APOBEC3A can activate the DNA damage response and cause cell-cycle arrest

EMBO Rep. 2011 May;12(5):444-50. doi: 10.1038/embor.2011.46. Epub 2011 Apr 1.

Abstract

Human apolipoprotein-B mRNA-editing catalytic polypeptide-like 3 (APOBEC3) proteins constitute a family of cytidine deaminases that mediate restriction of retroviruses, endogenous retro-elements and DNA viruses. It is well established that these enzymes are potent mutators of viral DNA, but it is unclear whether their editing activity is a threat to the integrity of the cellular genome. We show that expression of APOBEC3A can lead to induction of DNA breaks and activation of damage responses in a deaminase-dependent manner. Consistent with these observations, APOBEC3A expression induces cell-cycle arrest. These results indicate that cellular DNA is vulnerable to APOBEC3 activity and deregulated expression of APOBEC3A could threaten genomic integrity.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Blotting, Western
  • Bromodeoxyuridine
  • Cell Cycle / physiology*
  • Cell Line
  • Cytidine Deaminase / metabolism*
  • DNA Damage / genetics*
  • Fluorescent Antibody Technique
  • Histones / metabolism
  • Humans
  • In Situ Nick-End Labeling
  • Nucleotide Deaminases / metabolism
  • Phosphorylation
  • Proteins / metabolism*
  • Uracil-DNA Glycosidase / metabolism

Substances

  • H2AX protein, human
  • Histones
  • Proteins
  • Uracil-DNA Glycosidase
  • Nucleotide Deaminases
  • APOBEC3A protein, human
  • Cytidine Deaminase
  • Bromodeoxyuridine