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DNA repair

It takes two

Nature Reviews Molecular Cell Biology volume 5, pages 424–425 (2004)Cite this article

Mice that lack the NHEJ-specific factor DNA ligase IV (Lig4) have a moderate mutant-repair phenotype, whereas deficiency for the HR factor Rad54 causes a milder phenotype. Mills et al. created double-mutant mice that lacked both Rad54 and Lig4 to study the relationship between HR and NHEJ in DSB repair. They found that embryonic fibroblasts that were derived from these mice showed a severe proliferation defect compared with cells derived from either Rad54 or Lig4 single-mutant mice.

To examine whether this proliferation defect was due to a high level of DSBs, the authors carried out immunofluorescence experiments to detect the phosphorylated histone-H2A variant of H2ax (γ-H2ax), which is a marker for the presence of DSBs. Nearly 100% of double-mutant cells contained γ-H2ax foci, compared with 50% of Lig4−/− cells.

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ORIGINAL RESEARCH PAPERS

  1. Mills, K. D. et al. Rad54 and DNA ligase IV cooperate to maintain mammalian chromatid stability. Genes Dev. 18, 1283–1292 (2004)

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  2. Couëdel, C. et al. Collaboration of homologous recombination and non-homologous end-joining factors to the survival and integrity of mice and cells. Genes Dev. 18, 1293–1304 (2004)

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Authors
  1. Arianne Heinrichs
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Heinrichs, A. It takes two. Nat Rev Mol Cell Biol 5, 424–425 (2004). https://doi.org/10.1038/nrm1410

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  • DOI: https://doi.org/10.1038/nrm1410

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