VCE Biology Question Thread

[Angelx001]

Hey guys,
Do we need to know about communication between cells (occluding, communicating & anchoring junctions)?

[vox nihili]

Hey guys,
Do we need to know about communication between cells (occluding, communicating & anchoring junctions)?

No

-Penicillin works by damaging the cell wall of bacteria
-The cell wall is composed of peptidoglycan
-Peptidoglycan is not found in human cells, so penicillin has no effect

Pretty much been answered well by calebark, also I don't know much about penicillin so:
Penicillin is an antibiotic which acts as a growth inhibitor to bacteria. It does this by interfering with the normal function/ growth of bacterial cells, and by considering that bacterial cells are prokaryotes and humans eukaryotes. The human cells will be structurally different to bacterial cells, therefore, penicillin will be able to kill bacterial cells but not human cells due to its specificity.

Perfect answers guys. Needless to say, nobody needs to know the function of penicillin. All you need to acknowledge is that bacteria are prokaryotes and thus contain structures that do not exist in human cells. Thereby, targeting those structures allows you to selectively kill bacteria, without harming humans.

Penicillin is a fairly special antibiotic actually. Except in those in which it causes an allergic reaction, it's one of the safest drugs known.



Two different types of adipose (fat) tissue have been identified in humans. In adult humans, so-called white fat predominates; whereas in children, high levels of brown fat are observed. Over time, brown fat is replaced with white fat.

One critical difference between brown fat and white fat, is the production of a protein called UCP1 in brown fat. UCP1 effectively stalls the electron transport chain, preventing it from producing ATP. Energy produced by the ETC is instead used to fuel heat production.

Some scientists have suggested that it might be possible to treat obesity by converting existing white fat into brown fat in adults. Explain why.

[Calebark]

Two different types of adipose (fat) tissue have been identified in humans. In adult humans, so-called white fat predominates; whereas in children, high levels of brown fat are observed. Over time, brown fat is replaced with white fat.

One critical difference between brown fat and white fat, is the production of a protein called UCP1 in brown fat. UCP1 effectively stalls the electron transport chain, preventing it from producing ATP. Energy produced by the ETC is instead used to fuel heat production.

Some scientists have suggested that it might be possible to treat obesity by converting existing white fat into brown fat in adults. Explain why.

-Excess energy is stored as glycogen in fat cells
-Obese people produce too much energy for too little activity
-Brown fat fuels heat production, so possible excess energy is instead converted to heat energy
-Thus it is not stored
-Thus converting white fat to brown fat could decrease obesity

[solution]

I don't understand the second part of the answer. Explanation please?

Pseudogenes are the remains of broken genes which are unable to function and can be considered to be genetic fossils. Some are relics of genes lost through evolution while others reflect an earlier version of a present functional gene. Pseudogenes are able to accumulate all kinds of mutations.
The gene G in mice makes an enzyme that helps synthesise vitamin C, but this gene became faulty in primates more than 40 million years ago and is now a pseudogene in humans.

Why are pseudogenes able to accumulate mutations that do not exist in functional genes? (2 marks)

My answer:
Pseudogenes do not code for proteins. As a result, they are not checked for mutations (and repaired), allowing mutations to accumulate across many generations.

Examiner's report:
pseudogenes are not expressed and any mutation in them does not harm the offspring when passed on
functional genes become inoperative or produce a different protein which could affect the survival of offspring.

[vox nihili]

-Excess energy is stored as glycogen in fat cells
-Obese people produce too much energy for too little activity
-Brown fat fuels heat production, so possible excess energy is instead converted to heat energy
-Thus it is not stored
-Thus converting white fat to brown fat could decrease obesity

This is a really tricky question, no doubt. Have another crack, I don't think this is quite there.

Also, glycogen is stored in muscle and the liver. Fat is stored in fat tissue.

Try to think about how we produce energy and what our major energy source (i.e. to produce ATP) is. Then consider what happens if you have too much of it.

I don't understand the second part of the answer. Explanation please?

Pseudogenes are the remains of broken genes which are unable to function and can be considered to be genetic fossils. Some are relics of genes lost through evolution while others reflect an earlier version of a present functional gene. Pseudogenes are able to accumulate all kinds of mutations.
The gene G in mice makes an enzyme that helps synthesise vitamin C, but this gene became faulty in primates more than 40 million years ago and is now a pseudogene in humans.

