of you
I feel like an idiot but I get it now
Better to feel like an idiot here than on the exam right? :)
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Haha don't worry you're not an idiot. I got a 50 in Biology and I started off asking the same question about how replication and gene expression would tie together but they really need to be treated as separate but similar processes imo. Learning is best helped by clarification!
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Haha don't worry you're not an idiot. I got a 50 in Biology and I started off asking the same question about how replication and gene expression would tie together but they really need to be treated as separate but similar processes imo. Learning is best helped by clarification!
I love when the questions start off with "well this is probably a stupid question but..." then by the end of it I'm left thinking "oh god, I got a 43 and I'm studying BIOmedicine and I don't even know that".
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I'm studying Photosynthesis and I was wondering if someone could check whether my descriptions of photosynthesis are accurate. Thanks :)
Light-dependent Stage:
- Chlorophyll molecules absorb light energy.
- A H2O molecule is split into H+ ions and O2.
- ATP is formed from ADP + Pi.
- NADP molecules collect H+ ions to form NADPH+ molecules.
Light-independent stage:
- CO2 reacts with H+ ions provided by NADPH+ to synthesis glucose.
- ATP provides energy to synthesise glucose.
- A H2O molecule is formed when H+ ions are accepted by oxygen atoms.
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I'm studying Photosynthesis and I was wondering if someone could check whether my descriptions of photosynthesis are accurate. Thanks :)
Light-dependent Stage:
- Chlorophyll molecules absorb light energy.
- A H2O molecule is split into H+ ions and O2.
- ATP is formed from ADP + Pi.
- NADP+ molecules collect H+ ions to form NADPH molecules.
Light-independent stage:
- CO2 reacts with H+ ions provided by NADPH to synthesis glucose.
- ATP provides energy to synthesise glucose.
- A H2O molecule is formed when H+ ions are accepted by oxygen atoms.
remember that when the CO2 is split, the carbon is used in synthesising the glucose (obviously 6-C are needed) aka carbon fixation
light dependant- grana (contains chlorophyll, accessory pigments)
light independant - stroma (contains necessary enzymes)
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remember that when the CO2 is split, the carbon is used in synthesising the glucose (obviously 6-C are needed) aka carbon fixation
light dependant- grana (contains chlorophyll, accessory pigments)
light independant - stroma (contains necessary enzymes)
Yeah I figured.
Carbon fixation is required to reduce carbon dioxide from its highly oxidised state as carbon dioxide and reduce it to carbon that can be used to synthesise organic glucose.
Carbon Fixation:
* CO2 reacts with RuBP (ribulose bi-phosphate) to form a unstable 6-C compound. The reaction between carbon dioxide and ribulose bi-phosphate is catalysed by RuBisCO.
* The unstable 6-C compound splits into two 3-C compounds.
* Once of these 3-C compounds continues through the Calvin-Benson Cycle, while the other 3-C compound leaves the cycle and eventually becomes organic glucose.
Light-Dependent Stage occurs in the grana of the chloroplast organelle, while the Light-Independent Stage occurs in the stroma of the chloroplast. Grana are stacks of thylakoid-membrane bound discs that contain chlorophyll and other accessory pigments. The stroma refers to the gel-like matrix that surrounds the grana and is rich in dissolved enzymes.
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Yeah I figured.
Carbon fixation is required to reduce carbon dioxide from its highly oxidised state as carbon dioxide and reduce it to carbon that can be used to synthesise organic glucose.
Carbon Fixation:
* CO2 reacts with RuBP (ribulose bi-phosphate) to form a unstable 6-C compound. The reaction between carbon dioxide and ribulose bi-phosphate is catalysed by RuBisCO.
* The unstable 6-C compound splits into two 3-C compounds.
* Once of these 3-C compounds continues through the Calvin-Benson Cycle, while the other 3-C compound leaves the cycle and eventually becomes organic glucose.
Light-Dependent Stage occurs in the grana of the chloroplast organelle, while the Light-Independent Stage occurs in the stroma of the chloroplast. Grana are stacks of thylakoid-membrane bound discs that contain chlorophyll and other accessory pigments. The stroma refers to the gel-like matrix that surrounds the grana and is rich in dissolved enzymes.
I don't think you need such an extensive knowledge about carbon fixation, as long as you know the inputs/outputs of each stage (which you seem to know well), you should be fine.
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I don't think you need such an extensive knowledge about carbon fixation, as long as you know the inputs/outputs of each stage (which you seem to know well), you should be fine.
I agree. Though of course it can be handy if you do know the full process to remember the other things :)
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Hey guys, I have a question, : what could possibly pop up in the DNA manipulation SAC?
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Hey guys, I have a question, : what could possibly pop up in the DNA manipulation SAC?
Gene cloning, restriction enzymes, ligation, gel electrophoresis, PCR.
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PCR and gel electrophoresis for forensic investigations is pretty common
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fe, thank-You :) :) :) :)
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Hey guys, I just have 2 more questions, any help would be really great :-[ :)
Q1:our class had a SAC today in which we performed electrophoresis on DNA fragments from certain similar species of glofishes but from different countries, and then there was a question, "by seeing the results of electrophoresis, what can you state about the origins of the glofishes?" and I was not sure what to write for that?
Results:
(-) (+)
Standard Fish :: ] ] ] ]
Control Fish :: ] ] ]
---------- Fish 1 :: ] ] ] ]
---------- Fish 2 :: ] ] ] ]
---------- Fish 3 :: ] ] ] ]
---------- Fish 4 :: ] ] ] ]
WHERE ] REPRESENTS A BAND
....
So my question is, what would be an appropriate answer for the origins of the fishes?
Q2: "How would you isolate a COPY of a gene? List 2 ways."
I wrote PCR or Gene Cloning, as I focused more on the word COPY, but now I'm confused because I remembered the word ISOLATE....
Thanks
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Hey guys, I just have 2 more questions, any help would be really great :-[ :)
Q1:our class had a SAC today in which we performed electrophoresis on DNA fragments from certain similar species of glofishes but from different countries, and then there was a question, "by seeing the results of electrophoresis, what can you state about the origins of the glofishes?" and I was not sure what to write for that?
Results:
(-) (+)
Standard Fish :: ] ] ] ]
Control Fish :: ] ] ]
---------- Fish 1 :: ] ] ] ]
---------- Fish 2 :: ] ] ] ]
---------- Fish 3 :: ] ] ] ]
---------- Fish 4 :: ] ] ] ]
WHERE ] REPRESENTS A BAND
....
So my question is, what would be an appropriate answer for the origins of the fishes?
Q2: "How would you isolate a COPY of a gene? List 2 ways."
I wrote PCR or Gene Cloning, as I focused more on the word COPY, but now I'm confused because I remembered the word ISOLATE....
Thanks
Based on the bands being extremely similar, this suggests that they are genetically identical and so have originated from the same fertilised egg. Their genome would be the same, and thus, separating DNA fragments by electrophoresis would yield the same results.
^ Someone should clarify if my reasoning is right though :)
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Yeah (thanks for replying though :) ) based on the similarity, I also stated that they must have originated from the same ancestors, how-ever if someone could clarify this, it would be great :) ....
Also, please do answer the second question :)
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Yeah (thanks for replying though :) ) based on the similarity, I also stated that they must have originated from the same ancestors, how-ever if someone could clarify this, it would be great :) ....
Also, please do answer the second question :)
What DNA fragments were used? I wouldn't say ancestral because there would be some genetic variability over time. Again, I could be wrong.
PCR and Gene cloning sound like good ways to isolate multiple copies of a gene. Of course, a restriction endonuclease would cut & isolate a particular gene, and then multiple copies of the gene, that is isolated, would then be made.
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I wouldn't say ancestral because there would be some genetic variability over time. Again, I could be wrong.
It really depends on the trait. I haven't really got the time to have a proper look into the question you're doing, but just as a relevant aside.
Whether or not there is a lot of variability in particular genes really depends on the gene that you're looking at. If the gene codes for a limb (let's pretend there's only one for a second) then you could expect variability, as minor changes are unlikely to impact the survival of the organism that much. As we know, over time minor changes become big changes. If the gene coded for, for example, something to do with the metabolism of the cell, you can expect a much smaller amount of variation even between species with a fairly distant ancestor. This is because minor changes really do make a massive difference. So it really depends on what the gene does and whether selection will wipe out the mutations quickly or not.
Think about it like a car. Replace a seat cover, no biggie. Replace the gear box, we may have a problem.
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At different times of the year, members of a population of water fleas vary in the size and shape of their outer head covering. Suggest a reason for this.
Some help please? Thanks
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My guess would be that the head shape is varying with the seasons, or with the mating cycle, and hence is motivated by changing temperatures, changing diets or sexual selection. Different head shapes might have different properties in terms of heat loss, catching prey or finding a mate and reproducing.
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My guess would be that the head shape is varying with the seasons, or with the mating cycle, and hence is motivated by changing temperatures, changing diets or sexual selection. Different head shapes might have different properties in terms of heat loss, catching prey or finding a mate and reproducing.
I was thinking on the lines of heat loss and surface area to volume ratio of their heads affecting heat loss and containment during various seasons of the year.
Thanks!
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I was thinking on the lines of heat loss and surface area to volume ratio of their heads affecting heat loss and containment during various seasons of the year.
Thanks!
With these kind of questions the answer just needs to be reasonable. I can't think of any additional ones to SocialRhubarb's, so all of them are fine I daresay! As long as you can justify it.
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DO we have to know about the Hardy-Weinberg Equilibrium?
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Yep! It useful to know how to calculate allele frequency etc
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Yep! It useful to know how to calculate allele frequency etc
Should we just know how to interpret a graph? Or I mean, what else should we know about it?
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Know how to interpret graphs to a basic extent. Understand the equation and how it can be used to calculate allele and genotype frequencies from it too :)
(This is what I was taught in VCE, not sure if its actually in the course - but it certainly helps in understanding population dynamics etc)
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DO we have to know about the Hardy-Weinberg Equilibrium?
Absolutely do not need to know HW Equilibrium. It is not in the course.
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Is a selecting agent the same thing as a selection pressure?
And is it accurate to state that members of a population with a high genetic fitness have a selective advantage to members of the same population with a low genetic fitness?
Thanks!
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Is a selecting agent the same thing as a selection pressure?
And is it accurate to state that members of a population with a high genetic fitness have a selective advantage to members of the same population with a low genetic fitness?
Thanks!
Essentially. They're slightly different, but the difference I don't think is particularly important. Intuitively, selective agent is the thing doing the selecting, selection pressure is the thing causing selection. In most cases, you'll find that these are identical.
I'd be weary about using the term genetic fitness. Like I said in my previous post on this, HW equilibrium is not part of the course and language like genetic fitness is very typical of population genetics, something that isn't explicitly studied in the course. You'd be better to go with selective advantage. And you will not be asked things about heterozygous advantage and so on. The questions will not require a level of complexity such that you need to talk about things like genetic fitness.
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Essentially. They're slightly different, but the difference I don't think is particularly important. Intuitively, selective agent is the thing doing the selecting, selection pressure is the thing causing selection. In most cases, you'll find that these are identical.
I'd be weary about using the term genetic fitness. Like I said in my previous post on this, HW equilibrium is not part of the course and language like genetic fitness is very typical of population genetics, something that isn't explicitly studied in the course. You'd be better to go with selective advantage. And you will not be asked things about heterozygous advantage and so on. The questions will not require a level of complexity such that you need to talk about things like genetic fitness.
Fair enough :) Thanks for the heads up. Could someone check whether my definitions are correct
Gene pool:
Refers to the total genetic material of a population, in a given environment.
Fitness:/b]
A measure of genetic contribution to the next generation of a particular phenotype compared to other phenotypes controlled by the same gene.
Selective advantage:
A higher genetic fitness of one phenotype relative to other phenotypes in a given environment, of a trait controlled by the same gene.
Selecting agent:
An environmental factor that acts differentially on various phenotypes in a given population.
Allele frequency:
The frequency of a particular alleles in a given population, living in a given environment.
Phenotype Frequency:
The frequency of particular phenotypes in a population, living in a given environment.
