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FEBS Lett. 2011 Sep 16;585(18):2772-9. doi: 10.1016/j.febslet.2011.06.005. Epub 2011 Jun 23.

Ubiquitin-family modifications in the replication of DNA damage.

Author information

  • Genome Damage and Stability Centre, University of Sussex, Falmer, Brighton BN1 9RQ, UK. a.r.lehmann@sussex.ac.uk

Abstract

The cell uses specialised Y-family DNA polymerases or damage avoidance mechanisms to replicate past damaged sites in DNA. These processes are under complex regulatory systems, which employ different types of post-translational modification. All the Y-family polymerases have ubiquitin binding domains that bind to mono-ubiquitinated PCNA to effect the switching from replicative to Y-family polymerase. Ubiquitination and de-ubiquitination of PCNA are tightly regulated. There is also evidence for another as yet unidentified ubiquitinated protein being involved in recruitment of Y-family polymerases to chromatin. Poly-ubiquitination of PCNA stimulates damage avoidance, and, at least in yeast, PCNA is SUMOylated to prevent unwanted recombination events at the replication fork. The Y-family polymerases themselves can be ubiquitinated and, in the case of DNA polymerase η, this results in the polymerase being excluded from chromatin.

Copyright © 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

PMID:
21704031
[PubMed - indexed for MEDLINE]
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