VCE Biology Question Thread

[katiesaliba]

Indeed we are required to know the various forms of a mutation. These include a single base substitution, addition, or deletion. This may lead to a frameshift mutation, whereby everything is shifted across, or a mutation in which the final protein isn't effected as the same amino acid is produced. Furthermore, a knowledge of chromosome mutations is somewhat needed, such as a chromosome mutation involves many base pairs and significantly alters protein functioning.

Just to add some useful terminology to this-

Point mutation types:
-substitutions,
-additions,
-deletions.

Deletions or additions result in frameshift mutations.

POINT MUTATION EFFECTS:
Missense mutations: Codes for different amino acid.
Silent mutations: Codes for same amino acid (as DNA is degenerative)
Nonsense mutations: (my personal favourite...has the best name :')) Codes for stop codons (UGA, UAA, UAG)

Some handy chromosomal mutations include translocation mutations and of course non-disjunction mutations

 

[kk.08]

Cholesterol's primary role is to regulate the fluidity and flexibility of the plasma membrane. This is done by preventing it from bunching up, and freezing in cold conditions. Conversely, it keeps the phospholipids closer together in cases of high temperature to prevent it from breaking or loosing its selective permeability.

Thanks!

[katiesaliba]

Can someone please check my understanding:

HUMORAL DEFENSE-
-Antibodies on B-cell complex with a complementary antigen.
-Concurrently, the antigen-complementary Th cell becomes activated upon binding with same antigen, releasing interleukin-2.
-Interleukin-2 stimulates B-cell clonal expansion, resulting in the differentiation and proliferation into plasma and memory B-cells.
-Plasma B cells synthesise and secrete immunoglobulins which either deactivate the concerned pathogen, or induce opsonisation, for example.
-Memory B-cells remain present, ready for future exposure.

CELL-MEDIATED RESPONSE:
-Cytotoxic T-cell receptor binds with a complementary antigen which is complexed with MHC I (e.g. infected cells).
-Concurrently, the antigen-complementary Th cell becomes activated upon binding with same antigen, releasing interleukin-2.
-Interleukin-2 stimulates Cytotoxic T-cell clonal expansion, resulting in the differentiation and proliferation into effector and memory Cytotoxic T-cells.
-Upon identification of foreign antigen (complexed with MHC I), cytotoxic T-cells secrete granzyme and perforin to 1) create perforations in the cell's membrane, and 2) induce apoptosis. This consequently kills infected SELF cells which express foreign antigens.
 -Memory cytotoxic T-cells remain present, ready for future exposure.


Is this all we need to know about the adaptive immune response?   

[dankfrank420]

Thanks!

It's a good answer, but far beyond what is required for the VCE Bio course. For all the VCAA past exams I've done, the answer to "what is the function of cholesterol" is simply to provide fluidity and flexibility to the plasma membrane.

[dankfrank420]

Can someone please check my understanding:

HUMORAL DEFENSE-
-Antibodies on B-cell complex with a complementary antigen.
-Concurrently, the antigen-complementary Th cell becomes activated upon binding with same antigen, releasing interleukin-2.
-Interleukin-2 stimulates B-cell clonal expansion, resulting in the differentiation and proliferation into plasma and memory B-cells.
-Plasma B cells synthesise and secrete immunoglobulins which either deactivate the concerned pathogen, or induce opsonisation, for example.
-Memory B-cells remain present, ready for future exposure.

CELL-MEDIATED RESPONSE:
-Cytotoxic T-cell receptor binds with a complementary antigen which is complexed with MHC I (e.g. infected cells).
-Concurrently, the antigen-complementary Th cell becomes activated upon binding with same antigen, releasing interleukin-2.
-Interleukin-2 stimulates Cytotoxic T-cell clonal expansion, resulting in the differentiation and proliferation into effector and memory Cytotoxic T-cells.
-Upon identification of foreign antigen (complexed with MHC I), cytotoxic T-cells secrete granzyme and perforin to 1) create perforations in the cell's membrane, and 2) induce apoptosis. This consequently kills infected SELF cells which express foreign antigens.
 -Memory cytotoxic T-cells remain present, ready for future exposure.


Is this all we need to know about the adaptive immune response?   

Don't memory Cells travel to the lymph nodes and are stored there?

[katiesaliba]

Yeah, they do (I'm pretty sure). Didn't take the location into account, whoops 

[Reus]

-Memory cytotoxic T-cells remain present, ready for future exposure.

I thought that Tc cells were harmful to the body after the response? Hence Suppressor T cells come in to play, suppressing the Tc cells from acting onwards (on self cells)?

[howlingwisdom]

I thought that Tc cells were harmful to the body after the response? Hence Suppressor T cells come in to play, suppressing the Tc cells from acting onwards (on self cells)?

Suppressor T cells can eliminate Tc cells after an infection has passed (in order to conserve energy and the like) but memory cells would also be generated (which is why they are still present in the body). I think that we are not required to know much detail about T-memory cells at all, except that like B memory cells, memory cells for T cells are formed as well.

[howlingwisdom]

How can we tell whether a genetic disease has occurred from non-disjunction in Anaphase 1 or Anaphase 2?

[Tyleralp1]

How can we tell whether a genetic disease has occurred from non-disjunction in Anaphase 1 or Anaphase 2?

Anaphase 1 would imply that all four gametes are affected.
Anaphase 2, only two gametes are affected.

Basically when there is extra chromosome, or double up on a homologous pair, refers to a non-disjunction. I hope that makes sense

[howlingwisdom]

Anaphase 1 would imply that all four gametes are affected.
Anaphase 2, only two gametes are affected.

Basically when there is extra chromosome, or double up on a homologous pair, refers to a non-disjunction. I hope that makes sense

Thanks! That makes logical sense

[shivaji]

So in cell-mediated immunity, after the cytotoxic t-cell is activated by a Th cell, the Tc celll undergoes clonal expansion to produce more cytotoix t cells (effector T cells) and also some T-memory cells as well?

[RazzMeTazz]

I don't really understand how infected cells signal cytotoxic T cells?

Once infected with the pathogen do they break down the antigens of the pathogen and display it on the surface of their MHC class 1 markers?

thanks!

[Tyleralp1]

I don't really understand how infected cells signal cytotoxic T cells?

Once infected with the pathogen do they break down the antigens of the pathogen and display it on the surface of their MHC class 1 markers?

thanks!

The Cell Mediated Response.

1. Pathogen/Antigen is detected as non-self and harmful.
2. Phagocytes (Macrophages) migrate to the site of infection and engulf the pathogen, breaking it down.
3. It presents an antigen fragement on its MHC Class II markers.
4. T Helper cells recognise this antigen, and stimulate the T cells to undergo clonal expansion and divide into Cytotoxic T Cells.
5. They move to the pathogen and release toxic granules to destroy it. Memory T cells are formed in the process for future occurences, and suppresor T cells supress the immune response.

[shivaji]

The Cell Mediated Response.

1. Pathogen/Antigen is detected as non-self and harmful.
2. Phagocytes (Macrophages) migrate to the site of infection and engulf the pathogen, breaking it down.
3. It presents an antigen fragement on its MHC Class II markers.
4. T Helper cells recognise this antigen, and stimulate the T cells to undergo clonal expansion and divide into Cytotoxic T Cells.
5. They move to the pathogen and release toxic granules to destroy it. Memory T cells are formed in the process for future occurences, and suppresor T cells supress the immune response.

So the cells which T-helper cells stimulate to undergo colonal expansion are T-Cells, which then go onto produce Cytotoxic T-cells and memory cells? So it is not cytotoxic cells which get stimulated directly by T-helper cells?

thanks