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Essentially. They're slightly different, but the difference I don't think is particularly important. Intuitively, selective agent is the thing doing the selecting, selection pressure is the thing causing selection. In most cases, you'll find that these are identical.
so in the example of the industrial revolution and moths and all that (hopefully you're all familiar with this example lol...):
The selecting agent would be the change in the color of the tree trunks (due to all the soot from the industrial revolution)
The selecting pressure would be predators of the moths (eg. birds), which would be killing of those who expressed phenotypes that did not camouflage them well in these new conditions.
Is that right?
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so in the example of the industrial revolution and moths and all that (hopefully you're all familiar with this example lol...):
The selecting agent would be the change in the color of the tree trunks (due to all the soot from the industrial revolution)
The selecting pressure would be predators of the moths (eg. birds), which would be killing of those who expressed phenotypes that did not camouflage them well in these new conditions.
Is that right?
I don't think so. It's kind of a tricky one, so I've done a little bit of googling to try and get it straight in my head. In most cases they're essentially synonyms.
In the case of the moths:
The selection agent is predation, the selective pressure is to avoid predation. So the fact that the birds want to eat the moths (agent) will increase the frequency of the wildtype allele (because of the selective pressure of the predation).
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I don't think so. It's kind of a tricky one, so I've done a little bit of googling to try and get it straight in my head. In most cases they're essentially synonyms.
In the case of the moths:
The selection agent is predation, the selective pressure is to avoid predation. So the fact that the birds want to eat the moths (agent) will increase the frequency of the wildtype allele (because of the selective pressure of the predation).
For VCE Bio, are we expected to know the difference between selective pressure and selective agent?
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Yes, because examiners have historically been very picky with terminology. You will lose marks if you call a pressure an agent, and vice versa.
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Yes, because examiners have historically been very picky with terminology. You will lose marks if you call a pressure an agent, and vice versa.
Selecting pressure causes the selection, selection agent is what does the selecting.
E.g. Tall plants vs short plants
Tall plant phenotype is favourable over short plant phenotype due to taller plants being able to photosynthesise more effectively.
Selecting agent: Light intensity
Selection pressure: Increased photosynthetic rate of the tall plants
^ Could someone please fix that up. I'm pretty sure its wrong, but I'd just like someone to explain what the right answers are and why.
Thanks :)
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Yes, because examiners have historically been very picky with terminology. You will lose marks if you call a pressure an agent, and vice versa.
Was my definition right?
Selecting pressure causes the selection, selection agent is what does the selecting.
E.g. Tall plants vs short plants
Tall plant phenotype is favourable over short plant phenotype due to taller plants being able to photosynthesise more effectively.
Selecting agent: Light intensity
Selection pressure: Increased photosynthetic rate of the tall plants
^ Could someone please fix that up. I'm pretty sure its wrong, but I'd just like someone to explain what the right answers are and why.
Thanks :)
Assuming what I said was correct.
The agent is correct, the pressure is to harvest more energy from it though. The pressure isn't the result, it's the thing that's "pressuring" selection to occur.
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The selecting agent exerts the pressure on the population, if that helps clarify things. The agent selects for or against a phenotype; the pressure is what results from that.
Edit: t-rav, I'm not confident that your definition is correct. I'd say that the selection agent is the bird, and the selection pressure is predation.
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The selecting agent exerts the pressure on the population, if that helps clarify things. The agent selects for or against a phenotype; the pressure is what results from that.
Edit: t-rav, I'm not confident that your definition is correct. I'd say that the selection agent is the bird, and the selection pressure is predation.
I think what we've clearly got here is that the difference is bloody tricky.
I just had a quick look at a textbook and it said "the selective agent is the environmental or biotic factor that causes selection to occur", and gave climate change, predation and bacteria/viruses as examples.
Another source though, which was a journal article, gave a really specific selective agent, it was an antibiotic.
So now I've got no idea :| haha!
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I'd go with the journal hahaha, probably a bit more reliable and reviewed than a textbook in most cases :P
I tend to think of selecting agents as entities, and selecting pressures as occurrences/events. It fits to most credible definitions that I see, an it helps draw a distinction between the two
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I'd go with the journal hahaha, probably a bit more reliable and reviewed than a textbook in most cases :P
I tend to think of selecting agents as entities, and selecting pressures as occurrences/events. It fits to most credible definitions that I see, an it helps draw a distinction between the two
Selection pressure: constraints upon phenotype from the environment that produce differential gene transmission.
That's from the penguin dictionary of Biology. To be honest though, it's a relatively unclear definition and there's nothing provided for agent.
In my opinion, selective agent is factor that results in selection and the selective pressure is the effect of that factor upon the organism, in terms of gene transmission. So with that, back to the moths, predation is both the pressure and the agent, to some extent. I think in most cases they're just accepted as being the same thing to be honest. The distinct lack of resources that Google seems to shoot back suggests that there probably isn't a significant difference, if any.
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haha we biologists have more important things to worry about :P
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haha we biologists have more important things to worry about :P
Hahah exactly. I kind of got half way through the last reply and thought "actually, who gives a shit?".
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Okay so just clarifying a couple of things:
A selecting agent is a biotic or abiotic factor that selects for or against a particular phenotype in a population, living in a given environment. Selection pressure is exerted upon a population living in a given environment, by the selecting agent.
Also, do we have to know the three different forms of natural selection:
(a) Directional selection
(b) Stabilising selection
(c) Disruptive selection
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Okay so just clarifying a couple of things:
A selecting agent is a biotic or abiotic factor that selects for or against a particular phenotype in a population, living in a given environment. Selection pressure is exerted upon a population living in a given environment, by the selecting agent.
Also, do we have to know the three different forms of natural selection:
(a) Directional selection
(b) Stabilising selection
(c) Disruptive selection
I agree with that definition, though there is very little difference between the two, if there is even a difference at all.
You don't need to know about the different types of selection. As I've said, you're not expected to understand population genetics. As an aside though, I think you'd enjoy what we're doing in maths at the moment (which is all about that!).
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In terms of a historical basis, how much should I know about the Darwin-Wallace theory of evolution by natural selection other than the fact that it is a theory that agents of selection act differentially on different phenotypes present amongst members of a population, without any human intervention?
Should I know about how this theory of evolution compares with other theories - for instance, that Darwinism provides a substantial means by which evolution can occur, and also that Darwinism explains how evolution is a change in the genetic composition of a population over many successive generations, opposed to evolution occurring in just one or few members of a population in a short period of time?
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In terms of a historical basis, how much should I know about the Darwin-Wallace theory of evolution by natural selection other than the fact that it is a theory that agents of selection act differentially on different phenotypes present amongst members of a population, without any human intervention?
Should I know about how this theory of evolution compares with other theories - for instance, that Darwinism provides a substantial means by which evolution can occur, and also that Darwinism explains how evolution is a change in the genetic composition of a population over many successive generations, opposed to evolution occurring in just one or few members of a population in a short period of time?
You should understand the key concepts and postulates of the Darwin-Wallace theory, but the historical context is just there because textbooks love to pretend that they're fancy.
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You should understand the key concepts and postulates of the Darwin-Wallace theory, but the historical context is just there because textbooks love to pretend that they're fancy.
Thanks for that!
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Thanks for that!
You can buy the chapter from Origin of Species about natural selection (It's called On Natural Selection) as one of those penguin classics. It's a good read. Darwin's quite funny really. He's just like a dotting old man who really loves his flowers hahah. That and he uses the words progeny, genera and commonest all the time...it's just so British.
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You can buy the chapter from Origin of Species about natural selection (It's called On Natural Selection) as one of those penguin classics. It's a good read. Darwin's quite funny really. He's just like a dotting old man who really loves his flowers hahah. That and he uses the words progeny, genera and commonest all the time...it's just so British.
I recently bought the penguin classics version of On the Origin of Species. Not necessary for VCE, but if you have any spare time, it's a brilliant read, as t-rav says.
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Could someone verify whether my knowledge of sticky ends/ blunt ends is accurate?
Sticky ends are cut, DNA fragments with overhanging (exposed) nitrogenous bases, formed when a restriction enzyme cuts a strand of DNA at a diagonal to its complementary strand.
Blunt ends are cut, DNA fragments with no overhanging (exposed) nitrogenous bases, formed when a restriction enzyme cuts two complementary DNA polynucleotide strands at the same location.
Also, would it be useful to mention that restriction enzymes cut at a restriction site, which is in fact located in a specific recognition sequence? It's just because from what I understand, a restriction sequence is a sequence of DNA of about 4-8 nitrogenous bases that a restriction endonuclease recognises. Then, within that recognition, is a restriction site where the restriction enzyme actually cuts. What I'm trying to say is that it may be useful to distinguish between a recognition sequence and a restriction site.
Thanks!
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Could someone verify whether my knowledge of sticky ends/ blunt ends is accurate?
Sticky ends are cut, DNA fragments with overhanging (exposed) nitrogenous bases, formed when a restriction enzyme cuts a strand of DNA at a diagonal to its complementary strand.
Blunt ends are cut, DNA fragments with no overhanging (exposed) nitrogenous bases, formed when a restriction enzyme cuts two complementary DNA polynucleotide strands at the same location.
Also, would it be useful to mention that restriction enzymes cut at a restriction site, which is in fact located in a specific recognition sequence? It's just because from what I understand, a restriction sequence is a sequence of DNA of about 4-8 nitrogenous bases that a restriction endonuclease recognises. Then, within that recognition, is a restriction site where the restriction enzyme actually cuts. What I'm trying to say is that it may be useful to distinguish between a recognition sequence and a restriction site.
Thanks!
yes to all
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yes to all
Thanks so much :)
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Are the following descriptions for each step of PCR correct? Thanks
(1) DNA is heated to 95oC for 2 minutes; the DNA molecule denatures, breaking the hydrogen bonds between the two polynucleotide strands and dissociating the DNA molecule.
(2) DNA is subject to 55oC for 2 minutes; a primer (synthetic, single strand of DNA or RNA) anneals (hybridises) to the 3' end of the single DNA strands by complementary base pairing.
(3) DNA is heated to 72oC for 1 minute; the primer is extended by taq polymerase ( a type of DNA polymerase), which collects free DNA nucleotides to construct complementary polynucleotide strands to the target sequence.
(4) The cycle is repeated.
Is it accurate to say the following about primers:
- A primer is a synthetic, single strand of DNA or RNA that brackets the target DNA sequence that scientists wish to amplify.
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Are the following descriptions for each step of PCR correct? Thanks
(1) DNA is heated to 95oC for 2 minutes; the DNA molecule denatures, breaking the hydrogen bonds between the two polynucleotide strands and dissociating the DNA molecule.
(2) DNA is subject to 55oC for 2 minutes; a primer (synthetic, single strand of DNA or RNA) anneals (hybridises) to the 3' end of the single DNA strands by complementary base pairing.
(3) DNA is heated to 72oC for 1 minute; the primer is extended by taq polymerase ( a type of DNA polymerase), which collects free DNA nucleotides to construct complementary polynucleotide strands to the target sequence.
(4) The cycle is repeated.
Is it accurate to say the following about primers:
- A primer is a synthetic, single strand of DNA or RNA that brackets the target DNA sequence that scientists wish to amplify.
I don't think a RNA primer is used in PCR.
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I don't think a RNA primer is used in PCR.
It can be used; its just better to use a DNA primer for stability and DNA primers anneal more efficiently to 3' end of polynucleotide strands than RNA primers.
But I see what you mean :) Thanks!
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It can be used; its just better to use a DNA primer for stability and DNA primers anneal more efficiently to 3' end of polynucleotide strands than RNA primers.
But I see what you mean :) Thanks!
also, I think you'd have to remove it to replace it with DNA nucleotides (using DNA polymerase), which isn't spoken of in PCR
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Can someone please explain what an STR is?
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Short tandem repeats (STRs) are very short pieces of DNA - like, ridiculously short, ~2-6 bp in length. You may have seen them mentioned as microsatellites when studying PCR or DNA fingerprinting. Basically, we can use these STRs for many, many forms of DNA amplification for multitude purposes. In PCR, the microsatellite/STR is what allows for the extension of existing nucleotide sequences.
