VCE Biology Question Thread

[Gogo14]

Dot points are particularly good if you're prone to waffling








Malaria is called by a variety of species of the genus Plasmodium, with the most severe form of malaria being the result of infection with P.falciparum.

Plasmodium species infect red blood cells. Once inside a red blood cell, the Plasmodium parasite produces proteins that it exports into the red blood cell to alter the cell to its specifications. One of these exported proteins, PfEMP1, is placed on the surface of the red blood cell. It is used to anchor the infected red blood cells to vessel walls, thereby preventing the red blood cell from moving in the blood to the spleen.

1. Suggest one reason why Plasmodium has developed a mechanism to prevent red blood cells infected with it from going to the spleen.

P.falciparum has about 60 different genes that code for PfEMP1, though only one of these genes is expressed at a time.

2. Suggest why P.falciparum has 60 genes that code for PfEMP1

Plasmepsin is an enzyme produced by Plasmodium species. It helps to mediate the export of proteins from Plasmodium into the red blood cell.

3. How many genes do you think there would be for plasmepsin? Why? 

1. The spleen is a lymph node containing cytotoxic T cells and phagocytes.
-when it infects the cell, the malaria antigen is expressed on the surface of the red blood cell
- by anchoring the cell to vessel walls, it prevents circulation of the cell into the lymph node, hence preventing Cytotoxic T cells detecting the foreign antigen on the surface
- Therefore the red blood cell will not be destroyed and plasmodium can continue to grow within the cell

2.
- PfEMp1 protein anchors the cell; hence is essential for the survival of plasmodium
- Because the protein is vital for the survival of the species, it cannot afford to have any mutations that will lead to a non-functional protein
- therefore there exists 60 genes to ensure that sufficient, functional PfEMp1 proteins are produced

3.
- a lot, 60 or more genes
- plasmepsin is a vital enzyme for the survival of plasmodium, as it allows the proteins to be secreted
- the correct production of this enzyme is equally important to the anchoring protein because it allows secretion of the protein

[AhNeon]

Dot points are particularly good if you're prone to waffling








Malaria is called by a variety of species of the genus Plasmodium, with the most severe form of malaria being the result of infection with P.falciparum.

Plasmodium species infect red blood cells. Once inside a red blood cell, the Plasmodium parasite produces proteins that it exports into the red blood cell to alter the cell to its specifications. One of these exported proteins, PfEMP1, is placed on the surface of the red blood cell. It is used to anchor the infected red blood cells to vessel walls, thereby preventing the red blood cell from moving in the blood to the spleen.

1. Suggest one reason why Plasmodium has developed a mechanism to prevent red blood cells infected with it from going to the spleen.

P.falciparum has about 60 different genes that code for PfEMP1, though only one of these genes is expressed at a time.

2. Suggest why P.falciparum has 60 genes that code for PfEMP1

Plasmepsin is an enzyme produced by Plasmodium species. It helps to mediate the export of proteins from Plasmodium into the red blood cell.

3. How many genes do you think there would be for plasmepsin? Why? 

Even though its already been answered pretty well i think
1
-There are an abundance of lymph nodes in the spleen which contain numerous T and B lymphocytes as well as other leukocytes which aim to destroy the pathogenic protozoa
-Once it has infected a red blood cell, Plasmodium anchors the cell to the vessel walls in order to prevent it from circulating with the blood to lymph nodes such as the spleen-where the protozoa would be susceptible

2   (was gonna talk about mutations but someone beat me to it so not sure if this is right)
-The PfEMP1 protein is one of great significance for the survival of Plasmodium
-This protein likely acts by attaching to a specific receptor on the red blood cell which then activates a signal transduction pathway
-In order to ensure specificity to a wide arrange of red blood cells on different species able to be infected by Plasmodium, different genes allow the construction of PfEMP1 with a slightly different conformational shapes
-The 60 genes coding for slightly different shapes of PfEMP1 could also be a way for the Plasmodium to get around vaccines which allow for the recipient to have T and B memory cells for a specific form of the protein

3 (0 clue)
This could be either very little due to Plsmepsin only having to work inside the cell and thus not having to have a variety of forms
Or the same number as PfEMP1 (60) or more as it would have to work with the proteins and thus would need to have a wide variety of specific shapes in order to work with a specific protein

[sweetcheeks]

Malaria is called by a variety of species of the genus Plasmodium, with the most severe form of malaria being the result of infection with P.falciparum.

