VCE Biology Question Thread

[cosine]

Seems a bit ambiguous. Allopatric speciation or natural selection?

Doesn't answer my question, can this be divergent evolution or not?

[bananabreadbelle]

Doesn't answer my question, can this be divergent evolution or not?

From what I understand, I reckon 'divergent evolution' is more to describe what is happening/the pattern of change rather than the process that would have "given-rise" to the adapted species.
Natural selection/allopatric speciation would be what caused the plant to evolve into what it did - which is what I think the question is emphasizing?
 

EDIT: After doing a bit more research in the differences between the terms 'divergent evolution' and 'speciation', I understand that 'divergent evolution' is more of a broader term that refers to the accumulation of differences that have arised from a common ancestral species - 'evolving to be more and more different over time'
while 'speciation' refers to the SPECIFIC EVENT of a species splitting into two or more species.

Hence, the way it correlates to me is that as lets say a single common species spreads out to different geographical locations, this can lead to SPECIATION (as the populations develop different adaptations (due to natural selection(?)) and become genetically isolated from each other) and as those new species continue to diverge over time (giving rise to more speciation/new species), differences have accumulated (relative to that first common ancestral species) = which is then as whole, from that first common ancestral species to the 'latest' species that arised from that line, referred to as DIVERGENT EVOLUTION

 

[sunshine98]

Can someone tell me if this info on the third line of defence is accurate?
Humoral Immune Response (humoral because it occurs in body fluids) 
•   Phagocyte (macrophage or dendritic cells) engulf pathogen and present pieces of the digested pathogen on the MHC II markers. Travels to lymphoid tissue. 
•   A T helper cell (with a specific receptor complementary to the antigen on the MHC II marker) will bind.
•   Binding triggers the release of Interleukin I by the phagocyte
•   This then triggers the T helper cell to produce Interleukin II and receptors for it. Autocrine signalling occurs and the Interleukin II binds to the newly made receptors on the T helper cell. The T helper cell begins to divide
•   B-cell (which are found in secondary lymph organs - spleen and lymph nodes) will encounter the same antigen as the macrophage, engulf it and present it on their MHC II markers.
•   Activated T helper cells will bind to the antigen on MHC II markers and release cytokines which trigger the proliferation of the B cells into both memory and plasma B cells .
•   Plasma B cells are clone of the activated B cells. Their function is  to produce specific antibodies . Note: They produce so much antibodies that they are worn out (lack of energy)  and die early. 
•   Function of memory B cells- to rapidly produce antibodies if the infection recurs at a later time. Stored in lymph nodes and spleen, and last for a long time.
Cell mediated immune response- this occurs in virally infected cells or cancerous cells
•   An infected cell (virally infected or cancerous) will present antigen on MHC I marker
•   Cytotoxic T cell with specific receptor will bind to the it
•   Cell releases cytokines which activate T cell
•   The Cytotoxic T cell will produce Interleukin II and receptors for it. Autocrine signalling occurs and the Interleukin II binds to the newly made receptors on the T helper cell. The Cytotoxic T cell begins to divide.
•   Activated Cytotoxic T cells will recognise antigens on the MHC I markers of more infected cells
•   Binding causes the release of perforins which form a pore in cell membrane and act as opening for more molecules of the Cytotoxic T cell to enter and destroy the cell.
Thanks

[Biology24123]

Can someone tell me if this info on the third line of defence is accurate?
Humoral Immune Response (humoral because it occurs in body fluids) 
•   Phagocyte (macrophage or dendritic cells) engulf pathogen and present pieces of the digested pathogen on the MHC II markers. Travels to lymphoid tissue. 
•   A T helper cell (with a specific receptor complementary to the antigen on the MHC II marker) will bind.
•   Binding triggers the release of Interleukin I by the phagocyte
•   This then triggers the T helper cell to produce Interleukin II and receptors for it. Autocrine signalling occurs and the Interleukin II binds to the newly made receptors on the T helper cell. The T helper cell begins to divide
•   B-cell (which are found in secondary lymph organs - spleen and lymph nodes) will encounter the same antigen as the macrophage, engulf it and present it on their MHC II markers.
•   Activated T helper cells will bind to the antigen on MHC II markers and release cytokines which trigger the proliferation of the B cells into both memory and plasma B cells .
•   Plasma B cells are clone of the activated B cells. Their function is  to produce specific antibodies . Note: They produce so much antibodies that they are worn out (lack of energy)  and die early. 
•   Function of memory B cells- to rapidly produce antibodies if the infection recurs at a later time. Stored in lymph nodes and spleen, and last for a long time.
Cell mediated immune response- this occurs in virally infected cells or cancerous cells
•   An infected cell (virally infected or cancerous) will present antigen on MHC I marker
•   Cytotoxic T cell with specific receptor will bind to the it
•   Cell releases cytokines which activate T cell
•   The Cytotoxic T cell will produce Interleukin II and receptors for it. Autocrine signalling occurs and the Interleukin II binds to the newly made receptors on the T helper cell. The Cytotoxic T cell begins to divide.
•   Activated Cytotoxic T cells will recognise antigens on the MHC I markers of more infected cells
•   Binding causes the release of perforins which form a pore in cell membrane and act as opening for more molecules of the Cytotoxic T cell to enter and destroy the cell.
Thanks

Do B cells engulf the antigens or just bind to receptors on the membrane?

For humoral response, it is T helper cells that trigger Cytotoxic T cells to divide, not the infected cell

[sunshine98]

Do B cells engulf the antigens or just bind to receptors on the membrane?

For humoral response, it is T helper cells that trigger Cytotoxic T cells to divide, not the infected cell

Got all this from a youtube video , and then was unsure because Wikipedia said that B cells simply present antigens on their B cell receptors. Is Wikipedia right , then?

