Did anyone need to read that last sentence like 50 times because the author refuses to use better grammar. Just frustrating.
For this one I think what you had to know is that Transcription (DNA-->RNA) is performed by RNA polymerase. It was not DNA polymerase because this one replicates (DNA-->DNA)
This is a good picture of an experiment showing this:
Oncogene volume 26, pages 2212–2219 (2007)
The grammar of the actual Q was confusing.
To make better sense, it should say "Which of the following is the most likely result on the transcription of genes that inhibit cell division and that contain the consensus sequeence TATA..."
So, the Q is asking about the tp53 gene and specifically about the tp53 gene promoter region.
Promoter regions have a TATA box (obviously, meaning rich in A-T base pairs). A-T base pairing has 2 hydrogen bonds, which makes them easier to cleave --> allows for DNA transcription to occur more easily. RNA Pol does transcription of DNA into RNA.
The entire Q-stem talks about how Li-Fraumeni is due to a mutation in tp53 gene, leading to a lack of tumor suppression activity.
So, if the promoter region TATA box of the tp53 gene is mutated, then the tp53 gene will not get transcribed --> this is why there will be decreased RNA Pol binding. RNA Pol will have a reduced ability to bind tp53 --> less tumor supressor gene transcription --> less tumor suppression.
p53 is mutated and cant bind the TATA box, so what happens to transcription of inhibitory proteins?
Is basically what this question is trying to ask...
So no TATA box promoter => Decreased binding of RNA polymerase
Does anyone have any specific idea on the mechanism of the p53 mutation question regarding the TATA box (the one with the single amino acid conversion and the different hydrogen bonding)?
I chose the decreased binding of RNA polymerase on the TATA sequence of genes that inhibit cell division based solely on the fact that p53 is a tumor suppressor (aka mutated p53->less inhibition of division->multiple divisions).
Why is this not increased binding of DNA polymerase?
This mutation should cause cellular division ie DNA replication and cause increased binding to origin replication sequences ie TATA by DNA polymerase.