AQA BIOL5 ~ 17th June 2013 ~ A2 Biology

how is ATP required for the cross-bridge formation between myosin heads and actin filaments? I thought it was the ADP molecule that allowed the myosin head to bind to the actin?

Could someone please explain what a palindromic sequence is? This term is new to me.

I'll try..
A palindromic sequence is a sequence of DNA base pairs are a anti-parallel to each other.
An example would be say, if one DNA strand had the sequence : GAATTC, the other, complimentary strand would have the sequence: CTTAAG, if you notice both sequences are palindromes to each other.
Restriction endonuclease enzymes are enzymes that recognize these specific palindromic sequences, which are also known as recognition sequences
Hope that helped

So are palindromic sequences just bases sequences that can be read backwards and forwards like one strand shows the DNA sequence being read forward whilst the other strand shows the sequence as it would be read backwards


Does this also mean that the endonuclease can join on ether side of the recognition site because it's a palindromic sequence?

Yes that's pretty much it!

Restriction endonucleases cut at palendromic sequences in the DNA, which are specific to the enzyme, which creates sticky ends. RE also do this to the vector (plasmid) i believe, so that the sticky ends of the target DNA and the plasmid are complimentary to each other, this way they stick together, with help of an enzymes called DNA ligase, this process is called ligation.

Hope that helped

just wondering, if possible please could you post one of your essays here? Do you ask your teachers to mark them? Thank u

Have a couple of questions on glucose control


Firstly, which target cells do glucagon, insulin and adrenaline bind to.


Secondly, when insulin is released, in the exams should I write enzymes released which increase glycogenesis or just increased glyogenesis.


thirdly, how much do we need to know about adrenaline in terms of glucose control?

Finally, in the book I read that people with type II diabetes can produce insulin but receptors on target cells dont work properly but on other pages I read that insulin cannot be produced. Which is the truth?

Any help will be appreciated

Have a couple of questions on glucose control


Firstly, which target cells do glucagon, insulin and adrenaline bind to.


Secondly, when insulin is released, in the exams should I write enzymes released which increase glycogenesis or just increased glyogenesis.


thirdly, how much do we need to know about adrenaline in terms of glucose control?

Finally, in the book I read that people with type II diabetes can produce insulin but receptors on target cells dont work properly but on other pages I read that insulin cannot be produced. Which is the truth?

Any help will be appreciated

Could anyone please summarise the effects of indoleacetic acid (IAA)?

Can anyone explain the secondary messenger model for me please?

Thanks

Someone a few pages asked the exact same question I think but I'll answer this,

The Secondary messenger model is basically when a hormone/compound binds to receptors on target cells which activates enzymes inside those target cells to carry out changes e.g. metabolic.

To put it into context, I talked about adrenaline earlier on this page is an example of this model.

Could anyone please summarise the effects of indoleacetic acid (IAA)?

Can someone explain the main steps which are needed in genetic fingerprinting?

Thanks