So T helper cells , not cytotoxic. Got it.
So is this right now?
-T helper cells bind to the MHC I marker of the infected cell and cell releases cytokines which activate T helper cell.
-T helper will produce Interleukin II and receptors for it. Autocrine signalling occurs and the Interleukin II binds to the newly made receptors on the T helper cell, which then begins to divide.
-Activated T helper then binds to cytotoxic T cell and then  release cytokines. These cytokines cause the Cytotoxic T cells to divide.
-Activated Cytotoxic T cells will recognise antigens on the MHC I markers of more infected cells
-Binding causes the release of perforins which form a pore in cell membrane and act as opening for more molecules of the Cytotoxic T cell to enter and destroy the cell.


Thanks 

[Biology24123]

Got all this from a youtube video , and then was unsure because Wikipedia said that B cells simply present antigens on their B cell receptors. Is Wikipedia right , then?

So T helper cells , not cytotoxic. Got it.
So is this right now?
-T helper cells bind to the MHC I marker of the infected cell and cell releases cytokines which activate T helper cell.
-T helper will produce Interleukin II and receptors for it. Autocrine signalling occurs and the Interleukin II binds to the newly made receptors on the T helper cell, which then begins to divide.
-Activated T helper then binds to cytotoxic T cell and then  release cytokines. These cytokines cause the Cytotoxic T cells to divide.
-Activated Cytotoxic T cells will recognise antigens on the MHC I markers of more infected cells
-Binding causes the release of perforins which form a pore in cell membrane and act as opening for more molecules of the Cytotoxic T cell to enter and destroy the cell.


Thanks 

Sorry I may have confused you with what I said. T helper cells ONLY bind with MHC II
- Cell mediated response
- APC engulfs pathogen and presents the antigen on it's MHC II
- Specific T helper cell binds to MHC II and is activated
- T helper cell activates cytotoxic T cell, the cells proliferate
- The specific cytotoxic T cell will now destroy any cell with foreign antigens on the MHC I

Humoral response
- APC engulfs pathogen and presents the antigen on it's MHC II
- Specific T helper cell binds to MHC II and is activated
- T helper cell activates B cell, which has bound with free antigens
- The B cell proliferates into plasma and memory cells
- Plasma cell produce antibodies against the specific antigen

[sunshine98]

Sorry I may have confused you with what I said. T helper cells ONLY bind with MHC II
- Cell mediated response
- APC engulfs pathogen and presents the antigen on it's MHC II
- Specific T helper cell binds to MHC II and is activated
- T helper cell activates cytotoxic T cell, the cells proliferate
- The specific cytotoxic T cell will now destroy any cell with foreign antigens on the MHC I

Humoral response
- APC engulfs pathogen and presents the antigen on it's MHC II
- Specific T helper cell binds to MHC II and is activated
- T helper cell activates B cell, which has bound with free antigens
- The B cell proliferates into plasma and memory cells
- Plasma cell produce antibodies against the specific antigen

Thank youuuu so much. Makes much more sense

[vox nihili]

Sorry I may have confused you with what I said. T helper cells ONLY bind with MHC II
- Cell mediated response
- APC engulfs pathogen and presents the antigen on it's MHC II
- Specific T helper cell binds to MHC II and is activated
- T helper cell activates cytotoxic T cell, the cells proliferate
- The specific cytotoxic T cell will now destroy any cell with foreign antigens on the MHC I

Humoral response
- APC engulfs pathogen and presents the antigen on it's MHC II
- Specific T helper cell binds to MHC II and is activated
- T helper cell activates B cell, which has bound with free antigens
- The B cell proliferates into plasma and memory cells
- Plasma cell produce antibodies against the specific antigen

This is v. gewd

[Biology24123]

This is v. gewd

It took way too long for me to finally understand immunity

[vox nihili]

It took way too long for me to finally understand immunity

has taken me three years.

Got 100% on my immuno sac in year 12 and still had no idea what any of it meant

[Biology24123]

has taken me three years.

Got 100% on my immuno sac in year 12 and still had no idea what any of it meant

It finally clicked for me a few weeks ago. 3/4 biology is just the basics, it get's extremely complex

[bananabreadbelle]

You just have to know that it's mediated by sodium and potassium and that the Sodium-potassium pump maintains a concentration gradient.

They've taken a lot of the detail about action potentials off the course, so what you need to know is really, really vague

Yeah I read in a VCAA Biology FAQ document that we don't need to know depolarisation, etc. but my teacher spent a bit of time on that in class if I remember correctly so I was a bit confuffled.
Thank you! 

[wobblywobbly]

For the attached question, can the answer be divergent evolution? Isn't divergent evolution a process? Ah I suck at evolution..

It specifically says process. The mechanism/process is natural selection.

[THEBEAST]

So during the humoral response, can B-cells be activated by the antigen on the pathogen directly binding to the antibodies on the B-cell's surface?

[cosine]

So during the humoral response, can B-cells be activated by the antigen on the pathogen directly binding to the antibodies on the B-cell's surface?

Although B cells have specific antibodies on their surfaces, which will bind to the specific antigens presented on the pathogen, this does not yet activate the B cell. The B cell must first engulf the antibody-antigen complex. Once engulfed, the B cells degrades the pathogen into fragments and presents antigenic fragments on it's surface via MHC Class II proteins. These proteins sit on the membrane until a specific T Helper Cell will come along, and form a MHC II - TCR complex, that is, when the T helper cell binds with the B cell's MHC II marker that holds the antigen fragment, the helper cell releases chemicals which stimulate/activate the B cell to proliferate into plasma B cells and memory B cells.