Plasmodium species infect red blood cells. Once inside a red blood cell, the Plasmodium parasite produces proteins that it exports into the red blood cell to alter the cell to its specifications. One of these exported proteins, PfEMP1, is placed on the surface of the red blood cell. It is used to anchor the infected red blood cells to vessel walls, thereby preventing the red blood cell from moving in the blood to the spleen.

1. Suggest one reason why Plasmodium has developed a mechanism to prevent red blood cells infected with it from going to the spleen.

P.falciparum has about 60 different genes that code for PfEMP1, though only one of these genes is expressed at a time.

2. Suggest why P.falciparum has 60 genes that code for PfEMP1

Plasmepsin is an enzyme produced by Plasmodium species. It helps to mediate the export of proteins from Plasmodium into the red blood cell.

3. How many genes do you think there would be for plasmepsin? Why? 

1) The spleen is a component of the immune system and contains many white blood cells that would likely detect an infected red blood cell, initiating an immune response against plasmodium. Plasmodium developed the mechanism to reduce the risk of being detected by the hosts immune system.

2) The PfEMP1 is placed on the red blood cells surface, where it is prone to detection by the white blood cells which will initiate an immune response against this specific antigen. By having many different genes, with only one activated per red blood cell, the PfEMP1 antigens will be differently shaped depending on the gene activated, making it harder for the immune system to completely detect and eradicate the plasmodium.

3) 60. One for each of the different PfEMP1 genes, as enzymes are specific to their substrate. The 60 different genes for PfEMP1, each will be a different shape, therefore there will need to be 60 enzymes, one to match each different PfEMP1.

[Vaike]

Malaria is called by a variety of species of the genus Plasmodium, with the most severe form of malaria being the result of infection with P.falciparum.

Plasmodium species infect red blood cells. Once inside a red blood cell, the Plasmodium parasite produces proteins that it exports into the red blood cell to alter the cell to its specifications. One of these exported proteins, PfEMP1, is placed on the surface of the red blood cell. It is used to anchor the infected red blood cells to vessel walls, thereby preventing the red blood cell from moving in the blood to the spleen.

1. Suggest one reason why Plasmodium has developed a mechanism to prevent red blood cells infected with it from going to the spleen.

P.falciparum has about 60 different genes that code for PfEMP1, though only one of these genes is expressed at a time.

2. Suggest why P.falciparum has 60 genes that code for PfEMP1

Plasmepsin is an enzyme produced by Plasmodium species. It helps to mediate the export of proteins from Plasmodium into the red blood cell.

3. How many genes do you think there would be for plasmepsin? Why? 

Here's my best guess

1. -The spleen is a primary lymphoid organ, having an important role in the regulation of erythrocytes and immunity.
 -If the red blood cell containing the parasite was able to reach the spleen, it may be recognised as abnormal due to non self protein presented on MHC I markers, and thus potentially be destroyed, including the plasmodium inside.
-Therefore, by developing an anchoring mechanism, P.falciparum is able to avoid the risks associated with entering the spleen and instead grow in a more stable environment, upon the vessel wall.

2. -The immune systems primary method of dealing with parasites such as P.falciparum once inside the body is via a specific immune response.
-Specific immune responses act upon the principle that a particular pathogen will be able to be recognised by a particular antigen it displays.
-By containing 60 genes for the PfEMP1 gene, it allows the parasite to have at least 60 different variants of the PfEMP1 at it's disposal, allowing it to cycle through them, making it increasingly difficult for the specific immune system to identify which RBCs are affected due to the wide variety of antigens that may be displayed upon different infected RBCs surface's.

