VCE Biology Question Thread

[galaxy21]

Hi again, sorry to dump another bucket-load of questions, but...
1. Does the TAC DNA sequence come before the promotor region?
2. Why do B cells have MHC II complexes? Can they act as APC's? How?
3. What is involved in post translation modification? Is it just the folding of the amino acid chain in the endoplasmic reticulum, and then final modifications in the golgi complex before export?
4. With alternate splicing, does this involve cutting out different exons (as well as introns) or rearranging them, or both?
5. Can T helper cells leave the lymph nodes?
6. Are introns always introns, or do they become exons sometimes?
7. Are exons the triplets of nucleotides or single nucleotides?
8. When a question asks about describing somethings function at a "molecular level", is it asking to refer to the structure of what it is (e.g. an enzyme) and how this effects its function?

Thank you so much!

[Erutepa]

1) Quote from bio FAQ "Teachers should provide examples of plants’ structural, chemical and peptide-based defences that are adapted to stop invading organisms before they cause extensive damage."
For structural i know of intact cuticles and chemical could be resin, but i dont know any peptide-based defences. Would hormones be considered as defenses? Also is there a second line of defense in plants?
2) What kind of hypothesis is best to use: 1. the 'if then when' format (e.g. if growth of plant is effected by water given to the plant then there will be increased growth of plant)
 or 2. the 'if then' format (e.g. if there is increased water supply to the plant then there will be increased growth). I was taught the if then when format but it's really long and I feel like it's wasting time.
3) Are cancer cells always killed through the death receptor pathway? My guess is no because there could be damage within the cell which leads to extrinsic pathway of apoptosis being induced.
4) Do we need to know about the assimilation model?
5) Does gene cloning include the gene being replicated as well as the protein the gene codes for being produced?

Any help would be appreciated, and thanks in advance

1. Plant immune systems/disease resistance seems to be more organized into pre-existing factors and inducible factors, not so much a first, second and third line of defence that we talk about with respect to mammals.
Things like the thick waxy (intact) cuticle and antimicrobial proteins which are present in plants are constant defense mechanisms against pathogens.
Further antimicrobial chemicals and proteins (like defensins) can also be induced by plant cells upon recognition of pathogen.

2. not sure about this hypothesis question. I don't think it matters too much though.

3. Cancer cells are not always killed via death receptor, as mentioned cancerous cells can induce the intrinsic pathway upon recognition of aberrant activity, however, the intrinsic pathway may also be induced by the action of perforins and granzymes released by NK and cytotoxic T cells recognizing cancerous cells.

4. In terms of human evolution theories you need to know the out of Africa hypothesis and the regional continuity theories. You don't need to know about the assimilation model as far as I am aware.

5. Gene cloning only refers to the cloning of the gene, irrelevant of its expression in the organism.

Do we need to know about Southern blotting in gel electrophoresis?

And also the Sanger method?!

Sorry, just these revision booklets are filled with lots of stuff and I’m not sure if they’re relevant or not.

I think you will find that a lot of resources for any course will include a bunch of applications of the core theory described in the study design like those you have mentioned above. I would say that you don't need to know them, but it won't hurt being familiar with them as you may get a question which is based upon one of these applications.

Mod edit (PF): Merged posts. You can include multiple quotes in the same post (just scroll down and click 'insert quote' next to it - or scroll up if you're using the quick reply box)

[joanna120728]

Thanks for the help! Just another question, would you say denaturation causes any damage to the primary or secondary structure of the protein, or is it only the tertiary?

[leonm19]

Hi again, sorry to dump another bucket-load of questions, but...
2. Why do B cells have MHC II complexes? Can they act as APC's? How?
3. What is involved in post translation modification? Is it just the folding of the amino acid chain in the endoplasmic reticulum, and then final modifications in the golgi complex before export?
4. With alternate splicing, does this involve cutting out different exons (as well as introns) or rearranging them, or both?
5. Can T helper cells leave the lymph nodes?
7. Are exons the triplets of nucleotides or single nucleotides?
8. When a question asks about describing somethings function at a "molecular level", is it asking to refer to the structure of what it is (e.g. an enzyme) and how this effects its function?

Thank you so much!

