Edexcel A2 Biology Unit 5 (6BIO5) - 22/06/2011- OFFICIAL THREAD !

First you need to be aware of the reaction that takes place

RED LIGHT - Day
FAR RED LIGHT - Night
So in red light/DAY Pr is changed to Pfr
and in far red light/NIGHT Pfr is is changed to Pr

You need to be aware of two types of plants:


LDP can be referred to as SNP 'short night plants' for better understanding but do not call them this during the exam!



SDP 'Long night plants'


Remember its the length of DARKNESS that determines whether a plant flowers. This can be demonstrated by:
Placing a SDP 'long night plant' and exposing it to say 3 hours of day and 9 hours of darkness. The result is flowering. However if you distrub this single period of darkness by flashing red light (day - changes Pr to Pfr) there is NO flowering.
Therefore the conclusion is that the period of darkness is the CRITICAL FACTOR in inducing flowering.
Hope that helps!

Thanks a lot.. cheers !

But i still dont get how Pr stimulates germination if it is converted to Pfr..? If you look at the last 2 lines on page 22 on the orange text book, it says that Pr stimulates germination and Pfr inhibits germination. Thats whats confusing me

me too... i'd just argue that pfr is biologically active, whereas the books says pr is just more 'stable'

You forgot the main part of oxidative phosphorylation ^^ which is oxygen acting as the terminal electron acceptor forming h20 in the process Without O2, the electrons in the ETC can't be 'disposed' of (which is done by combining with oxygen and forming water) and so the ETC stops functioning as all the carriers are loaded with an electron - ETC stops so no ATP formation

Will we ever be tested on the HSW (how science works) boxes??

Does anyone revise/note-take on them?

But i still dont get how Pr stimulates germination if it is converted to Pfr..? If you look at the last 2 lines on page 22 on the orange text book, it says that Pr stimulates germination and Pfr inhibits germination. Thats whats confusing me

another question on the ETC.
My teacher keeps on saying when a molecule accepts hydrogen it is the same as accepting an electron. For some reason it doesnt seem right to me. Can you please explain this?
thanks

Your teacher is kind of right Basically H breaks down to form H+ and e-
Reduction is the gain of electrons so when NAD accepts a H atom, its basically taking up a H+ AND an e- which is why some books may refer to redNADP as NADPH+

thanks

Can anyone explain oxidative phophorylation. I have a general idea of what it is and I know it happens in the inner membrane of the cristae but i'm not entirely sure of what I should write if it comes up in the exam. Thanks

Okay I've seen the other post; not meaning to be a pedant. However, it's not called oxidative phosphorylation because it is dependent on Oxygen, of course it is dependent on Oxygen. It's oxidative because the energy required to synthesize the ATP comes from the Oxidation of the Co-enzymes

NAD + FAD both give up H+ and 2e-: Oxidation

If you wonder where the energy comes from, it comes from the idea that in the co-enzymes the electrons are in a really excited state, as they pass through the electron transport chain through a series of redox reactions their energy state is lowered, and of course energy is never lost, it is transferred, and the energy goes towards moving the H+ across into the inter membrane space and creating the electrochemical gradient.

Hope everyone understands this, I tried to make the chemistry quite basic.

Some possible Q's our teacher gave us for section 1, to have a go at. We might be given more but im not sure. Just thought i'd share them.

Muscles, genes and gym in a bottle.

1.Why does bolstering the delivery of oxygen to labouring tissues increase performance?
2.Describe how Mantyranta's genetic mutation could have altered the receptor for the the hormone EPO.
3.Explain the feedback mechanism involved in maintaining red blood cell production.
4.Explain how EPO could be produced by recombinant bacteria.
5.Explain how gene therapy could be used to 'aquire the equivalent of Mantyranta's super-gene with a single shot'.
6.Why are viruses used to 'carry EPO genes into cells?
7.Why are Adenoviruses 'easily recognised by the immune system'.
8.What safety issues are involved with gene therapy?
9.Outline the stages that would be involved in the EPO gene therapy clinical trials.
10.One side effect of EPO gene therapy is likely to be high blood pressure. Why does high BP increase the risk of atherosclerosis and how can this lead to a heart attack or a stroke?

cn u provide the answers ?