AQA BIOL5 Biology Unit 5 Exam - 22nd June 2011

Can somebody please explain transcription factors to me?

I don't really unterstand it either but I think it either acts as avtivators or suppressors in the rate of transcription of the targt gene.
Like repressors stop the te rna polymerase from attaching by blocking the start of the target gene.
activators help rna polymerase attach to the start of the target gene.

oestrogen is involved but I don't unterstand that fully either. :/
sorry, this is probably no help.

I think with the control of heart rate, its best not to link it with homeostasis cause less CO2 doesn't lead to the blood being alkaline (in homeostasis the change can go in both directions)

My personal opinion would be to not link the two. Control of heart is studied to realise the importance of receptors.

can someone please help me:
on the spec paper, on question 5)a)i) there is a question about action potentials and it asks to explain the shape of the curve when it is increasing in +.. the answer is:

'Sodium ions move out of axon; By diffusion/down concentration gradient; Through sodium ion channels/sodium ion channels open;'
i am SO confused, because i thought it was the inward diffusion of sodium ions and then the further influx INTO the axon membrane that caused an action potential :/

can someone please explain...

yes please, that would b really good thanks!

Can somebody please explain transcription factors to me?

yes this involves the parasympathetic system (although i'm not sure when co2 levels will fall below normal in the real world? as increased metabolic ativity means more co2, so when there is very metaboli activity or muscular activity im guessing co2 level will fall?) but yh in logical terms im sure the process is the complete reverse of the above, where chemorecptors detect the decrease send this to the medulla oblongatat which then decreases the frequency of impulses via the sinoatrial node which decreases the heart rate which leads to less co2 being removed and so the ph in th blood returns to normal, hence the ph lowers to normal and the chemorecptors which detect ph change then reduced impulses frequency and to the mo and this redcues the frequency to the san which increases heart rate back to normal

control of heart rate is an example of negative feedback and is in some aspect slighlty realted to homeostais whereby the co2 level and 02 levels are controlled as a result of ph homeostatic control

Can somebody please explain transcription factors to me?

hiyaa
that mark scheme is totally WRONG!
your right..i had the same problem and my teach said it was wrong

Can somebody please explain transcription factors to me?

oh ok
hmm it is rather confusing.

chemoreceptors detect a rise in pH
chemoreceptors send impulses to the medulla oblongata, precisely the inhibitory centre
the medulla oblongata sends impulses via the parasympathetic nerve to the SAN
at the end of the parasympathetic nerve, acetylcholine is secreted, which causes SAN to decrease the frequency at which it produces waves of electrical activity
reduced blood flow means that less co2 is removed
pH falls back to normal

am i right?

An increase in blood C02 concentration will lead to a fall in blood pH not a rise. CO2 forms an acid in solution and the more acidic something is the lower its pH.

When the chemorecepors detect this fall in pH they send impulses to the medulla oblongata which sends impulses down the sympathetic nervous system, causing the SAN to increase the frequency of waves of electrical activity and hence increasing heart rate.

The increased heart rate means that CO2 is removed by the lungs more rapidly and blood pH rises to the set level.

Transcription factors:

Basicallly these are what determines if a gene is expressed or not.
For a gene to be expressed, that part of the DNA has to be stimulated by something, and that something is the transcriptional factor - it moves from the cytoplasm into the nucleus.
It has a site that is specific to that region of the DNA and so when it binds with it, it stimulates that region to begin transcription -> mRNA -> poly peptide etc.

When a gene is NOT expressed, the site on the transcriptional factor is blocked by an inhibitor molecule. This means the transcriptional factor is prevented from binding to the DNA -> no transcription of the gene -> no poly peptide etc.

OESTROGEN:
The role of this is to express a gene -
It is lipid soluble, so can relatively easily pass through the phospholipid portion of the cell membrane.
So, when inside, it combines with the site on the receptor molecule of the transcriptional factor (they're both complementary) and this causes the receptor molecule to change shape!
The receptor molecule is also attached to the inhibitor molecule, so when oestrogen combines, the change in shape of receptor molecule releases the inhibitor molecule from the DNA binidng site of Transcriptional factor.

The TF can now bind to the specific part of the DNA and stimulate it to being transcription.

Hope that helps

Transcription factors control transcription. They bind to the promoter region which is upstream of the gene to be transcribed and this enables the mRNA polymerase to attach to the start of the gene. If an inhibitor molecule blocks the DNA binding site on the transcription factor it can no longer bind to the promoter region preventing transcription as the mRNA doesn't attach to the gene to be transcribed.

In the case of oestrogen, the transcription factor and inhibitor molecule form a complex so the normally the inhibitor molecule is blocking the DNA binding site on the transcription factor preventing transcription. However, when oestrogen enters the cytoplasm (it's small and lipid soluble so it can diffuse easily through the phospholipid bilayer), it binds to a site on a receptor molecule of the transcription factor causing a conformational shape change and this releases the inhibitor molecule. This means that the DNA binding site of the transcription factor is no longer blocked, it can bind to the promotor region, causes transcription to start and hence polypeptide synthesis can take place.

Adrenaline, Insulin and Glycagon work by the 2nd messenger model-they are hydrophillic.

Oestrogen is capable of diffusing straight through the phospholipid bilayer as it is hydrophobic (lipid soluble).

For transcription to begin the gene needs to be stimulated-transcriptional factors.

Oestrogen simply intiates the synthesis of a particular protein by binding to a receptor causing the receptor molecule to change shape and so release the inhibitor exposing the DNA binding site.

Oestrogen causes the repair of the lining of the uterus wall-it doesnt do it itself.

i'm talking about what happens if co2 level falls below normal.

For the role of calcium ions in muscle contraction, when they activate ATPase, do we need to know what bonds ATPase breaks in order to give Pi and ADP?

Ooh, okay. I wonder when it would. I guess if you hyperventilate CO2 is decreased in blood levels but in that case the pH of body fluids increases. I would be cautious about writing about chemoreceptors and heart rate when blood CO2 concentration falls purely because we're not taught if it does work the other way round.