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Short tandem repeats (STRs) are very short pieces of DNA - like, ridiculously short, ~2-6 bp in length. You may have seen them mentioned as microsatellites when studying PCR or DNA fingerprinting. Basically, we can use these STRs for many, many forms of DNA amplification for multitude purposes. In PCR, the microsatellite/STR is what allows for the extension of existing nucleotide sequences.
They're also extremely helpful in forensics, because regions with heaps of STRs tend to be "junk" and thus are highly mutable.
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Do we need to know about the child from Tuang and Lucy the hominin (the fossils)?
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Do we need to know about the child from Tuang and Lucy the hominin (the fossils)?
nope :P
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nope :P
Okay thanks (:
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Sea anemones produce an organic compound called anthopleurine. When eaten by sea slugs, the chemical is released from the sea slug, warning the other anemones that a predator is approaching. Anthopleurine would best be described as a:
(A) Hormone
(B) Pheromone
(C) Trigger Substance
(D) Neurotransmitter
The given answer is B; but pheromones are signalling molecules that act exclusively on members of the same species from which a particular organism released it. So, how could a signalling molecule released by a sea slug and acting upon other anemones be a pheromone? The only explanation I could think of is that the anemone actually releases the anthopleurine as it is being consumed by the sea slug, which acts on other anemones. I chose C by the way :)
Could someone please explain? Thanks
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Anthopleurin is definitely a toxin but it also functions as a pheromone; it's used by anemones to retract their tentacles when a predator is detected. When a predator consumes the anemone, areas of the anemone exposed to the environment contain larger-than-usual amounts of anthopleurin, which is then dispersed to the environment so as to warn other anemones.
As a flowchart summary, the action is anemone --> other anemones (as required by pheromones), where the predator acts as a vehicle for the dispersion of the pheromone.
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Anthopleurin is definitely a toxin but it also functions as a pheromone; it's used by anemones to retract their tentacles when a predator is detected. When a predator consumes the anemone, areas of the anemone exposed to the environment contain larger-than-usual amounts of anthopleurin, which is then dispersed to the environment so as to warn other anemones.
As a flowchart summary, the action is anemone --> other anemones (as required by pheromones), where the predator acts as a vehicle for the dispersion of the pheromone.
Okay yeah I get it :) Thanks alondouek
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Are australopiths and australopithecines the same thing?
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Are australopiths and australopithecines the same thing?
Presumably
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I've completed a unit 3 paper (insight 2010) and I've found that there are many questions where the suggested solutions seem to be different to mine, but I feel mine are still in a way, correct.
For instance, what is acquired immunity?
My answer: Defence against disease that involves the production of antibodies and memory cells in response to a pathogenic agent.
The answer: Defence against pathogenic agents that is mediated by B and T lymphocytes that is specific, has memory and self-non self recognition.
How do I deal with questions like that? How do I know how harsh to be with my marking?
For instance, another question:
What is amylase and what is its relationship with starch?
I answered that: amylase is an enzyme that catalyses the breakdown of starch into glucose sub-units. But I gave myself 1 out of 2 for it because the answer said that starch was its substrate and you needed to indicate that.
I just feel terrible after all these practice exams because a lot of my answers are still right, just not specific enough. Fml I need help :( Thanks for any advice/suggestions
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I've completed a unit 3 paper (insight 2010) and I've found that there are many questions where the suggested solutions seem to be different to mine, but I feel mine are still in a way, correct.
For instance, what is acquired immunity?
My answer: Defence against disease that involves the production of antibodies and memory cells in response to a pathogenic agent.
The answer: Defence against pathogenic agents that is mediated by B and T lymphocytes that is specific, has memory and self-non self recognition.
How do I deal with questions like that? How do I know how harsh to be with my marking?
Their answer is better, as acquired immunity involves both the cell-mediated and humoral responses. Your response pretty much centers on the humoral with antibody production; you don't really touch upon the cell-mediated response, and this might be perceived as a lack of understanding.
tbh just give yourself 0 if there's any doubt. You honestly shouldn't care what you score on trials anyway, so long as you're improving.
What is amylase and what is its relationship with starch?
I answered that: amylase is an enzyme that catalyses the breakdown of starch into glucose sub-units. But I gave myself 1 out of 2 for it because the answer said that starch was its substrate and you needed to indicate that.
Well, saying it acts on amylase is basically saying that starch is its substrate. I wouldn't mention glucose because that's not necessarily correct. Just say it catalyses the breakdown of starch (substrate) into simple sugars.
Actually on second thought it is a 2 mark question and it explicitly mentions its relation to starch, so yeah, guess you had to have the bit about substrate there. Should only be worth a mark tbh...
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Yeah guess your right. I wont worry too much about how much I score on trial exams; I'd much rather improving. Thanks :)
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Just for future reference, glucose and maltose are the products of amylase-catalysed starch hydrolysis
And if you say that amylase acts on starch you are implying that it's the substrate, so you're more than likely going to get the marks
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Just for future reference, glucose and maltose are the products of amylase-catalysed starch hydrolysis
And if you say that amylase acts on starch you are implying that it's the substrate, so you're more than likely going to get the marks
Scooby I started my first official Biology unit 3 exam and I got 87% (65/75), which for 2010 was an A+ - I did the 2010 unit 3 Biology Insight exam. Trying to be as picky as possible, so I gave myself only 1 mark out of 2 for that. Just to be on the safe side, should I avoid mentioning the product of an enzyme-substrate reaction unless it specifies?
Any tips other than actually documenting errors? And is it true that questions tend to be repeated in exams that have been used before? (i.e. structure wise)
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As long as you didn't word your answer in such a way that implied that glucose is the only product, I doubt you'd lose a mark (unless they were looking for you to write maltose as well, which I kinda doubt).
Oh, and try to avoid definitives wherever possible - there's pretty much always going to be an exception, and depending on how much of a hardass your examiner is you may or may not be marked down for it
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Glucose and maltose aren't the only possible products for amylases though, so I'm not sure why you'd be more specific for the sake of specificity anyway
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Yeah for that answer I would have just stuck with:
Amylase is an enzyme that catalyses the breakdown of starch (its substrate).
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Glucose and maltose aren't the only possible products for amylases though, so I'm not sure why you'd be more specific for the sake of specificity anyway
Well, yeah, but I'm just talking about alpha-amylase here
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Can someone help me clarify my understanding of this:
In the blood condition known as Immune Thrombocytopenic Purpura (ITP), the immune system destroys platelets in the blood but does not damage the cells in the bone marrow that manufacture them. Since the blood platelets are always low in number, the cells in the bone marrow of ITP sufferers are continually stimulated in the feedback loop.
ITP is an example of:
(a) an allergic disorder
(b) a hypersensitivity
(c) an immune deficiency
(d) an autoimmune disease
I answered C, but the answer is D. I answered C because it mentions that the cells in the bone marrow that produce the platelets are not damaged. An autoimmune disease is an immune deficiency where the self-non self recognition is deficient and as a result, are attacked and destroyed as an immune defence mechanism.
Can someone please clarify this? Thanks
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Can someone help me clarify my understanding of this:
In the blood condition known as Immune Thrombocytopenic Purpura (ITP), the immune system destroys platelets in the blood but does not damage the cells in the bone marrow that manufacture them. Since the blood platelets are always low in number, the cells in the bone marrow of ITP sufferers are continually stimulated in the feedback loop.
ITP is an example of:
(a) an allergic disorder
(b) a hypersensitivity
(c) an immune deficiency
(d) an autoimmune disease
I answered C, but the answer is D. I answered C because it mentions that the cells in the bone marrow that produce the platelets are not damaged. An autoimmune disease is an immune deficiency where the self-non self recognition is deficient and as a result, are attacked and destroyed as an immune defence mechanism.
Can someone please clarify this? Thanks
Immune deficiency is when the immune system loses ability to fight infectious disease. eg. AIDS
Autoimmune disease is when the immune system identifies self cells as non-self and attacks them. eg. Type 1 Diabetes
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Immune deficiency is when the immune system loses ability to fight infectious disease. eg. AIDS
Autoimmune disease is when the immune system identifies self cells as non-self and attacks them. eg. Type 1 Diabetes
Okay then fe :)
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Would the following explanations regarding the levels of molecular organisation of proteins be good?
Primary structure:
Refers to the linear sequence of amino acids of a polypeptide, determined by the coded instructions of DNA.
Secondary structure:
The secondary structure of a protein refers to partial folding of the polypeptide chain as a result of hydrogen bonds forming between H and O atoms in the backbone of the polypeptide, causing the polypeptide folding upon itself.
-Alpha Helix:
Results when tight polypeptide coils are held together by hydrogen bonds at every fourth amino acid.
-Beta-pleated sheet:
Results when regions of a polypeptide chain life parallel to each other, and hydrogen bonds form between parallel parts of the backbone of the polypeptide chain to hold the structure together.
Random coil:
Refers to hydrogen bonds forming as a result of H and O interactions in the backbone of the polypeptide, and folding to form a coiled shape not common to an alpha-helix or beta-pleated sheet.
Tertiary Structure:
Refers to the overall, three-dimensional structure of a protein as a result of the complex molecular shape forming (conformation). The tertiary structure of a protein is formed as a result of interactions between the side chains of a polypeptide. The tertiary structure of a protein is critical to the biological function of the protein.
Quaternary Structure:
Refers to a protein made up of two or more polypeptide chains. The quaternary structure results from the combined overall shape of all linked polypeptide chains.
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Would the following explanations regarding the levels of molecular organisation of proteins be good?
Primary structure:
Refers to the linear sequence of amino acids of a polypeptide, determined by the coded instructions of DNA.
Secondary structure:
The secondary structure of a protein refers to partial folding of the polypeptide chain as a result of hydrogen bonds forming between H and O atoms in the backbone of the polypeptide, causing the polypeptide folding upon itself.
-Alpha Helix:
Results when tight polypeptide coils are held together by hydrogen bonds at every fourth amino acid.
-Beta-pleated sheet:
Results when regions of a polypeptide chain life parallel to each other, and hydrogen bonds form between parallel parts of the backbone of the polypeptide chain to hold the structure together.
Random coil:
Refers to hydrogen bonds forming as a result of H and O interactions in the backbone of the polypeptide, and folding to form a coiled shape not common to an alpha-helix or beta-pleated sheet.
Tertiary Structure:
Refers to the overall, three-dimensional structure of a protein as a result of the complex molecular shape forming (conformation). The tertiary structure of a protein is formed as a result of interactions between the side chains of a polypeptide. The tertiary structure of a protein is critical to the biological function of the protein.
Quaternary Structure:
Refers to a protein made up of two or more polypeptide chains. The quaternary structure results from the combined overall shape of all linked polypeptide chains.
Yup. You don't need that much detail for any of the sub-secondary structures.
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Can someone check if my knowledge of allergies is accurate:
* The immune system comes into contact with an allergen; plasma cells secrete IgE antibodies with antigen-binding sites complementary to the shape of the antigens of the allergen.
* Some of these IgE antibodies bind to the surface of mast cells.
* On a subsequent occasion, when the allergen binds to the IgE antibodies on the surface of mast cells, degranulation of histamine occurs and the release of histamine results in difficulty breathing and other signs and symptoms common to allergies.
Something to add or take off? Thanks!
Do we need to know that a person is sensitised to a particular allergen when immature B-lymphocytes come into contact with the antigens of the allergen?
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Are these good ways of describing the effects of temperatures on enzymes?
At temperatures below the optimum temperature of an enzyme, enzymatic activity is reduced due to less kinetic energy being present, and thus, reduced molecular movement. Hence, there are fewer collisions between enzymes and their substrate molecules, resulting in the decrease of the enzyme's activity rate.
At temperatures above the optimum temperature of an enzyme, the enzyme begins to denature. The active site configuration is permanently altered as a result of disruptions in the bonds forming the active site, preventing the substrate molecules from being able to attach to the enzyme, and thereby decreasing the enzyme's activity rate.
Could someone just add/remove/change anything that needs ammendments ?
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Are these good ways of describing the effects of temperatures on enzymes?
At temperatures below the optimum temperature of an enzyme, enzymatic activity is reduced due to less kinetic energy being present, and thus, reduced molecular movement. Hence, there are fewer collisions between enzymes and their substrate molecules, resulting in the decrease of the enzyme's activity rate.