3. -It is likely that there is more than 60 genes for plasmepsin.
-PfEMP1 is only one of potentially many proteins that P.falciparum exports
-Each enzyme is specific to a certain substrate, and thus there must be a large variety of enzymes to be able to export a large variety of proteins
-Therefore, it is probable that there are 60 different genes coding for Plasmepsin for the PfEMP1 protein alone, with many other potential Plasmepsin genes coding for other exported proteins.   


Thanks so much for doing these questions by the way, I've found them super helpful and I really appreciate it

[vasuk]

SOMEONE PLEASE HELP ME!!
How does the Cell-Mediated immune response occur? I'm not sure as I have heard two different ways, one from each 3/4 teacher at my school.

One teacher says:
- Antigen engulfed, by an phagocytic antigen presenting cell which then displays a fragment of the antigen on an MHC marker (Does it matter which class of MHC? A lot of people are saying only MHC class II)
- Naive T Cell binds to epitope displayed on the MHC marker via the T-Cell Receptor
- It becomes activated and is stimulated to divide and differentiate into 4 types
- Helper T Cell which secretes interleukins, stimulates Cytotoxic T Cells and stimulates B-lymphocytes to divide and differentiate
- Cytotoxic T Cell which recognise antigens presented on MHC Class I marker, on surface of abnormal/infected cell. Tc cells bind with these cells, and release cytotoxins inducing cell destruction
- Memory T Cell which remains in blood after infection has passed to prevent reinfection, quickly reactivated if pathogen reinvades
- Suppressor T Cell which stops immune response when infection passes

OR I have also been told by the other teacher:
- An antigen presenting cell engulfs and presents a fragment of an antigen on a MHC Class II marker
- A HELPER T CELL binds to the antigen fragment via the T-Cell Receptor
- The Helper T Cell is stimulated to divide and differentiate into all 4 types of T Cells
- Helper T Cell also secretes interleukins, stimulates Cytotoxic T Cells and stimulates B-lymphocytes to divide and differentiate
-  Then the 4 T Cells go about their various roles as listed above


The main difference being, in the 1st method a naive T Cell is the one which binds to the antigenic fragment displayed on an MHC marker (which class, I don't know) and therefore causes division and differentiation into the 4 types of T Cells.

In the 2nd method, the Helper T Cell is heavily involved being the one which binds to the antigenic fragment displayed on the MHC marker and therefore it itself becomes activated to divide and differentiate into the 4 types of T Cells. There is no mention of naive T cells here.

I am very confused

[HasibA]

there is no difference between polygenic and polygenetic is there? thanks!
edit: why and when do we use potassium-argon dating vs carbon 14 dating?

[AhNeon]

SOMEONE PLEASE HELP ME!!
How does the Cell-Mediated immune response occur? I'm not sure as I have heard two different ways, one from each 3/4 teacher at my school.

One teacher says:
- Antigen engulfed, by an phagocytic antigen presenting cell which then displays a fragment of the antigen on an MHC marker (Does it matter which class of MHC? A lot of people are saying only MHC class II)
- Naive T Cell binds to epitope displayed on the MHC marker via the T-Cell Receptor
- It becomes activated and is stimulated to divide and differentiate into 4 types
- Helper T Cell which secretes interleukins, stimulates Cytotoxic T Cells and stimulates B-lymphocytes to divide and differentiate
- Cytotoxic T Cell which recognise antigens presented on MHC Class I marker, on surface of abnormal/infected cell. Tc cells bind with these cells, and release cytotoxins inducing cell destruction
- Memory T Cell which remains in blood after infection has passed to prevent reinfection, quickly reactivated if pathogen reinvades
- Suppressor T Cell which stops immune response when infection passes

OR I have also been told by the other teacher:
- An antigen presenting cell engulfs and presents a fragment of an antigen on a MHC Class II marker
- A HELPER T CELL binds to the antigen fragment via the T-Cell Receptor
- The Helper T Cell is stimulated to divide and differentiate into all 4 types of T Cells
- Helper T Cell also secretes interleukins, stimulates Cytotoxic T Cells and stimulates B-lymphocytes to divide and differentiate
-  Then the 4 T Cells go about their various roles as listed above


The main difference being, in the 1st method a naive T Cell is the one which binds to the antigenic fragment displayed on an MHC marker (which class, I don't know) and therefore causes division and differentiation into the 4 types of T Cells.