Hi sorry I can only answer some of your questions

2. I think B cells such as B memory cells have MHC II markers to bind to foreign antigens to be stimulated (this after the person has been infected at least once before). There might be other reasons though, I'm not entirely sure.
3. That sounds right, I think that's all you need to know.
4. Alternative splicing involves cutting out both introns and sometimes exons (not always), but I think that what you're referring to about rearranging exons is exon juggling.
5.Yes T helper cells can leave the lymph nodes. They can go to the site of infection and release cytokines to attract other immune cells such as during inflammation.
7. I'm not too sure about this one, but I think exons are coding regions so they might refer to just a general region of a gene (multiple nucleotides).
8. Yes I think so. I have seen a question about describing an antibody's function at a molecular level, which involved talking about its complementary shape to the specific antigen. Don't forget to mention specificity for some molecules.

Hope I helped! Feel free to correct me if I'm wrong for any answers.

[Erutepa]

Hi again, sorry to dump another bucket-load of questions, but...
1. Does the TAC DNA sequence come before the promotor region?
2. Why do B cells have MHC II complexes? Can they act as APC's? How?
3. What is involved in post translation modification? Is it just the folding of the amino acid chain in the endoplasmic reticulum, and then final modifications in the golgi complex before export?
4. With alternate splicing, does this involve cutting out different exons (as well as introns) or rearranging them, or both?
5. Can T helper cells leave the lymph nodes?
6. Are introns always introns, or do they become exons sometimes?
7. Are exons the triplets of nucleotides or single nucleotides?
8. When a question asks about describing somethings function at a "molecular level", is it asking to refer to the structure of what it is (e.g. an enzyme) and how this effects its function?

Thank you so much!

1. this 'TAC' DNA triplet actually codes for the first amino acid of the protein. Therefore, it comes after the promoter region. While this codes for the 'start' codon, it is translated into an amino acid while the 'stop' codons are not translated.

2. B cells have MHC class II protein receptors because they play a crucial role in their activation. In order to be activated, a B cell first needs to encounter a free antigen which will bind to its BCRs (b cell receptors) of which are membrane-bound antibodies. These antibodies once bound to the antigen will be engulfed by the B cell which will then process the antigen (like a dendritic cell would) and present it on its MHC II protein receptors. This allows the T helper T cell of complimentary specificity (already activated by its own interaction with an APC like a dendritic cell) to bind to the B cell through the TCR (T cell receptor) binding to the MHCII.
I don't think you need to know all this though, so don't worry.

3. As far as our course is concerned, that is all the post-translational modifications that will occur to the polypeptide chain.

4. It can be both. (although if you just say they are rearranged I would struggle to think you will be marked off)

5. Pretty much all the lymphocytes will migrate around the body in a circadian manner, however, they congregate in lymph tissues like the lymph nodes such that they can effectively filter antigen circulated in the lymph. Interestingly, activated T helper cells (at least specific subsets) will migrate to sites of infection and stimulate stronger immune responses by macrophages (but this is another thing that is not relevant).

6. I think they are only introns and are less of a classification of whatever segment is removed and more of an evolved genetic tool.

7. Exons are segments which would be composed of triplet codes.

8. Yes. When they ask what is happening 'at a molecular level' they are asking for the specific mechanisms. For a process such as transcription, they are wanting you to talk about the actions of the molecules involved, not just the inputs and outputs of the process.

[leonm19]

Thanks for the help! Just another question, would you say denaturation causes any damage to the primary or secondary structure of the protein, or is it only the tertiary?

I think denaturation causes damage to tertiary structures and potentially secondary structures. But it wouldn't be strong enough to damage primary structures, as for that to happen it would have to break the peptide bonds.

[Erutepa]

Thanks for the help! Just another question, would you say denaturation causes any damage to the primary or secondary structure of the protein, or is it only the tertiary?

Denaturation will not change the primary structure. The primary structure is the sequence of amino acids and heat or acidity will not change that.
Rather, for excessive temperatures, for example, the denaturation consists of the breaking of hydrogen bonds (which are susceptible to heat so to say) in both the tertiary and secondary structures. This alters the protein's conformation, thus altering its functionality.

[Erutepa]

Question 12

In aerobic respiration the final product of the electron transport chain combines with
A. oxygen.
B. glucose.
C. pyruvate.
D. carbon dioxide.

could anyone please explain how this is glucose? I thought the final products of the electron transport chain was 6H20 and 32 ATP

I would agree with you, the final product of the ETC (electrons) would combine with Oxygen and hydrogen ions. I don't see how glucose could be the correct answer.

