Feedback inhibition of L1 and alu retrotransposition through altered double strand break repair kinetics.

ABSTRACT:

Background

Cells adapt to various chronic toxic exposures in a multitude of ways to minimize further damage and maximize their growth potential. Expression of L1 elements in the human genome can be greatly deleterious to cells, generating numerous double strand breaks (DSBs). Cells have been reported to respond to chronic DSBs by altering the repair of these breaks, including increasing the rate of homology independent DSB repair. Retrotransposition is strongly affected by proteins involved in DSB repair. Therefore, L1 expression has the potential to be a source of chronic DSBs and thus bring about the changes in cellular environment that could ultimately restrict its own retrotransposition.

Results

We demonstrate that constitutive L1 expression leads to quicker DSB repair a

SUBMITTER: Wallace NA 

PROVIDER: S-EPMC3164224 | biostudies-literature | 2010 Oct

REPOSITORIES: biostudies-literature