VCE Biology Question Thread

[PhoenixxFire]

Hey guys,

Do we need to know anything about plant immunity?

Thanks!

Yes, but not that much.
Study design:
• invading cellular and non-cellular pathogens as a source of non-self antigens, and preventative strategies
including physical, chemical and microbiological barriers in animals and plants that keep them out

Plants don't have adaptive immunity so you just need to know about physical and chemical barriers.

Here's an old stolen quote from heidi because I don't remember many off the top of my head.

So these are answers from past questions they've asked:

Barriers in plants:
•   Waxy layers on outside surface
•   Intact or thick cuticle
•   Chemicals that repel potential pathogen vectors such as insects
(Not from the exam report but my own knowledge: another could be thorns and hairs to deter vectors, or excreting nasty chemicals that kill pathogens - no need to be specific)

And if infection does occur in plants:
•   Grow ‘gall’ tissue round area containing infective agent to prevent spread to other areas
•   Produce chemicals e.g. tannins
•   Produce ‘gum’ to seal off wounded area
•   Drop infected leaf to inhibit spread to other areas

[Scribe]

Could someone briefly explain monoclonal antibodies please? My class was told to just make notes from the Nature of Biology textbook and I'm not sure what we need.

Thanks!

[PhoenixxFire]

Could someone briefly explain monoclonal antibodies please? My class was told to just make notes from the Nature of Biology textbook and I'm not sure what we need.

Thanks!

It's new to the study design, so your teacher probably isn't too sure themself.

The study design dot point is very small - it just says that you need to know their role in treating cancer.

Here's what i wrote in my notes about them:

Monoclonal antibodies: Antibodies made synthetically in a lab, they all have the same antigen specificity.

They are made by fusing a plasma B cell that produces antibodies with a desired antigen specificity to a cancerous cell, resulting in a B cell that will divide indefinitely.

If antibodies that were specific to proteins only expressed by cancerous cells could be made, they could travel around a patient’s body and stick to cancerous cells.

These antibodies could be modified to carry things such as radioactive isotopes.
They could be used to set off complement cascades.
A toxin could be attached to antibodies that will be delivered straight to cancerous cells.
Antibodies could be made to stimulate fas R receptors and therefore trigger apoptosis in cancerous cells.
Antibodies could also carry a non-self antigen to allow phagocytes to find the cancerous cells.
Antibodies can also be used to damage blood vessels that lead to tumours (tumours can sometimes cause new blood vessels to form).

[Scribe]

Another question,

What's the difference between natural killer cells and cytotoxic T cells? Do they both work via degranulation?

Thanks 

[darkz]

Another question,

What's the difference between natural killer cells and cytotoxic T cells? Do they both work via degranulation?

Thanks 

Hey so heres some info from a past post. And just to add, NK are apart of the innate immune response and TC from the adaptive and yes, they both work via degranulation through the action of destroying the integrity of the plasma membrane

This is outside of the scope of the VCE course, but its some extra interesting info about it and you can find it in the Nature of Biology textbook if you use it. So basically, Natural Killer cells have two receptors, a killer activation receptor (KAR) and killer inhibitory receptor (KIR). KAR binds with surface proteins released by virally infected cells or cancerous cells in distress, while KIR binds to MHC Class I markers on the cell. If the KIR binds with a sufficient number of MHC Class I markers, then the order to kill is overridden. (We can get a lack of MHC Class I markers when viruses or cancer cells inhibit or destroy MHC Class I markers on the cell surface). Therefore, if the cell is lacking of MHC Class I markers, then the signal to kill won't be overridden and then the NK cell will secrete perforin damaging the plasma membrane leading to lysis. If the cell has sufficient MHC Class I markers, then I'm pretty sure that those cells are left for cytotoxic T cells.

[PopcornTime]

Can someone check the following:

High cytokinin and low auxin causes shoot growth and low cytokinin and high auxin causes root growth due to:
- the synergistic effect between the two hormones

MHC2 markers are present in:
- APC's

MHC1 markers are present in:
- all nucleated cells

Thanks.

[darkz]

Can someone check the following:

High cytokinin and low auxin causes shoot growth and low cytokinin and high auxin causes root growth due to:
- the synergistic effect between the two hormones

MHC2 markers are present in:
- APC's

MHC1 markers are present in:
- all nucleated cells

Thanks.

Yeh, looks good!

[Abi21]

Hi,
So I've heard that what happens is with bio, your cohort is ranked based upon exam grades and Sac rankings. If you're exam rank is 10 and your sac rank is 26, what happens?

[PhoenixxFire]

Hi,
So I've heard that what happens is with bio, your cohort is ranked based upon exam grades and Sac rankings. If you're exam rank is 10 and your sac rank is 26, what happens?

Basically:
Your SAC rank (for each of unit 3 and 4) will get scaled to the 26th best exam score (assuming you're the same rank for both U3 and U4). Your exam rank doesn't matter - you'll get your exam score as your GA3.

[juntyhee]

Can someone check the following:

High cytokinin and low auxin causes shoot growth and low cytokinin and high auxin causes root growth due to:
- the synergistic effect between the two hormones

MHC2 markers are present in:
- APC's

MHC1 markers are present in:
- all nucleated cells

Thanks.

Not always for the first one, i.e. root growth occurs when cytokinin concentration is equal to 0.

[darkz]

So here's a graph of time vs antibody titres after a previously uninfected individual was infected with a virus. How do we explain the 1st dip in the graph? Is it because the antibodies are being used up quicker than being produced or something?

[TheBigC]

So here's a graph of time vs antibody titres after a previously uninfected individual was infected with a virus. How do we explain the 1st dip in the graph? Is it because the antibodies are being used up quicker than being produced or something?

Just to clarify, is the above graph a depiction of a primary infection? To me, it looks analogous to both the primary and secondary immune responses mapped over time... if so, the 'dip' in the graph is simply deterioration of antibodies (as they only last for so long within the bloodstream). However, if it represents a single response, then a different explanation must be had.

[darkz]

Just to clarify, is the above graph a depiction of a primary infection? To me, it looks analogous to both the primary and secondary immune responses mapped over time... if so, the 'dip' in the graph is simply deterioration of antibodies (as they only last for so long within the bloodstream). However, if it represents a single response, then a different explanation must be had.

Its a single infection over the course of around 50 days

[TheBigC]

Its a single infection over the course of around 50 days

You're explanation of antibody consumption versus antibody production seems plausible at that 'dip', however, I would probably just add that this would have likely occurred as a result of the specific pathogen undergoing rapid replication after a possible initial 'elimination'. For example, the pathogen - upon replicating (immediately prior to the observed 'dip') would have caused agglutination, opsonisation, neutralisation etc. which used up antibodies, however then begun to exponentially increase in population, which warranted a secondary response.

Now, another plausible explanation could have been the degradation of antibodies (given the 50-day period) and the occurrence of a subsequent secondary immune response due to a coincident explanation as above...

[juntyhee]

Hey friends, few questions:

1. "...apoptosis is tidy and splits the cell into little parcels that can be taken up and recycled by other cells."
What does it mean by "recycle"? If these "little parcels" are phagocytosed and destroyed, then how can they be 'recycled'?

2. Can second messengers act as effector molecules? And do they always amplify cellular responses?

Also, can you please confirm the following definitions?

Second Messenger: Molecules that relay signals through the cytoplasm after the binding of a signalling molecule, by activating a cascade of events to trigger an amplified cellular response.
Signal Amplification: The ability of one signalling molecule to cause the activation of many molecules inside the cell, initiating a cascade of events that amplify the response.