At temperatures above the optimum temperature of an enzyme, the enzyme begins to denature. The active site configuration is permanently altered as a result of disruptions in the bonds forming the active site, preventing the substrate molecules from being able to attach to the enzyme, and thereby decreasing the enzyme's activity rate.
Could someone just add/remove/change anything that needs ammendments ?
The big issue with these are that they describe enzyme action in terms of chemistry, so you may find that this is beyond the Biology course. In my understanding though, the first is correct, the second is not strictly true.
The reason enzymes do not function as well above optimum temperature is not necessarily related to the denaturation of the enzyme. An enzyme in a human, for example, is not denatured at 38°C for examples, nor is it beginning too. The reason it won't function as well is because the interaction (binding) between the enzyme and its substrate isn't as stable at higher temperatures, probably because higher temperatures deliver enough energy to break that bond.
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The big issue with these are that they describe enzyme action in terms of chemistry, so you may find that this is beyond the Biology course. In my understanding though, the first is correct, the second is not strictly true.
The reason enzymes do not function as well above optimum temperature is not necessarily related to the denaturation of the enzyme. An enzyme in a human, for example, is not denatured at 38°C for examples, nor is it beginning too. The reason it won't function as well is because the interaction (binding) between the enzyme and its substrate isn't as stable at higher temperatures, probably because higher temperatures deliver enough energy to break that bond.
I guess it would depend upon the context of the question and the specification regarding the temperature (and then determining how much higher it is than the optimum temperature of the enzyme). So to be on the safe side, should I just reference the disruptions in bonds holding together the active site subsequently altering the configuration of the active site as a result of heating an enzyme above its temperature optima?
Thanks for your help.
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Could someone check whether my descriptions for each stage of photosynthesis are accurate?
Light-dependent stage:
- In the grana of the chloroplast, light energy is absorbed by chlorophyll molecules.
- Water is split to form H+ ions and oxygen gas.
- ATP is formed from ADP + Pi (i.e. the phosphorylation of ADP)
- NADPH is formed.
Light-independent stage:
- In the stroma of chloroplasts, the Calvin Cycle occurs.
- In the Calvin Cycle, carbon dioxide reacts with H+ (provided by NADPH) to synthesize glucose.
- ATP provides the energy to synthesise the glucose.
I'm trying not to deviate too much from the study design and so that's why I'm trying to simplify it without explaining things like the carbon fixation, etc.
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^you should know that electron transport occurs in light dependent stage. VCAA had a multiple choice question where that knowledge was necessary.
Hence, for light dependent:
-Chlorophyll in grana absorb light energy, exciting their electrons which enter an electron transport chain
-Water is split to replenish chlorophyll's lost electrons, producing H+ and molecular oxygen
-As a product of electron transport, ATP and NADPH are formed, which go to the light independent stage
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^you should know that electron transport occurs in light dependent stage. VCAA had a multiple choice question where that knowledge was necessary.
Hence, for light dependent:
-Chlorophyll in grana absorb light energy, exciting their electrons which enter an electron transport chain
-Water is split to replenish chlorophyll's lost electrons, producing H+ and molecular oxygen
-As a product of electron transport, ATP and NADPH are formed, which go to the light independent stage
Ah I see :) Was light independent okay?
SO Light-dependent:
- In the grana, chlorophyll molecules absorb light energy, exciting electrons that then enter an electron transport chain.
- Water is split to form H+ ions and oxygen gas to compensate for the chlorophyll's lost electrons.
- ATP (ADP is phosphorylated) and NADPH are formed, as a result of the electron transport chain.
- ATP and NADPH go to the light-independent stage.
Thanks!
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I guess it would depend upon the context of the question and the specification regarding the temperature (and then determining how much higher it is than the optimum temperature of the enzyme). So to be on the safe side, should I just reference the disruptions in bonds holding together the active site subsequently altering the configuration of the active site as a result of heating an enzyme above its temperature optima?
Thanks for your help.
I don't think you'll be asked to account for the Chemistry of enzymes in this case. It's not a part of the course.
It is safest to mention both if you were asked about it.
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I don't think you'll be asked to account for the Chemistry of enzymes in this case. It's not a part of the course.
It is safest to mention both if you were asked about it.
I reckon you should know a little bit of enzymatic chemistry, such as how the function by lowering the activation energy of a reaction, and how denaturation affects the chemical structure of the enzyme (it being a protein).
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I reckon you should know a little bit of enzymatic chemistry, such as how the function by lowering the activation energy of a reaction, and how denaturation affects the chemical structure of the enzyme (it being a protein).
Absolutely! Just not in that case I don't think. It's useful to know it, but no biggy if you don't of course.
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Can anyone please help me with these questions from chapter 2 review (Nature of biology book two, fourth edition).
Q5-The folded internal membranes of mitochondria have many stalked particles on their innermost surfaces (figure 2.31). Given the function of mitochondria and where most of the reactions occur, of what advantage might the presence of these particles be for the production of ATP in the organelle?
Q6 In figure 2.31, you may have noted the holes in the folds of the inner membrane of mitochondria. Explain a possible function of these holes
If the first question is referring to the cristae, then it is the increased surface area that allows for greater generation of ATP through the electron transport chain, that the cristae offer.
Q6 holes? These pores in the membrane allow for ATP transport molecules to carry ATP out of the mitochondria and/or these could be the pores through which hydrogen ions are pumped (but that would be more explicit, hard to tell without the diagram)
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Q6 holes? These pores in the membrane allow for ATP transport molecules to carry ATP out of the mitochondria and/or these could be the pores through which hydrogen ions are pumped (but that would be more explicit, hard to tell without the diagram)
They may also hide some ribosomes.
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I think I'm being driven to my destruction.
To describe the function of a restriction enzyme, would it be most accurate to say:
Restriction enzymes catalyse the cutting and isolation of a DNA fragment.
or would it be find to say
Restriction enzymes cut and isolate DNA fragments
Some prac exams solutions say you aren't allocated the marks unless you mention catalysis. I'm being driven mad.
Also, for genetic cross questions asking what the chance of offspring having a particular trait is, this is my template:
- Parental Genotypes
- Punnet Square
- Offspring genotype ratio
- Offspring phenotype ratio
Statement (e.g.): There is a 25% chance that John and Cathy will have a child with blue eyes.
^ Would that be sufficient for an explanation of two parents having a child with a particular trait and the possibility of this?
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Just mention catalysis in case and I would also add to my definition that it cuts at a specific recognition site.
Yes, but I would also always state parental phenotypes before parental genotypes even if they're written in the question. It's kind of like showing your working; usually in the question it will be like a female with brown fur was crossed to a male with white fur and blah blah blah blah and you need to show where you pulled the important info out of the paragraph...I guess it's each to their own though! Just like to be as thorough as possible.
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Yes, but I would also always state parental phenotypes before parental genotypes even if they're written in the question. It's kind of like showing your working; usually in the question it will be like a female with brown fur was crossed to a male with white fur and blah blah blah blah and you need to show where you pulled the important info out of the paragraph...I guess it's each to their own though! Just like to be as thorough as possible.
Thanks for that!
I'm going to construct a log book and put all of this in there!
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Is it correct to say the Second Line of Defence involves recognising 'self' from 'non-self'? Or is that in the 3rd line?
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Yup thats correct, the Second Line does recognise self from non self (E.g phagocytes engulf non self cells)
Is it correct to say the Second Line of Defence involves recognising 'self' from 'non-self'? Or is that in the 3rd line?
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Is it correct to say the Second Line of Defence involves recognising 'self' from 'non-self'? Or is that in the 3rd line?
The second line of defence involves macrophages recognising non-self (foreign) matter, and then binding to, engulfing & eventually destroying this antigen. However, the macrophages do not distinguish between different pathogens in the 2nd line of defence. Instead, they initiate the same response to any type of antigen that they come across, disregarding how often the immune system has come into contact with this pathogen, because there is no immunological retention of memory involved.
So in a sentence, you can say that the second line has self-non self recognition; however, it is the 3rd (adaptive) line of defence that initiates specific responses when exposed to specific pathogens, possessing specific antigenic markers
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This is from Lisa Chem, 2006.
For the 2nd row my answers were as follows:
Carbohydrates ... ... Glucose
I initially thought I could have written proteins but the description provided, "organic catalyst used in glycolysis" suggested it wasn't, as enzymes can't be consumed in a reaction.
But the answers suggested they were, protein and amino acids.
Confused :-\
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This is from Lisa Chem, 2006.
For the 2nd row my answers were as follows:
Carbohydrates ... ... Glucose
I initially thought I could have written proteins but the description provided, "organic catalyst used in glycolysis" suggested it wasn't, as enzymes can't be consumed in a reaction.
But the answers suggested they were, protein and amino acids.
Confused :-\
The wording of that section is wrong; VCAA would have the accurate expression. But the inference to it being a catalyst used in glycolysis should tell you its an enzyme, hence a protein, made up of amino acid subunits.
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In the studydesign it states "disorders of the human immune response including the allergic response and autoimmune diseases"
Does this mean we should only know the details on allergic response and autoimmune disease?
Or must we know all the disorders of the human immune response such as Rhesus incompatibility, immunodeficiency, etc?
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In the studydesign it states "disorders of the human immune response including the allergic response and autoimmune diseases"
Does this mean we should only know the details on allergic response and autoimmune disease?
Or must we know all the disorders of the human immune response such as Rhesus incompatibility, immunodeficiency, etc?
Information about specific examples would be provided within the stem of the question. You should know about the allergic response and autoimmune disease.
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This is from Lisa Chem, 2006.
For the 2nd row my answers were as follows:
Carbohydrates ... ... Glucose
I initially thought I could have written proteins but the description provided, "organic catalyst used in glycolysis" suggested it wasn't, as enzymes can't be consumed in a reaction.
But the answers suggested they were, protein and amino acids.
Confused :-\
Anything that says organic catalyst is referring to an enzyme (or an RNA but that's out of the course). Carbohydrates are the substrates.
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Would it be accurate to say that a regulatory gene is a unit of DNA that codes for a polypeptide, that in turn, regulates the activity of another gene.
Also:
* The leading strand is synthesised continuously in a 5' to 3' direction because the replication fork immediately exposes the leading strand DNA template
* The lagging strand is synthesised discontinuously in a 5' to 3' direction because the replication fork does not immediately expose the lagging strand DNA template. As a result, short okazaki fragments are produced, which are then ligated by DNA ligase to form a continuous polynucleotide strand.
^ Is that accurately expressed?
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Hey guys, how would you infer that lethal alleles are involved within this question,
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Is mRNA longevity just a reference to how long mRNA is able to last? And by regulating mRNA longevity, is energy conserved by the cell? Because if the mRNA lasts a shorter time, then it would not be continually translated and thus polypeptides that are not required will not be produced.
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Few questions:
1) Does interferon just cause cells to produce an enzyme that inhibits the biosynthesis of viral particles, if the virus were to enter the cell?
2) If I were asked to indicate HOW the immune system cells distinguish 'self' from 'non-self', would this be acceptable:
* Cells of the immune system possess receptors that are able to recognise different MHC markers, and thereby be able to distinguish self from non-self.
3) Plant defence mechanisms - should I only know a couple:
E.g. thick (intact) waxy cuticle, hairy epidermal layer, and more active responses like the production of galls to trap pathogens.
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Few questions:
1) Does interferon just cause cells to produce an enzyme that inhibits the biosynthesis of viral particles, if the virus were to enter the cell?
2) If I were asked to indicate HOW the immune system cells distinguish 'self' from 'non-self', would this be acceptable:
* Cells of the immune system possess receptors that are able to recognise different MHC markers, and thereby be able to distinguish self from non-self.
3) Plant defence mechanisms - should I only know a couple:
E.g. thick (intact) waxy cuticle, hairy epidermal layer, and more active responses like the production of galls to trap pathogens.
1. you could say they are antiviral agents
secreted by activated T cells
Their production and secretion is triggered by the presence of double-stranded RNA, which does not occur in uninfected cells
Interferons act by preventing the synthesis of viral RNA and therefore
the produc tion of viral proteins. They have little or no effect on uninfected
cells.