Can you tell me where this question is from so I can have a look myself?

[AISHAB]

I would agree with you, the final product of the ETC (electrons) would combine with Oxygen and hydrogen ions. I don't see how glucose could be the correct answer.

Can you tell me where this question is from so I can have a look myself?

Hi,
Thank you. Sorry I mistakenly read the wrong question the answer was A

[EllingtonFeint]

What are sticky ends?
A. Short sequences of single stranded DNA
B. Long sequences of double stranded DNA
C. Untranslated pieces of mRNA
D. Genetically engineered restriction enzymes

So by process of elimination I was able to work this out, but is this a weird definition?
My understanding of sticky ends was cut DNA with overhangs. Anything else I should add?


Should we know about how PCR is semi conservative?

[vox nihili]

What are sticky ends?
A. Short sequences of single stranded DNA
B. Long sequences of double stranded DNA
C. Untranslated pieces of mRNA
D. Genetically engineered restriction enzymes

So by process of elimination I was able to work this out, but is this a weird definition?
My understanding of sticky ends was cut DNA with overhangs. Anything else I should add?


Should we know about how PCR is semi conservative?

They are really just short bits of ssDNA though. I guess it’s not a very VCE definition.

Yes, you should know that PCR is semi-conservative, although that language may not be used in VCE anymore. The concept is still important though, even without a title

[PhoenixxFire]

Do we need to know about continuous and discontinuous variation?


Do we also need to know DNA replication? Like drawing it, identifying all stages and about Okazaki fragments?

Definitely don't need to know anything about either of these.

2) What kind of hypothesis is best to use: 1. the 'if then when' format (e.g. if growth of plant is effected by water given to the plant then there will be increased growth of plant)
 or 2. the 'if then' format (e.g. if there is increased water supply to the plant then there will be increased growth). I was taught the if then when format but it's really long and I feel like it's wasting time.

Either. It really doesn't matter so long as you include the IV and it's predicted effect on the DV.

6. Are introns always introns, or do they become exons sometimes?
7. Are exons the triplets of nucleotides or single nucleotides?

6. Generally in alternative splicing it's the other way around. Exons are sometimes removed from pre-mRNA when it is processed.
7. Exons are stretches of nucleotide bases - it could be several thousand bases in each exon that are then joined together.

I was just wondering how a large sample size increases validity

Larger sample size increases validity as it reduces the effect of random errors that may be present. It's basically just averaging data - if you measured, for example, how fast people could run 100m (completely unrelated to bio but still), and 99 people took between 20-25 seconds, and one person took 45 seconds because they tripped over half way through (a (pretty terrible) example of an error), the effect that this person would be reduced, as so many of the other runners were within a small range. If the test was out of 5 people, and one person took significantly longer, then the results would be more greatly influenced by this. It's the same for an experiment - if there is an outlier in the results, its effect on the general data is greatly reduced if we have a sample size of 100 rather than 3.
It means that the data can be generalised more as well, as it is more reliable.

If you're talking about validity, make sure to mention that reducing the effects of random errors increases the chances that you're measuring the effect of the IV (or something along those lines) as well, because that's what validity is about.

[randy123]

Hi

Does anyone know how monoclonal antibodies carry drugs to target cells?

thanks,

[PhoenixxFire]

Hi

Does anyone know how monoclonal antibodies carry drugs to target cells?

thanks,

The drug is attached to an antibody. The antibody has antigen binding sites complementary to a molecule associated with that disease. The antibody bonds to that molecule, and the drug is therefore in the right spot.

[C14M8S]

1) Are cytotoxic T cells activated in a similar process to B cells (i.e by T helper cells' cytokines after both being exposed to the same antigen?)
2) Would the membrane structure be considered an argument supporting endosymbiotic theory? I always thought that it wasn't, due to bacteria not having double membranes.
3) Would it be ample to state that the steps of apoptosis are as follows:
 - Crucial proteins digested by caspases i.e cytoskeleton
 - Chromosomes condense, organelles digested
 - Cell shrinks
 - Cell blebs and breaks apart
 - Sends signals to macrophages to consume remains
4) What is the purpose of regular integral proteins that aren't carrier/channel proteins in cell membranes?