In the 2nd method, the Helper T Cell is heavily involved being the one which binds to the antigenic fragment displayed on the MHC marker and therefore it itself becomes activated to divide and differentiate into the 4 types of T Cells. There is no mention of naive T cells here.

I am very confused

Both are correct just different ways of looking at it. It would be best to combine both so you know the immune system as detailed as possible.
Not sure if it's a must know but yes, it is MHC II in this case. Cytotoxic T cells bind to MHC I whilst Helper T cells bind to MHC II. MHC I is present on all nucleated cells (everything but mature red blood cells) whilst MHC II is only on antigen presenting cells like macrophages and dendrites.

[plsbegentle]

there is no difference between polygenic and polygenetic is there? thanks!
edit: why and when do we use potassium-argon dating vs carbon 14 dating?

carbon 14 dating is only useful for ages up to 60,000. while K/Ar is useful for a very very long time ( not sure about the exact figure). We use radioactive isotopes to figure the absolute age of when the organism died

[Vaike]

there is no difference between polygenic and polygenetic is there? thanks!
edit: why and when do we use potassium-argon dating vs carbon 14 dating?

As far as I'm aware they (polygenic and polygenetic) are two of the same

Carbon 14 has a half life of 5,730 years. This means, after this time, only half of the original C14 will remain, the other half will have decayed into Nitrogen 14. Carbon 14 is useful for dating organic compounds up to and around 50,000 years old, but not any older, because past this point the amount of C14 left will be so small it's difficult to measure (I assume, not 100% on this part)

On the other hand, K40 has a much, much longer half life than C14, with a half life of 1,300,000,000 years. This means that it can be used to date substances, often rocks, from 0.5 myo, due to decaying into 40Ar at a much slower rate.

It's also important to consider that not all compounds will have a particular element, the subject being dated has to contain the element in the first place, for example not all. For example, most igneous rocks cannot be dated with C14, as they often do not have C14, or they haven't directly obtained it from the atmosphere (unlike living organisms who breath it in, and thus have a known initial concentration of C14, concentration the same as the atmosphere), and also because they are often older than 50,000 years old. 

Hopefully this helps you

[Gogo14]

Why is it that when you inbreed animals, the offspring often has a high chance of genetic problems.i.e. pedigree dogs

[Vaike]

Why is it that when you inbreed animals, the offspring often has a high chance of genetic problems.i.e. pedigree dogs

My understanding is that related individuals, due to having similar/same parents, will potentially have many loci upon which both are heterozygotes for recessive conditions, but since they still have one normal gene, they display the normal phenotype. However, when two genetically similar individuals breed, they will have a greater degree of similarity in the conditions they are heterozygous for than say if compared to an unrelated individual, due to inheritance from the same parents, and thus it is more likely that an offspring of the inbreeding inherits a recessive condition as a result. Not 100% sure on this though, I could be wrong, this is just what I've been told.

[HasibA]

thanks for the help guys. is carbon and potassium/argon dating the only elements we have to know that relate to absolute dating?
more q's

1) difference between lysosome and lysozyme?
2) is a definition of apoptosis all we have to know? or more?
3)what do restriction endonucleases do/ endonucleases in general?
4) what do we have to know about mitochondrial dna, and mitochondrial inheritance? never came across this type of inheritance
5) what is the purpose of having many chlorophyll pigments? to absorb different wavelengths of light, to support photosynthetic reactions etc.?
6) a question i did was- 'explain why fossilized feet bones consist of only a few fragments'- i wrote it was because they're intricate structures and could easily be damaged etc.
7)'the stride of homo erectus is the similar to the stride of a modern man. what advantage did this give homo erectus?'- i wrote more efficient walking, able to travel large distances easier, saving energy etc. this sound ok?
'how might climate change affect an organism that has undergone a series of genetic bottlenecks'- didnt really get this one.

thanks guys- sorry to spam!