2. sounds good
3. as long as you can apply your knowledge to situations
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secreted by activated T cells
You'd want to avoid definitives. They can also be produced by cells that are affected by a virus in an attempt to warn other cells and hence the production of an anti viral protein coat within non affected cells.
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You don't need to know the specifics of #1 and #2
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Russ is right. All you need to know is that interferons are proteins released by virus-infected cells that trigger surrounding cells to produce anti-viral enzymes
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Definition of reflex arc:
A reflex arc is a pathway of nerves, from a receptor to an effector, that involves the electrical impulse bypassing the brain.
^ Is that accurate? It definitely needs a bit of touching up, so if anyone has anything I could incorporate into that/remove, it would be much appreciated.
Also, would an advantage of a reflex arc over a normal stimulus-response model be that a reflex arc is a rapid response to a stimulus that would minimise tissue damage, in events like touching a hot plate, standing on a pin, etc?
Thanks!
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Definition of reflex arc:
A reflex arc is a pathway of nerves, from a receptor to an effector, that involves the electrical impulse bypassing the brain.
^ Is that accurate? It definitely needs a bit of touching up, so if anyone has anything I could incorporate into that/remove, it would be much appreciated.
Also, would an advantage of a reflex arc over a normal stimulus-response model be that a reflex arc is a rapid response to a stimulus that would minimise tissue damage, in events like touching a hot plate, standing on a pin, etc?
Thanks!
It's a hard one to define, but that should suffice
And yeah, the advantage is speed
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Hey guys, how would you infer that lethal alleles are involved within this question,
We know that 'When the hairy dogs are mated, they tend to produce larger litters and never produce hairless offspring" meaning that they must be homozygous recessive.
The hairless dogs can be either heterozygotes or homozygous dominant.
(but their litters are smaller, which suggests something is different)
if you add up all the hairless offspring, you get 16.
If you add up all the hairy offspring, you get 8.
A ratio of 2:1 hairless to hairy. "Other breeders of Mexican hairless dogs always obtained similar overall ratios." suggests that this 2:1 ratio is reliable.
If you label the hairless dogs as HH, draw a punnet square, you'll see that their offspring will be 100% HH, which we know is not true (due to the difference of the ratio of phenotypes)
If you label the hairless dogs as Hh, draw a punnet square, you'll see that their offspring will be 25% homozygous dominant (HH), 50% heterozygous (Hh), and 25% homozygous recessive (hh). Since we can infer that the genotype of a hairy dog is hh, the genotype of hairless dogs must be Hh. The ratio 2:1 reinforces that HH is a lethal allele.
(apologies if this doesn't help!)
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We know that 'When the hairy dogs are mated, they tend to produce larger litters and never produce hairless offspring" meaning that they must be homozygous recessive.
Alternatively, couldn't they be homozygous dominant? That's where my confusion lies
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Alternatively, couldn't they be homozygous dominant? That's where my confusion lies
(by logic, yes) But not every hairy dog will be homozygous dominant, and if we cross heterozygous and heterozygous, we'll end up with a 25% chance of a hairless offspring, which is untrue.
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(by logic, yes) But not every hairy dog will be homozygous dominant, and if we cross heterozygous and heterozygous, we'll end up with a 25% chance of a hairless offspring, which is untrue.
Ah makes sense, thanks mate :)
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Is the purpose of a dihybrid test cross to determine the genotype of the parent who phenotypically expresses the dominant trait at both gene loci under investigation, AND to determine whether two genes are linked/independently assorted?
Thanks :)
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Is the purpose of a dihybrid test cross to determine the genotype of the parent who phenotypically expresses the dominant trait at both gene loci under investigation, AND to determine whether two genes are linked/independently assorted?
Thanks :)
Yeah, it can be used to do both.
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Yeah, it can be used to do both.
Thank you. Would it be accurate describe independent assortment as pairs of genes being assorted randomly into gametes independent of the behaviour of other genes? That is, considering the genes are unlinked.
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Thank you. Would it be accurate describe independent assortment as pairs of genes being assorted randomly into gametes independent of the behaviour of other genes? That is, considering the genes are unlinked.
It would be a bit more accurate to say that the alleles are assorted randomly, not genes.
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It would be a bit more accurate to say that the alleles are assorted randomly, not genes.
But the genes do independently assort. I mean, we're talking at the chromosome level here, hence, the gene loci they carry. But I see what you mean. I'd probably mention that pairs of genes (alleles) assort independently of other pairs of genes (alleles). That would probably make up for it :) Thanks for the input.
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If you want to be a real pain, it's actually technically the gene loci that assort independently. But yeah, that is an accurate description. It's not accurate to say that the gene loci are on different chromosomes though, because gene loci on the same chromosomes can assort independently, so it is a good definition.
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Do we need to know anything about liposomes other than the fact that they are hollow structures used as vectors in gene therapy? I mean, I know that liposomes wrap around a gene, and with the target cell membrane to deliver the gene into the cell. Must I know more?
Retroviruses and adenoviruses - I know that these are both vectors used to transfect cells. But do we need to know, for instance, how retroviruses use reverse transcriptase to create a DNA template from an inserted mRNA strand complementary to the gene of interest, and then how integrase is used to catalyse the incorporation of the gene into the genetic material of the cell.
Also, is it right to say that gene therapy does not involve the integration of a normal functioning allele of a gene into the chromosomal DNA of a cell, and rather just involves the delivery of an allele to a cell through a liposome for instance? I found this to be a logical way of explaining how gene therapy does not involve the removal of a defective allele for a gene.
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1. There really isn't much else to know.
2. No. I explained that earlier for interest purposes/explanation purposes you don't have to know it.
3. There is no requirement for integration in gene therapy but if you want your allele to be maintained through division you would want it to be integrated. You could still have a gene inserted into the genome elsewhere and have both the defective allele and the functional allele in the genome in completely different places. For eg your defective allele might be on chromosome 6 but you might insert it into some junk DNA on chromosome 11. You don't have to remove the defective allele in this case/replace it you can just add to what is already there. Most of the time your defective allele is going to produce a nonfunctional product. You would only want to actually eliminate the defective allele specifically if you have a dominant negative.
Let me know if I didn't understand your question correctly as I'm worried I may have misinterpreted.
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1. There really isn't much else to know.
2. No. I explained that earlier for interest purposes/explanation purposes you don't have to know it.
3. There is no requirement for integration in gene therapy but if you want your allele to be maintained through division you would want it to be integrated. You could still have a gene inserted into the genome elsewhere and have both the defective allele and the functional allele in the genome in completely different places. For eg your defective allele might be on chromosome 6 but you might insert it into some junk DNA on chromosome 11. You don't have to remove the defective allele in this case/replace it you can just add to what is already there. Most of the time your defective allele is going to produce a nonfunctional product. You would only want to actually eliminate the defective allele specifically if you have a dominant negative.
Let me know if I didn't understand your question correctly as I'm worried I may have misinterpreted.
That's fine :) thank you simpak!
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It looks like you already know the stuff anyway. My teacher didn't even mention this stuff in class. I learnt all of this stuff from you just now.
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It looks like you already know the stuff anyway. My teacher didn't even mention this stuff in class. I learnt all of this stuff from you just now.
Trust me, I feel the same. At times, I feel that I so rapidly went through unit 4 that my knowledge of this unit is superficial. Nevertheless, the topics and concepts are less intricate than unit 3, so I guess its a good unit. :) Good luck!
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Would this be sufficient for describing how apoptosis is an example of signal transduction:
Apoptosis occurs when a specific target cell receives a death signal, triggering a cascade of events (including the activation of caspases, blebbing of the cell) that leads to the cell self-destructing (the response).
Also, the sample Biology exam seems to suggest that we need to know about action potentials - the question asks to describe how the electrical signal travels across the axon of a post-synaptic neuron. I mean, would I just need to mention that an action potential travels from one node of Ranvier to the next across the myelinated axon. Could someone help me formulate a more appropriate response?
Another question from the sample exam:
A tissue that has been responsive to hormone X may, over time, lose its response to hormone X, even
though the concentration of hormone X remains unchanged.
Based on your understanding of how a hormone controls the functioning of cells, suggest reasons for
this decrease in responsiveness.
Some suggestions:
- The cells have become overstimulated and so no longer respond to hormone X when it binds to specific receptors.
- The reception sites for the ligand molecules have been altered; there is no lock-and-key fit between hormone X and its specific receptor, and thus the effects of hormone X have been reduced.
What else could we mention as suggestions in that regard? Thanks for your help :)
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Would this be sufficient for describing how apoptosis is an example of signal transduction:
Apoptosis occurs when a specific target cell receives a death signal, triggering a cascade of events (including the activation of caspases, blebbing of the cell) that leads to the cell self-destructing (the response).
Also, the sample Biology exam seems to suggest that we need to know about action potentials - the question asks to describe how the electrical signal travels across the axon of a post-synaptic neuron. I mean, would I just need to mention that an action potential travels from one node of Ranvier to the next across the myelinated axon. Could someone help me formulate a more appropriate response?
Another question from the sample exam:
A tissue that has been responsive to hormone X may, over time, lose its response to hormone X, even
though the concentration of hormone X remains unchanged.
Based on your understanding of how a hormone controls the functioning of cells, suggest reasons for
this decrease in responsiveness.
Some suggestions:
- The cells have become overstimulated and so no longer respond to hormone X when it binds to specific receptors.
- The reception sites for the ligand molecules have been altered; there is no lock-and-key fit between hormone X and its specific receptor, and thus the effects of hormone X have been reduced.
What else could we mention as suggestions in that regard? Thanks for your help :)
The loss of the response to hormone x suggests that some sort of negative feedback witchcraft is going on. This might happen because a substance produced by the binding of hormone x to the receptors alters the shape of the receptors for hormone x.
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When discussing how a vaccine confers long-term immunity against a particular pathogen, do I only need to talk about the production of antibodies in the humoral response? Is there a need to discuss a cell-mediated response? Or maybe I can intertwine is subtly and mention that:
1. A specific immune response is coordinated against the pathogen.
2. Memory cells retain memory of the antigenic markers of the pathogen.
3. On subsequent infections caused by the same pathogen, a more rapid, emphatic attack against the pathogen is coordinated.
4. Long term immunity of the individual against the pathogen is conferred.
^ Is this sufficient.
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Don't be subtle. If I have a marking scheme and you're not mentioning the points on it, I can give you a half mark at best.
For example, your point for 2) is extremely vague (what does "retain memory" mean? Do cells just remember what happened?) and if I had a checklist that required you to say something about clonal expansion, I couldn't give you the full mark, even though you have (maybe) implied that it occurs.
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Don't be subtle. If I have a marking scheme and you're not mentioning the points on it, I can give you a half mark at best.
For example, your point for 2) is extremely vague (what does "retain memory" mean? Do cells just remember what happened?) and if I had a checklist that required you to say something about clonal expansion, I couldn't give you the full mark, even though you have (maybe) implied that it occurs.
Okay but my question was whether or not I needed to mention T cells when talking about vaccines? What do you suggest I write? I mean thanks for completely attacking what I wrote. I require assistance, not someone telling me how crap my answer is.
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I would probably approach it in terms of a timeline of sorts - what is actually happening.
For instance: the vaccine is administered and B cells with a B cell receptor specific to the particular vaccine antigen administered bind the antigen and are activated. The B cell proliferates and differentiates and some of the differentiated cells develop into long lived memory B cells that produce antibody specific to the vaccine antigen to protect against that antigen should it be re-encountered in the future.
Additionally, the vaccine antigen is taken up by antigen presenting cells that process and present this antigen on MHCI and MHCII markers. T cells with a T cell receptor specific to the particular vaccine antigen will be activated by these antigen presenting cells. Activated T cells will proliferate and differentiate to produce memory T cells with a TCR specific to the vaccine antigen. These cells will be long-lived and respond to the antigen immediately should it be re-encountered.
That would probably be modified to make it better, go ahead and see what you can do with it!
Don't be mad at Russ for pointing out that your response to the question may have been too vague - he's trying to help you to think about what you would need to include to make it more specific without feeding you an answer. You will get much more out of that than being told exactly what to say.
What I've done above is feed you an answer that might cover your points because you've asked for one but he did hint on a couple of things that I've covered in that answer that you could have thought about yourself (for instance, clonal expansion and explaining how memory is maintained - specifically the production of antibodies or the maintenance of cells that respond to that antigen in the future). He wasn't just saying 'it is wrong' he did give some info about how he thought you could improve it, just not so transparently.