Why are pseudogenes able to accumulate mutations that do not exist in functional genes? (2 marks)

My answer:
Pseudogenes do not code for proteins. As a result, they are not checked for mutations (and repaired), allowing mutations to accumulate across many generations.

Examiner's report:
pseudogenes are not expressed and any mutation in them does not harm the offspring when passed on
functional genes become inoperative or produce a different protein which could affect the survival of offspring.

If you have a mutation in a gene you need, one of two things can happen: that gene can stop working, or it can produce a protein that does something different. That's all it's saying.

Your answer was pretty good, just don't forget to talk about the evolutionary context

[sweetcheeks]

@Solution

What it is saying is that if a mutation where to occur in a gene that was used by the organism (expressed), it could have a severe negative impact on the organism, having a higher chance of the mutation being removed from the gene pool. If the gene doesn't code for anything it is not expressed and mutations won't have an effect upon the organism as there is no product of the gene (i.e. no protein is produced).

[Gogo14]

What is a haplogroup? (Its in the context of mtDNA and evolution)
It came up on my teacher's notes, but it isn't really explained or define.
This is just one of those words where google only confuses you more

[Angelx001]

Do we need to know about amoeba, fungi, worms, arthropods, rabies?

[Gogo14]

No

Perfect answers guys. Needless to say, nobody needs to know the function of penicillin. All you need to acknowledge is that bacteria are prokaryotes and thus contain structures that do not exist in human cells. Thereby, targeting those structures allows you to selectively kill bacteria, without harming humans.

Penicillin is a fairly special antibiotic actually. Except in those in which it causes an allergic reaction, it's one of the safest drugs known.



Two different types of adipose (fat) tissue have been identified in humans. In adult humans, so-called white fat predominates; whereas in children, high levels of brown fat are observed. Over time, brown fat is replaced with white fat.

One critical difference between brown fat and white fat, is the production of a protein called UCP1 in brown fat. UCP1 effectively stalls the electron transport chain, preventing it from producing ATP. Energy produced by the ETC is instead used to fuel heat production.

Some scientists have suggested that it might be possible to treat obesity by converting existing white fat into brown fat in adults. Explain why.

- Adipose tissues store fat and energy for the organism, and when you convert white fat to brown fat, UCP1 is produced by the brown fat
- this protein essentially causes the electron transport chain to be inefficient as energy is converted to heat rather than chemical (in the form of ATP)
- therefore more fat would be used to produce the same amount of ATP in brown fats than white fats.
- So obese people with brown fat will use up more fat

[vox nihili]

What is a haplogroup? (Its in the context of mtDNA and evolution)
It came up on my teacher's notes, but it isn't really explained or define.
This is just one of those words where google only confuses you more

No need to worry about it, not part of the course

Do we need to know about amoeba, fungi, worms, arthropods, rabies?

You should recognise all of these except amoebae and rabies. Just remember, rabies is a virus!

- Adipose tissues store fat and energy for the organism, and when you convert white fat to brown fat, UCP1 is produced by the brown fat
- this protein essentially causes the electron transport chain to be inefficient as energy is converted to heat rather than chemical (in the form of ATP)
- therefore more fat would be used to produce the same amount of ATP in brown fats than white fats.
- So obese people with brown fat will use up more fat

Yep, would be happy to give that full marks.

Assuming your energy needs remain constant, you'd have to burn more fuel (in adipose tissue, that's gonna be fat) to produce the same amount of ATP. This is part of the reason that kids are so skinny compared to adults.

CFTR is a chloride channel expressed in the lungs. In patients with cystic fibrosis, the channel is defective.

One of the features of cystic fibrosis is thick, gluggy mucous. Explain how a non-functional CFTR channel could lead to thick, gluggy mucous.

[Butterflygirl]

No need to worry about it, not part of the course

You should recognise all of these except amoebae and rabies. Just remember, rabies is a virus!

Yep, would be happy to give that full marks.

Assuming your energy needs remain constant, you'd have to burn more fuel (in adipose tissue, that's gonna be fat) to produce the same amount of ATP. This is part of the reason that kids are so skinny compared to adults.

CFTR is a chloride channel expressed in the lungs. In patients with cystic fibrosis, the channel is defective.

