Ubiquitin-family modifications in the replication of DNA damage

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

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • DNA / genetics
  • DNA / metabolism
  • DNA Damage*
  • DNA Replication*
  • DNA-Directed DNA Polymerase / metabolism*
  • Humans
  • Models, Genetic
  • Proliferating Cell Nuclear Antigen / metabolism*
  • Protein Processing, Post-Translational
  • Ubiquitin / metabolism*

Substances

  • Proliferating Cell Nuclear Antigen
  • Ubiquitin
  • DNA
  • DNA-Directed DNA Polymerase
  • Rad30 protein