p53, G1 arrest and apoptosis
mepstein at helix.nih.gov
Thu Oct 27 13:23:06 EST 1994
Thank you for your help. Waiting for the DNA repair to occur before
replication is smart. That means that cells that recognise DNA damage
while in the cycle would then apoptose. This makes sense however, Dr.
Levine mentioned that there seemed to be a cell type dependence.
Fibroblasts head towards G1 arrest and thymocytes head towards apoptosis.
How do you think that a cell type dependence and the timing of the cell
cycle be explained in the same model?
On Thu, 27 Oct 1994 odin25 at netcom.com wrote:
> By arresting the cell prior to DNA replication the cell allows time for
> the DNA repair to occur. If p53 was not elevated p21 and others would
> not increase and the cell would progress to DNA replication before it had
> a chance to repair the DNA. Obviously this could lead to increased rates
> of mutant DNA being synthesized and hence carcinogenesis. If the only
> option were apoptosis then many cells which could be repaired would
> simply be lost. At least that is mycurrent thinking.
> X-Newsreader: TIN [version 1.2 PL1]
> In article <Pine.SGI.3.90.941026184113.120D-100000 at helix.nih.gov> you wrote:
> : Recently, I heard an interesting talk by Arnold Levine about the p53
> : suppressor gene and it's function. He proposed that the p53 gene product
> : is responsible for recognizing damaged DNA which would subsequently
> : result in one of two pathways: cell cycle arrest or apoptosis depending
> : on where the cell was in the cell cycle and possibly the cell type (eg
> : thymocytes/apoptosis).
> : I wasn't sure how the pivotal role of the p53 gene products and the cell
> : cycle interacted with ongoing repair of DNA by the DNA repair enzymes.
> : Does anyone know?
> : Is it known if there are defects in the DNA repair
> : enzymes associated with defects in p53 leading to a greater incidence
> : of carcinoma?
> : Why would a cell chose to arrest at G1 instead of
> : apoptosing in the face of damaged DNA and mutations?
> : Michelle
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