One of the features of cystic fibrosis is thick, gluggy mucous. Explain how a non-functional CFTR channel could lead to thick, gluggy mucous.

The chloride levels in cells in the lungs play a role in controlling mucous viscosity. If the CFTR channel is not present in individuals with cystic fibrosis, then chloride cannot be transported into and out of cells lining the lungs, leading to thick, gluggy mucous production.


Lol I tried but I have no idea about how factual any of the things I mentioned are (Just made up some stuff) 

[vox nihili]

The chloride levels in cells in the lungs play a role in controlling mucous viscosity. If the CFTR channel is not present in individuals with cystic fibrosis, then chloride cannot be transported into and out of cells lining the lungs, leading to thick, gluggy mucous production.


Lol I tried but I have no idea about how factual any of the things I mentioned are (Just made up some stuff) 

Not a bad answer, but not quite what I was looking for. You're right that chloride does play a role in determining the viscosity of mucous—that much we know from the stem—but how does it do it? Remember, you'll never get asked something in VCE that doesn't relate to what you've learned; likewise, I haven't asked you about anything you won't have learned here

[sweetcheeks]

I'll take a stab.

I'm thinking along the lines of osmosis. A defective chloride channel stops chloride ions being able to enter the lungs, this results in a hypotonic environment compared to the other side of the lungs. Water will move from an area of low solute concentration to an area of higher solute concentration. The water will move out of the lungs, resulting in a higher viscosity mucous.

[vox nihili]

I'll take a stab.

I'm thinking along the lines of osmosis. A defective chloride channel stops chloride ions being able to enter the lungs, this results in a hypotonic environment compared to the other side of the lungs. Water will move from an area of low solute concentration to an area of higher solute concentration. The water will move out of the lungs, resulting in a higher viscosity mucous.

Yep, this is the right idea. Good work!

Just be careful about the way you word it though. When you talk about chloride moving in and out of the lungs, it's hard to interpret whether you mean the lungs as the cells that create the lung tissue, or the breathing spaces (i.e. extracellular environment). The defect in CFTR prevents chloride from moving out of cells in the lungs, to the extracellular environment. This way, the cells are hypotonic and the extracellular environment is, by definition, therefore hypertonic.

An interesting follow up:

Cholera is a diarrhoeal disease that continues to ravage the developing world. It is caused by the bacterium Vibrio cholerae, which is transferred in water contaminated by faeces.

V.cholerae causes diarrhoea by producing a toxin that binds to a receptor on the intestinal mucosa. Binding to the receptor increases the production of cAMP in the cell, which in turn activates the CFTR chloride channel.

• What is the role of cAMP in this pathway?
• Explain how opening of CFTR can cause diarrhoea

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Edited to better reflect reality....i.e. I done fucked up :p

PS: interesting fact; you can't change the colour of lists on HTML..kden

[Butterflygirl]

Yep, this is the right idea. Good work!

Just be careful about the way you word it though. When you talk about chloride moving in and out of the lungs, it's hard to interpret whether you mean the lungs as the cells that create the lung tissue, or the breathing spaces (i.e. extracellular environment). The defect in CFTR prevents chloride from moving out of cells in the lungs, to the extracellular environment. This way, the cells are hypotonic and the extracellular environment is, by definition, therefore hypertonic.

An interesting follow up:

Cholera is a diarrhoeal disease that continues to ravage the developing world. It is caused by the bacterium Vibrio cholerae, which is transferred in water contaminated by faeces.

V.cholerae causes diarrhoea by producing a toxin that binds to a receptor on the intestinal mucosa. Binding to the receptor increases the production of cAMP in the cell, which in turn activates the CFTR chloride channel.

• What is the role of cAMP in this pathway?
• Explain how opening of CFTR can cause diarrhoea

[/b][/color]


Edited to better reflect reality....i.e. I done fucked up :p

PS: interesting fact; you can't change the colour of lists on HTML..kden

a) cAMP acts as a secondary signalling molecule that stimulates a signal cascade to then activate the CFTR chloride channel.
b) If the chloride channel opens, then chloride will move out of the cell via facilitated diffusion. This will then cause water to move out of the cell via osmosis from a low solute concentration (inside the cell) to a high solute concentration (outside the cell). The water levels in the intestine will increase, causing diarrhoea.

Maybe? Maybe not? I don't know