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I would probably approach it in terms of a timeline of sorts - what is actually happening.
For instance: the vaccine is administered and B cells with a B cell receptor specific to the particular vaccine antigen administered bind the antigen and are activated. The B cell proliferates and differentiates and some of the differentiated cells develop into long lived memory B cells that produce antibody specific to the vaccine antigen to protect against that antigen should it be re-encountered in the future.
Additionally, the vaccine antigen is taken up by antigen presenting cells that process and present this antigen on MHCI and MHCII markers. T cells with a T cell receptor specific to the particular vaccine antigen will be activated by these antigen presenting cells. Activated T cells will proliferate and differentiate to produce memory T cells with a TCR specific to the vaccine antigen. These cells will be long-lived and respond to the antigen immediately should it be re-encountered.
That would probably be modified to make it better, go ahead and see what you can do with it!
Don't be mad at Russ for pointing out that your response to the question may have been too vague - he's trying to help you to think about what you would need to include to make it more specific without feeding you an answer. You will get much more out of that than being told exactly what to say.
What I've done above is feed you an answer that might cover your points because you've asked for one but he did hint on a couple of things that I've covered in that answer that you could have thought about yourself (for instance, clonal expansion and explaining how memory is maintained - specifically the production of antibodies or the maintenance of cells that respond to that antigen in the future). He wasn't just saying 'it is wrong' he did give some info about how he thought you could improve it, just not so transparently.
Thanks simpak :)
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Okay but my question was whether or not I needed to mention T cells when talking about vaccines? What do you suggest I write? I mean thanks for completely attacking what I wrote. I require assistance, not someone telling me how crap my answer is.
You're completely misinterpreting what is constructive criticism and advice, not attacking what you wrote. I have no interest in giving people perfect answers to their questions (for various reasons), unless it's a factual knowledge deficit. It's much better for you as a student to get some prompts and advice and use that instead.
Be specific when writing an answer. Mention all the key points. Don't be vague or subtle, the person reading your answer will avoid making assumptions.
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Okay but VCAA doesn't provide 8 lines for a question like this. So I'm trying to be specific, yet shorten it do a degree where I can fit all the information. I know everything Simpak mentioned; this question, however, was worth 2 marks and had 3 lines.
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Also, the sample Biology exam seems to suggest that we need to know about action potentials - the question asks to describe how the electrical signal travels across the axon of a post-synaptic neuron. I mean, would I just need to mention that an action potential travels from one node of Ranvier to the next across the myelinated axon. Could someone help me formulate a more appropriate response?
-
Also, the sample Biology exam seems to suggest that we need to know about action potentials - the question asks to describe how the electrical signal travels across the axon of a post-synaptic neuron. I mean, would I just need to mention that an action potential travels from one node of Ranvier to the next across the myelinated axon. Could someone help me formulate a more appropriate response?
I think it's asking what actually causes the action potential itself, to describe the action potential. It's asking how it travels across, not where it goes if you see what I mean. I'm also fairly sure that the Nodes of Ranvier aren't part of the VCE course.
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Calcium channels are the only thing in the course to do with electrical impulses, This is what I would say:
During an action potential an electrical gradient from the dendrite of the neuron to its axon terminal is triggered, the gradient is caused by the opening of calcium ion channels on the neuron's membrane causing and influx of calcium ions, contributing to the continuation of the electrical gradient down the axon of the neuron, leading to an 'all or nothing response'
Would this do... or completely wrong...
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Calcium channels are the only thing in the course to do with electrical impulses, This is what I would say:
During an action potential an electrical gradient from the dendrite of the neuron to its axon terminal is triggered, the gradient is caused by the opening of calcium ion channels on the neuron's membrane causing and influx of calcium ions, contributing to the continuation of the electrical gradient down the axon of the neuron, leading to an 'all or nothing response'
Would this do... or completely wrong...
But doesn't the influx of calcium ions trigger the exocytosis of neurotransmitter molecules? They aren't involved in anything other than trigger the release of neurotransmitters (excitatory or inhibitory) from the pre-synaptic terminal by exocytosis.
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But doesn't the influx of calcium ions trigger the exocytosis of neurotransmitter molecules? They aren't involved in anything other than trigger the release of neurotransmitters (excitatory or inhibitory) from the pre-synaptic terminal by exocytosis.
You are right.
It's sodium and potassium channels that are opened that cause the action potential to make its way along the axon. Something which I think is mentioned in the course, though not in detail. The detail is quite boring and pretty fiddly to, to be honest.
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The detail is quite boring and pretty fiddly to, to be honest.
What?! It was easily one of the most interesting parts of the previous study design (and of uni thus far). It's mindblowing (hur hur) that the nervous system acts as a self-powered generator that controls and regulates all processes that you as a person carry out.
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If I were to approach that answer, it would probably involve discussing how an action potential is initiated as an excitatory neurotransmitter signal binds to a post-synaptic membrane receptor, to continue conducting the action potential through the neuron, across the axon. But again, this seems to vague. How can I add more without necessarily talking about Na+/K+ ions?
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What?! It was easily one of the most interesting parts of the previous study design (and of uni thus far). It's mindblowing (hur hur) that the nervous system acts as a self-powered generator that controls and regulates all processes that you as a person carry out.
It's cool overall, but I really couldn't give a rat's arse which channels are open when and ahhhh the exact details are so annoying with it!
Kudos for the mindblowing though...very nice hahaha!
If I were to approach that answer, it would probably involve discussing how an action potential is initiated as an excitatory neurotransmitter signal binds to a post-synaptic membrane receptor, to continue conducting the action potential through the neuron, across the axon. But again, this seems to vague. How can I add more without necessarily talking about Na+/K+ ions?
It's asking you how the action potential travels down the post-synaptic axon. The fact it's mentioned the axon specifically suggests it probably doesn't want you talk about how the action potential is initiated.
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Did u no the nervous system ALSO regulates the migration of immune cells? :D
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Did u no the nervous system ALSO regulates the migration of immune cells? :D
Learnt this on Friday :D
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Did u no the nervous system ALSO regulates the migration of immune cells? :D
Ooh, could you elaborate? Sounds interesting!
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About this question that was mentioned before
A tissue that has been responsive to hormone X may, over time, lose its response to hormone X, even
though the concentration of hormone X remains unchanged.
Based on your understanding of how a hormone controls the functioning of cells, suggest reasons for
this decrease in responsiveness.
Any ideas on a response..?
I remember confronting this question, and had no idea..
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About this question that was mentioned before
A tissue that has been responsive to hormone X may, over time, lose its response to hormone X, even
though the concentration of hormone X remains unchanged.
Based on your understanding of how a hormone controls the functioning of cells, suggest reasons for
this decrease in responsiveness.
Any ideas on a response..?
I remember confronting this question, and had no idea..
I think a reasonable solution would be that by increased concentrations of hormone X, the protein receptor conformational shape can be altered and the hormone can no longer effectively bind to the receptor. Also, overstimulating these cells could result in cells no longer responding to this hormone.
^^ but I'd get that clarified as I'm not 100% sure of its accuracy.
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I think a reasonable solution would be that by increased concentrations of hormone X, the protein receptor conformational shape can be altered and the hormone can no longer effectively bind to the receptor. Also, overstimulating these cells could result in cells no longer responding to this hormone.
The concentration of hormone x remains unchanged over the duration of their life. Wouldn't an over stimulation result from an increase in hormone conc.? However, I think Yacoubb is right as the conformational shape of the specific receptor would have changed.
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I think the product of the biochemical pathway initiated by the binding of hormone x to the receptor inhibits the response by binding to the specific receptor for hormone x.
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It could perhaps have something to do with gene regulation too. The genes expressed by a particular type of cell may change during various stages of growth and development (an example escapes me for the minute but it does happen).
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It could perhaps have something to do with gene regulation too. The genes expressed by a particular type of cell may change during various stages of growth and development (an example escapes me for the minute but it does happen).
It's a suggest type question so surely justifying it in some way would be sufficient to get the full marks! :)
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There are legit infinite possibilities but here are some:
1. Binding of hormone X causes internalisation of receptor-ligand complex so that receptors are no longer expressed on the cell surface.
2. Binding of hormone X alters the expression of the gene encoding the receptor for hormone X such that it is no longer expressed (a negative feedback type model)
3. Binding of hormone X causes the cell to produce hormone Y, which feeds back on the same cell (autocrine signalling) and reception of hormone Y inhibits components of the signalling cascade triggered by hormone X (classical negative feedback)
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Does the hyper variable regions in mtDNA mutate faster than those found in nuclear DNA? I initially thought it did but according to my teacher, it's the other way around
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Does the hyper variable regions in mtDNA mutate faster than those found in nuclear DNA? I initially thought it did but according to my teacher, it's the other way around
mtDNA mutates more slowly than nuclear DNA. This is because mutations in mtDNA are usually a hell of a lot worse than in nuclear DNA (think of what mtDNA is coding for!). Hypervariable, annoyingly, just means that there are heaps of molymorphisms, which is true. mtDNA is usually used in genealogical analysis though and is a pretty good way of detecting someone's ancestral roots. The other reason for that though is that it doesn't undergo any form of recombination!
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Does the hyper variable regions in mtDNA mutate faster than those found in nuclear DNA? I initially thought it did but according to my teacher, it's the other way around
The D loop in the hypervariable region of mtDNA has a very high mutation rate. This can be used t observe the evolutionary relationship between not so distantly-related species. However, the coding region of mtDNA has a very low mutation rate and so is used to determine the evolutionary relationship between distantly related species with common ancestry.
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Hey I've got a few questions
* Upon second encounter with a particular pathogen, I know the immune response is much faster and greater due to the presence of B-memory cells which recognize the antigen and know exactly which antibodies to create. But exactly how does the presence of B-memory cells speed up the rate and strength of the response? Does it mean that there is no need for plasma cells to undergo proliferation?
*And also, I came across a question asking why mast cells are perceived to play a positive role in the inflammatory response, but a negative role in hypersensitivity reactions.
I'm aware of their role in allergic response, but unsure of how they aid the inflammatory one.
*Finally, is the action of mast cells specific or non-specific?
Thanks guys :)
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Hey guys just wondering with autoimmune diseases which aspect of the immune system is destroying the self cells, the cytotoxic T cells or the B cells and antibodies? Also how are eukaryotic pathogens destroyed? I assumed the phagocytes would be too small to engulf them thus agglutination would be ineffective.
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Hey guys just wondering with autoimmune diseases which aspect of the immune system is destroying the self cells, the cytotoxic T cells or the B cells and antibodies? Also how are eukaryotic pathogens destroyed? I assumed the phagocytes would be too small to engulf them thus agglutination would be ineffective.
With autoimmune diseases, cytotoxic T-cells are primarily involved. Of course, helper T-cells activate cytotoxic T cells to act on self cells. Cytotoxic T-cells release perforin (a cytotoxic protein) that punches holes through the plasma membrane of these self cells, resulting in these cells lysing.
Hey I've got a few questions
* Upon second encounter with a particular pathogen, I know the immune response is much faster and greater due to the presence of B-memory cells which recognize the antigen and know exactly which antibodies to create. But exactly how does the presence of B-memory cells speed up the rate and strength of the response? Does it mean that there is no need for plasma cells to undergo proliferation?
*And also, I came across a question asking why mast cells are perceived to play a positive role in the inflammatory response, but a negative role in hypersensitivity reactions.
I'm aware of their role in allergic response, but unsure of how they aid the inflammatory one.
*Finally, is the action of mast cells specific or non-specific?
Thanks guys :)
I'll start off with your last question. You cannot really ask whether a mast cell is specific or non-specific. It really depends on the situation it is involved in. For instance, mast cells, which are found on the lining of blood vessels, release histamine during an inflammatory response to attract phagocytes to the infective area. In this instance, it is non-specific. Why? Mast cells release histamine to attract phagocytes irrespective of the types of pathogens that have penetrated the internal environment of the organism. However, when looking at hypersensitivities against allergens, the IgE antibodies that bind to the outer surface of these mast cells having paratopes (antigen binding sites) specifically complementary to the shape of the antigens of a specific allergen that the individual is sensitised to. In this instance, it is specific (adaptive). Why? Because mast cells will ONLY release histamine when a specific allergen that the organism is sensitised to binds to the IgE antibodies, which are in turn bound to the outer membrane of the mast cells.
