Chromosome ends teach unexpected lessons on DNA damage signalling

EMBO J. 2012 Aug 15;31(16):3380-1. doi: 10.1038/emboj.2012.199. Epub 2012 Jul 27.

Abstract

EMBO J 31 16, 3398–3410 (2012)

The ATM/ATR-dependent checkpoint kinases restrain mitotic entry when cells accumulate unrepaired DNA double-strand breaks (DSBs) or when telomeres become uncapped. New work by Thanasoula et al (2012) reveals an intricate network of checkpoint interactions in the wake of telomere uncapping through removal of TRF2 or POT1, providing compelling evidence that the mechanism of G2/M checkpoint activation at chromosome end is distinct from the canonical DNA damage response to ionizing radiation (IRs).

Publication types

  • Comment

MeSH terms

  • Ataxia Telangiectasia Mutated Proteins
  • Cell Cycle Proteins / metabolism*
  • Cytokinesis*
  • DNA-Binding Proteins / metabolism*
  • Gene Expression Regulation*
  • Humans
  • Protein Serine-Threonine Kinases / metabolism*
  • Telomere / metabolism*
  • Tumor Suppressor Proteins / metabolism*
  • cdc25 Phosphatases / biosynthesis*

Substances

  • Cell Cycle Proteins
  • DNA-Binding Proteins
  • Tumor Suppressor Proteins
  • ATM protein, human
  • ATR protein, human
  • Ataxia Telangiectasia Mutated Proteins
  • Protein Serine-Threonine Kinases
  • CDC25C protein, human
  • cdc25 Phosphatases