[sweetcheeks]

thanks for the help guys. is carbon and potassium/argon dating the only elements we have to know that relate to absolute dating?
more q's

1) difference between lysosome and lysozyme?
2) is a definition of apoptosis all we have to know? or more?
3)what do restriction endonucleases do/ endonucleases in general?
4) what do we have to know about mitochondrial dna, and mitochondrial inheritance? never came across this type of inheritance
5) what is the purpose of having many chlorophyll pigments? to absorb different wavelengths of light, to support photosynthetic reactions etc.?
6) a question i did was- 'explain why fossilized feet bones consist of only a few fragments'- i wrote it was because they're intricate structures and could easily be damaged etc.
7)'the stride of homo erectus is the similar to the stride of a modern man. what advantage did this give homo erectus?'- i wrote more efficient walking, able to travel large distances easier, saving energy etc. this sound ok?
'how might climate change affect an organism that has undergone a series of genetic bottlenecks'- didnt really get this one.

thanks guys- sorry to spam!

1) A lysosome is an organelle found in eukaryotic cells. Its role is to breakdown unneeded material. Lysozymes are enzymes that provide defense against pathogens
2) Not sure on that one.
3) Restriction endonucleases is another term for restriction enzymes. They simply cut genetic material at binding sites. They are commonly found in bacteria as a mechanism at protection against viruses (destroy their genetic material before it can be incorportated in the bacterias own). They can be used in gene manipulation and gel electrophoresis (fragment the DNA)
4) Mitchondrial DNA is maternally inherited (it only comes from your mother and her mother so forth). It is useful as it can show direct lineage and mutates at a known rate so accurate dating can be performed
5) Not 100% sure about this one, but it is likely to do with being able to utilise as much light as possible. It is common for rainforest plants to have multiple pigments to capture as much light as possible due to its low availability.
6) Not sure
7) Again not sure
Genetic bottlenecks are where a population is severely reduced. This can lead to a decreased genetic variation. If a change comes, there can be little variation between members, resulting in them all having the same impact (e.g. they all cannot cope with rising temperature). Another problem is that a smaller population also means that it is harder for variation to accumulate and those members that may be able to cope with the change are too few and the species cannot rebuild.

[AhNeon]

thanks for the help guys. is carbon and potassium/argon dating the only elements we have to know that relate to absolute dating?
more q's

1) difference between lysosome and lysozyme?
2) is a definition of apoptosis all we have to know? or more?
3)what do restriction endonucleases do/ endonucleases in general?
4) what do we have to know about mitochondrial dna, and mitochondrial inheritance? never came across this type of inheritance
5) what is the purpose of having many chlorophyll pigments? to absorb different wavelengths of light, to support photosynthetic reactions etc.?
6) a question i did was- 'explain why fossilized feet bones consist of only a few fragments'- i wrote it was because they're intricate structures and could easily be damaged etc.
7)'the stride of homo erectus is the similar to the stride of a modern man. what advantage did this give homo erectus?'- i wrote more efficient walking, able to travel large distances easier, saving energy etc. this sound ok?
'how might climate change affect an organism that has undergone a series of genetic bottlenecks'- didnt really get this one.

thanks guys- sorry to spam!

Just gonna answer the ones that aren't already answered
2) Vcaa has accepted "programmed cell death" as a definition in past exams
5) Different accessory pigments serve to allow a plant to absorb a wider array of wavelengths. However, it is ultimately only chlorophyll a that has a direct involvement in the light-dependent stage of photosynthesis
6) Not sure but likely due to the fact that only hard material fossilizes in addition to the likelihood that the fragile, thin bones in the foot may be damaged
7) Your answer sound about right                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                       

[Vaike]

2) is a definition of apoptosis all we have to know? or more?

The study design states:
-Apoptosis (regulated cell death) as an example of a cellular response to specific signals
So by the sounds of it, we only need a general idea, but I still think it wouldn't hurt to look up on the different pathways (mitochondrial and death receptor) and the general process involved in apoptosis and it's role in an organism compared to necrosis.