Acetylation regulates the DNA end-trimming activity of DNA polymerase beta

Mol Cell. 2002 Nov;10(5):1213-22. doi: 10.1016/s1097-2765(02)00745-1.

Abstract

We describe a novel regulatory mechanism for DNA polymerase beta (Polbeta), a protein involved in DNA base excision repair (BER). Polbeta colocalized in vivo and formed a complex with the transcriptional coactivator p300. p300 interacted with Polbeta through distinct domains and acetylated Polbeta in vitro. Polbeta acetylation was furthermore observed in vivo. Lysine 72 of Polbeta was identified as the main target for acetylation by p300. Interestingly, acetylated Polbeta showed a severely reduced ability to participate in a reconstituted BER assay. This was due to an impairment of the dRP-lyase activity of Polbeta. Acetylation of Polbeta thus acts as an intranuclear regulatory mechanism and implies that p300 plays a critical regulatory role in BER.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylation
  • Base Pair Mismatch*
  • Cell Line
  • DNA / chemistry*
  • DNA / metabolism
  • DNA Polymerase beta / metabolism*
  • DNA Repair*
  • DNA-Directed DNA Polymerase / metabolism
  • Humans
  • Immunohistochemistry
  • Lysine / chemistry
  • Microscopy, Fluorescence
  • Nuclear Proteins / metabolism*
  • Precipitin Tests
  • Protein Binding
  • Trans-Activators / metabolism*
  • Transcription, Genetic
  • Transcriptional Activation*

Substances

  • Nuclear Proteins
  • Trans-Activators
  • DNA
  • DNA Polymerase beta
  • DNA-Directed DNA Polymerase
  • Lysine