Next point: mast cells release histamine during the inflammatory response to attract phagocytes to the infective area, resulting in the phagocytosis of non-self, pathogenic matter, to prevent the spread of infection. However, in allergic responses, the release of histamine by mast cells causes profound, emphatic and dramatic responses to the detected allergen, including constriction of airways, itchiness, swelling, excessive production of mucous, etc. So that's how you can have mast cells acting positively in one instance, and not so positively in the other. Again, depends on the situation itself.
Memory B-cells retain immunological memory of the antigenic markers of the specific pathogen that the individual is now actively immunised against. When the pathogen is encountered on a subsequent occasion, there is no need for clonal selection. That is, clonal expansion (involving the rapid proliferation of B cells which differentiate into memory and plasma B cells that secrete specific immunoglobulins) occurs at an earlier time than when the individual first encountered the pathogen, because of the delay in the time required for the surface antibodies of a SPECIFIC B-cell to bind to the complementary antigenic marker of a pathogen, to then actually activate that B-cell to rapidly proliferate. The presence of memory just really speeds up the process by which a higher concentration of antibodies (in terms of humoral immunity) are produced, to elicit a more emphatic, rapid response to that specific pathogen.
Hope this helped!
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I got a question on a practice exam for unit 4 on transgenic zebra fish. A gene from sea coral was inserted into the genome of the zebra fish eggs. So the Glofish glew fluorescently.
Predict the chance of survival of the Glofish if it were released into the natural environment of the zebra fish. Explain your answer.
My answer was COMPLETELY opposite to VCAAs, in that I mentioned their chances of survival increased. This was my answer:
The chances of survival of the Glofish would increase because the bright fluorescent glow would trick predators into believing they are poisonous. Hence, predation is reduced, thereby increasing the chance of survival o the Glofish in the natural environment of the zebra fish.
VCAA's answer:
The survival of the Glofish is likely to be poor in the natural environment. The fish would be more noticeable to predators because it is red or glows in ultraviolet light, so may be captured more often.
Would my answer be considered right because of my justification.
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No, your answer would not be correct.
Take as an analogy the anglerfish; it has a luminous protrusion called an illicium that it uses to attract prey. Fish - living in a light-poor environment - are naturally attracted to fluorescence. From this, you can take that if we were to put a fish that fluoresces into the natural environment, it would become more appealing to predators. As such, the fishes chances of survival decrease.
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^Agreed, your answer is definitely incorrect.
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No, your answer would not be correct.
Take as an analogy the anglerfish; it has a luminous protrusion called an illicium that it uses to attract prey. Fish - living in a light-poor environment - are naturally attracted to fluorescence. From this, you can take that if we were to put a fish that fluoresces into the natural environment, it would become more appealing to predators. As such, the fishes chances of survival decrease.
Hmm, it's just because I've come across a question similar to this once and it was also a light-poor environment, and the fluorescent glow made them seem poisonous. Any tips on knowing when to go with what approach? For instance, how would I know the fluorescence in this instance decreased the biological fitness of the fish?
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Hmm, it's just because I've come across a question similar to this once and it was also a light-poor environment, and the fluorescent glow made them seem poisonous. Any tips on knowing when to go with what approach? For instance, how would I know the fluorescence in this instance decreased the biological fitness of the fish?
It's more common sense than anything, really - you need to apply wider biological principles to situations while maintaining a logical view (in biology, the logical way of something occurring is probably the true way it occurs, even if it isn't immediately obvious).
For the Glofish example, you need to think about 1. The characteristics of the aquatic environment, 2. The characteristics of unaltered fish in that environment and why they have the adaptations that they do, and 3. The characteristics of the altered fish and how these alterations affect fitness.
Just as a general rule (obviously fraught with exceptions) - the more colourful an organism is, the more attractive it is designed to be to prey.
The 'poisonous' example was probably something to do with the predator having a bright colour in order to entice prey, as opposed to our example where we've manipulated the prey in such a way that it is more enticing to the predator.
Hope this makes sense!
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When cells of a transplanted organ are detected as 'non-self' by cells of the immune system of the organ recipient, is the transplanted organ rejected as a result of specific antibodies being produced against these cells?
^ I thought that rejection of tissue/organs would involve cytotoxic t-cells, but that doesn't seem to be the case in an exam I did. They've mention that skin grafts detected as non-self by the immune system of mice were rejected as specific antibodies against the skin grafts were produced, leading to the rejection of the skin graft.
Could someone please just clarify this? Thanks :)
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When cells of a transplanted organ are detected as 'non-self' by cells of the immune system of the organ recipient, is the transplanted organ rejected as a result of specific antibodies being produced against these cells?
^ I thought that rejection of tissue/organs would involve cytotoxic t-cells, but that doesn't seem to be the case in an exam I did. They've mention that skin grafts detected as non-self by the immune system of mice were rejected as specific antibodies against the skin grafts were produced, leading to the rejection of the skin graft.
Could someone please just clarify this? Thanks :)
Antibodies sounds about right. It's because you're interacting with foreign antigens. That inherently suggests antibodies. It's the safer bet in any case. The VCE course is very light on immunology, so things like this often happen. You're trying to string together a picture with so few of the facts. Sadly the same thing happens in first year, so I've still got no clue about any of it!
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Antibodies sounds about right. It's because you're interacting with foreign antigens. That inherently suggests antibodies. It's the safer bet in any case. The VCE course is very light on immunology, so things like this often happen. You're trying to string together a picture with so few of the facts. Sadly the same thing happens in first year, so I've still got no clue about any of it!
Yeah I'll just stick with specific antibodies being produced against the detected non-self tissue. Thanks t-rav!
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You can definitely say antibodies, but there are actually three kinds of rejection responses and two are relevant here:
The first is 'hyperacute' and occurs because of antibody binding, the second is 'acute' and is largely T cell mediated.
T cells are the most important cell to coordinate a rejection response. They are the most important thing for most everything, though. Ever. In the world. :D
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OK can I get this straight
Does mitochondrial DNA have a faster or slower mutation rate than nuclear DNA? Is it faster in the coding/non-coding region, and slower in the other region?
A lot of the resources I have looked at are contradicting, and not one gives a definitive answer
Thank youuu
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And one more thing, what exactly is a haplogroup, and its relevance to Mitochondrial DNA?
How can haplogroups be used to compare polpulations more effectively than nuclear DNA?
Thanks again :)
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OK can I get this straight
Does mitochondrial DNA have a faster or slower mutation rate than nuclear DNA? Is it faster in the coding/non-coding region, and slower in the other region?
A lot of the resources I have looked at are contradicting, and not one gives a definitive answer
Thank youuu
The coding regions of mitochondrial DNA have a very slow mutation rate, and so this is used to determine evolutionary relationships between species with no recent common ancestry, and the non-coding region (D-loop in hypervariable region of mitochondrial DNA) has a very high mutation rate. Because of this, the non-coding region is used to determine the degree of not-too-distantly related species. That is, species with a recent common ancestor.
Hope this helped.
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And one more thing, what exactly is a haplogroup, and its relevance to Mitochondrial DNA?
How can haplogroups be used to compare polpulations more effectively than nuclear DNA?
Thanks again :)
You don't need to know about haplogroups. However, as part of the Out-of-Africa hypothesis, which states that Homo Sapiens evolved in Africa prior to emigrating from the African continent, and as a result, a large degree of variation is expected to exist in the mtDNA of the African population.
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The coding regions of mitochondrial DNA have a very slow mutation rate, and so this is used to determine evolutionary relationships between species with no recent common ancestry
Wasn't it to determine evolutionary relationships between species with common ancestry?
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All species will have common ancestry to some degree, but what Yacoubb is saying is that if species diverged from a common ancestor long ago you would use mitochondrial DNA to detect changes - otherwise the differences in the genome are too large to make any kind of direct comparison between the organisms.
Recent was the key word in his response.
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I thought the species had to have recent common ancestry?
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I thought the species had to have recent common ancestry?
As simpak mentioned, all species of organisms to some extent have common ancestry. But some are more recent than others.
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I have some things I'd like clarified.
+ Are operons only located on the single circular chromosome eukaryotic cells?
+ If a spontaneous mutation occurred in a sterile hybrid where the number of chromosomes doubled, would that make the hybrid fertile because as a result of the doubling process, the chromosomes are present in homologous pairs --> the chromosomes are able to line up during meiosis > functional gametes can be produced.
+ On the actual exam, I was contemplating on not reading through the MC during reading time & only focussing on short answer. I dunno, I feel like its probably not a good idea. If so, what are you all doing during reading time? I was thinking of maybe spending 5 mins reading through MC and then spend around 10 mins skimming through the short answer. Tips/advice would be appreciated.
Thank you (:
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+ Are operons only located on the single circular chromosome eukaryotic cells?
I'm not sure what you mean by this; you're more likely to find circular chromosomes in prokaryotic cells for starters.
The operon model is a way of describing a set of genes regulated by the same promoter. For example, the lac operon consists of a promoter, an inducer, an operator, a series of genes that code for several mRNA products that lead to multiple proteins, and a terminator. These genes are adjacent to one another.
Note that the lac operon is a prokaryotic mechanism. Eukaryotic operons are far less common (based on current findings).
+ If a spontaneous mutation occurred in a sterile hybrid where the number of chromosomes doubled, would that make the hybrid fertile because as a result of the doubling process, the chromosomes are present in homologous pairs --> the chromosomes are able to line up during meiosis > functional gametes can be produced.
It's possible, and if I recall correctly it's been induced experimentally in plants. The process you have described is correct. However, in the case of the mutated sterile hybrid, it's possible (or even likely) that there are other factors that will make the gametes unviable.
+ On the actual exam, I was contemplating on not reading through the MC during reading time & only focussing on short answer. I dunno, I feel like its probably not a good idea. If so, what are you all doing during reading time? I was thinking of maybe spending 5 mins reading through MC and then spend around 10 mins skimming through the short answer. Tips/advice would be appreciated.
A 5 min/10 min split is fine; what I found to be the case in the exam is that I'd read over both sections fairly quickly to get an idea of what I'd need theory-wise, then return to the beginning and read it again more thoroughly as much as possible. Often this second reading would only get me through the MCQs, but it definitely saved time later on as I had already considered the answers.
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What plant hormone/s are responsible for abscission in deciduous plants? I thought it was ABA hence the name, but has recent research proved otherwise?
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What plant hormone/s are responsible for abscission in deciduous plants? I thought it was ABA hence the name, but has recent research proved otherwise?
ABA was initially thought to be a hormonal cause of abscission (there are a number of other causes, such as structural or chemical causes), but recent research has found that auxin and ethylene are instead likely to be hormonal causes.
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ABA was initially thought to be a hormonal cause of abscission (there are a number of other causes, such as structural or chemical causes), but recent research has found that auxin and ethylene are instead likely to be hormonal causes.
Thanks alondouek :) so if a question does pop up on VCAA, would we be expected to mention both ethylene and auxin?
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Thanks alondouek :) so if a question does pop up on VCAA, would we be expected to mention both ethylene and auxin?
Good question - last year, ABA was an accepted answer even though the research that contradicted this is older than 2012. First things first, check the VCAA site for any document outlining amendments to theory (they usually release on each year); otherwise, check with your teacher.
If I were a marker, giving both ethylene and auxin would be the correct answer - but I don't know if VCAA has moved away from ABA causing abscission. You'd definitely have a case to argue if they marked you as wrong!
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Thought plant hormones were removed from the course?
This is from the VCAA Bio FAQs:
The distinction between different types of growth regulators (auxins, cytokinins, gibberellins, abscisic acid and ethylene) are not required
Can someone clarify?
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Thought plant hormones were removed from the course?
This is from the VCAA Bio FAQs:
The distinction between different types of growth regulators (auxins, cytokinins, gibberellins, abscisic acid and ethylene) are not required
Can someone clarify?
plant growth regulators are definitely on the study design.
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I'm not sure what you mean by this; you're more likely to find circular chromosomes in prokaryotic cells for starters.
The operon model is a way of describing a set of genes regulated by the same promoter. For example, the lac operon consists of a promoter, an inducer, an operator, a series of genes that code for several mRNA products that lead to multiple proteins, and a terminator. These genes are adjacent to one another.
Note that the lac operon is a prokaryotic mechanism. Eukaryotic operons are far less common (based on current findings).
It's possible, and if I recall correctly it's been induced experimentally in plants. The process you have described is correct. However, in the case of the mutated sterile hybrid, it's possible (or even likely) that there are other factors that will make the gametes unviable.
A 5 min/10 min split is fine; what I found to be the case in the exam is that I'd read over both sections fairly quickly to get an idea of what I'd need theory-wise, then return to the beginning and read it again more thoroughly as much as possible. Often this second reading would only get me through the MCQs, but it definitely saved time later on as I had already considered the answers.
Yeah sorry that was a typo; I meant circular chromosomes in prokaryotic cells.
Thanks so much!
And I think I'll do that for the exam. During reading time I'll quickly read over the paper & look at what I need, then skim through short answer first, leaving a few minutes for mc.
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http://www.vcaa.vic.edu.au/Documents/vce/biology/Biology-faqs.doc
This is what I've been reading for course info. Is this what everyone else is going off? If not, can someone give me a brief summary of what's been taken out of the course? So confused
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BASE YOUR STUDIES ON THE STUDY DESIGN.
The FAQ pretty much tells you what the study design tells you.
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BASE YOUR STUDIES ON THE STUDY DESIGN.
The FAQ pretty much tells you what the study design tells you.
Not necessarily, the FAQs were released afterwards and consolidates the required knowledge for the biology syllabus. The board may have rushed to release the study design PDF and may have included dot points that were irrelevant. I'm going off the FAQ, cross checking with the study design and if there's a misleading point/question, I'll revise it anyways :)
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Not necessarily, the FAQs were released afterwards and consolidates the required knowledge for the biology syllabus. The board may have rushed to release the study design PDF and may have included dot points that were irrelevant. I'm going off the FAQ, cross checking with the study design and if there's a misleading point/question, I'll revise it anyways :)
The FAQ, just summarises what the Study design tells you..
I'd like to know what points on the study design is misleading, or irrelevant...
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The FAQ, just summarises what the Study design tells you..
I'd like to know what points on the study design is misleading...
Reading the above comments, plant growth regulators was a dot point from the study design but discarded from the FAQs.
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Reading the above comments, plant growth regulators was a dot point from the study design but discarded from the FAQs.
No. If I remember correctly, it states the distinction between different types of growth regulators are not required. This doesn't necessarily mean you don't need to know it.
Also, on top of that statement It even says:
"Signalling molecules, specifically neurotransmitters, animal hormones, pheromones and plant growth hormones, should be distinguished at a functional (rather than a structural) level"
EDIT:
That was straight off the FAQ.
That's also stated on the study design.
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Another couple of questions guys
1) How does inhibition of acetylcholinesterase cause paralysis? I thought it would just cause muscle spasms due to over stimulation at the post-synaptic membrane?
2) And can someone explain the mechanics behind infertile hybrids? Can they not produce functional gametes? Is it because they have less than the diploid number of chromosomes? I never really understood this and it'd be good to get this cleared up, even if its like 4 days before the exam haha
Thanks in advance :)
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1) How does inhibition of acetylcholinesterase cause paralysis? I thought it would just cause muscle spasms due to over stimulation at the post-synaptic membrane?
Finally a question i'm actually qualified to answer.
It should be obvious from the name that acetylcholinesterase is an enzyme. It's responsible for the breakdown of acetylcholine. If it wasn't broken down, it would just continually hang around and build up (which is what you don't want and this is why our bodies are "designed" to break it down).
By inhibiting AchE, you inhibit the breakdown of Ach, thus increasing Ach levels. Ach stimulates receptors on muscles causing them to contract. However, in this case, so much Ach is present that the receptors are constantly stimulated, eventually, they develop a tolerance to Ach and cannot be stimulated anymore.
So, in this case, you'd see the person initially twitch a fair bit due to the increased stimulation and then they'd become paralyzed after their receptors become tolerant/desensitised to the effects of Ach.
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No. If I remember correctly, it states the distinction between different types of growth regulators are not required. This doesn't necessarily mean you don't need to know it.
Also, on top of that statement It even says:
"Signalling molecules, specifically neurotransmitters, animal hormones, pheromones and plant growth hormones, should be distinguished at a functional (rather than a structural) level"
EDIT:
That was straight off the FAQ.
That's also stated on the study design.
Well that was based on previous comments, nevertheless another that has been directly extracted from both documents:
"Homeostasis and feedback mechanisms have been deleted from unit 3" - FAQ
"Nature of the stimulus-response model" - Study Design
However, I'm not too sure if they are different topics.
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Quick shitty diagram i drew for those who are still confused. Just to note, it actually isn't 100% correct but it is "VCE correct" and helps illustrate the concept that you need to understand, namely it increases the levels of Ach (acetylcholine) not by making more but by preventing its breakdown. More Ach present = more receptors stimulated. If you prevent its breakdown, it hangs around in the synapse and receptor for longer continually stimulating it until it just gives up and stops responding. You can get more technical and talk about stuff like depolarization but you dont need to know that for VCE as far as i know.
On the right, you have the normal state where AchE (acetylcholine esterase) inactivates Ach. On the left, you have an absence of AchE (because its blocked and i couldnt be fucked drawing it either) and thus increased Ach levels.
(http://i.imgur.com/9B3DV8R.png)
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Well that was based on previous comments, nevertheless another that has been directly extracted from both documents:
"Homeostasis and feedback mechanisms have been deleted from unit 3" - FAQ
"Nature of the stimulus-response model" - Study Design
However, I'm not too sure if they are different topics.
FAQ:
"Signal transduction can be considered in terms of a stimulus-response model and should be described, in simple terms, as a three-step process: reception (information is received by a cell’s receptor), transduction (information from the receptor is passed on to an effector) and induction/response (various cellular responses are initiated)."
All the FAQ is, is pretty much a summary of the study design..
Now I'm going to stop proving my point..
time to study
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Hey guys, just had a couple of questions regarding the engage exam.
1. Could pain be a result of "inflammation from the non specific response"?
And what would you say for q 32? Answer was B I said C
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Hey guys, just had a couple of questions regarding the engage exam.
1. Could pain be a result of "inflammation from the non specific response"?
And what would you say for q 32? Answer was B I said C
One of the symptoms of inflammation is pain surrounding the infective area. An inflammatory response can also be associated with burning sensations near the affected area.
And I would have gone with B because it says it fluctuates around a constant; so this means that frequencies of alleles will eventually always remain in equilibrium, just varying mildly from time to time. But this is highly ambiguous and I think VCAA would be much better in wording!
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One of the symptoms of inflammation is pain surrounding the infective area. An inflammatory response can also be associated with burning sensations near the affected area.
And I would have gone with B because it says it fluctuates around a constant; so this means that frequencies of alleles will eventually always remain in equilibrium, just varying mildly from time to time. But this is highly ambiguous and I think VCAA would be much better in wording!
Thanks Yacoubb, so equilibrium doesn't necessarily mean the allele frequencies are exactly the same in future gens?
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1. Could pain be a result of "inflammation from the non specific response"?
Yes, non-specific immunity involves the release of histamines, prostaglandins (i think, im no immuno expert) and other pain sensitising substances.
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Thanks slothpomba, that cleared it up :)
Also, does anyone know if rational drug design is actually still in the course? I believe the study design says its deleted, but I'm not too sure if this is referring to rational drug design specifically..
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Thanks slothpomba, that cleared it up :)
Also, does anyone know if rational drug design is actually still in the course? I believe the study design says its deleted, but I'm not too sure if this is referring to rational drug design specifically..
It shouldn't matter if it is or isn't. Rational drug design is preeeety basic. It's just trying to design drugs to target specific structures, rather than just exposing microbes to a whole heap of random shit and seeing which one kills them!
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Why are Okazaki fragments necessary for the synthesis of a strand complementary to the lagging strand during DNA replication?
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Why are Okazaki fragments necessary for the synthesis of a strand complementary to the lagging strand during DNA replication?
Because the DNA polymerase adds DNA nucleotides to the 3' end. so as DNA helicase unzips the DNA molecule, only a certain part of the strand is exposed for the synthesis of a complementary DNA strand to occur. So the fragments are synthesised instead of a continuing strand (like the leading strand). Thus okazaki fragments form, and ligase must be used to catalyse the formation of the phosphodiester bond in the sugar phosphate backbone between the okazaki fragments.
I don't think we need to know about okazaki fragments though
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Why are Okazaki fragments necessary for the synthesis of a strand complementary to the lagging strand during DNA replication?
Okazaki fragments aren't used in the synthesis of lagging strand; they are actually the lagging strand constituents. During DNA replication, the lagging strand is built discontinuously 5' to 3' in okazaki fragments, because the lagging strand template is not exposed immediately by the replication fork.
So this means that because the RNA primer binds to the 5' end of the strand, and the replication fork is being formed (i.e. DNA is being unzipped), the RNA primer has to keep jumping, and that's why the lagging strand is built discontinuously.
Following DNA replication, okazaki fragments are ligated together to then form a continuous strand.
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Just some queries in regards to mutations. Could someone check my expression:
What occurs in translocation mutations:
A section of a chromosome breaks off and attaches to a non-homologous chromosome.
What occurs in inversion mutations:
A segment of a chromosome breaks off, flips around, and reattaches to the same chromosome.
What occurs in deletion mutations:
A segment of a chromosome is lost; genetic material is lost.
What occurs in a duplication mutation:
A section of a chromosome is repeated, resulting in an addition of genetic material.
________________________________________________________________________________
Explaining a non-sense mutation:
* As a result of the insertion/deletion/substitution of the base, a premature stop codon is present in the mRNA transcript of the gene, and a polypeptide with a shortened amino acid sequence is synthesised.
Explaining a missense mutation:
As a result of the base substitution mutation, a different amino acid is coded for at position ____. Thus, a polypeptide with an altered primary structure is produced.
Explaining a silent mutation:
Because the genetic code is redundant, and the amino acid ____ is coded for by different codons, the substitution mutation has no effect on the amino acid sequence of the polypeptide.
__________________________________________________________________________________
Explaining the effects of a Frameshift mutation:
When a base is added or deleted, all triplets beyond the mutation are altered. As a result, a dysfunctional polypeptide with a different amino acid sequence is produced.
Explaining a frameshift mutation:
- When a base is inserted or deleted, all bases beyond this mutation point are displaced one position. The reading template is frameshifted, triplets are altered and a dysfunctional polypeptide is synthesised.
^^ Is this fine?! Thank you! (:
And can someone PLEASE explain to me translocations in regards to gamete formation? Also, how do I know whether an extra X chromosome is a result of non-disjunction occurring in the mother or the father during meiosis? Thanks
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I have another quick question...
Is there a formal definition for 'non-competitive inhibition'?
Thanks... :)
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I have another quick question...
Is there a formal definition for 'non-competitive inhibition'?
Thanks... :)
I used a
molecule that binds to an enzyme at a site other than the active site; this changes the shape of the enzyme so that the substrate can no longer bind to
the active site
but there are no real "formal definitions" in bio :)
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A non-competitive inhibitor is a molecule that binds to the allosteric region of an enzyme; that is, the molecule binds to a region other than the active site of that enzyme. This inhibition induces a change in the shape of the active site of the enzyme. Consequently, the enzyme is no longer able to bind to its specific substrate molecules, and the activity rate of the enzyme decreases.
The first sentence ^^ would suffice as a definition of a non-competitive inhibitor.
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A non-competitive inhibitor is a molecule that binds to the allosteric region of an enzyme; that is, the molecule binds to a region other than the active site of that enzyme. This inhibition induces a change in the shape of the active site of the enzyme. Consequently, the enzyme is no longer able to bind to its specific substrate molecules, and the activity rate of the enzyme decreases.
The first sentence ^^ would suffice as a definition of a non-competitive inhibitor.
Thanks!:) That is actually amazing...