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DNA repair

New tales of an old tail

Nature volume 458, pages 581–583 (2009)Cite this article

Modifications of DNA-associated histone proteins maintain genome integrity. On damage to DNA, phosphorylation of histone H2A.X determines whether repair is justified or if the damaged cell must die.

Chromosomal DNA wraps around histone proteins to form a complex scaffold called chromatin1. The reorganization of these proteins following DNA damage is crucial for repairing the damage, and so maintaining genomic integrity and reducing the likelihood of cell death or cancer. One such histone modification — known as γ-H2A.X — follows DNA double-strand breaks (DSBs) and involves phosphorylation by the enzyme ATM of serine residue 139, which is located in the carboxy-terminal tail of the histone variant H2A.X (ref. 2). γ-H2A.X generates a chromosomal microenvironment that promotes recruitment of repair proteins3 and facilitates DNA repair to reduce the risk of mutations4. But how this modification is regulated and how it affects cell fate have remained elusive. Two papers5,6, including one on page 591 of this issue, provide insights into these questions.

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Figure 1: A matter of life or death5,6.

References

  1. Groth, A., Rocha, W., Verreault, A. & Almouzni, G. Cell 128, 721–733 (2007).

    CAS  Article  Google Scholar 

  2. Rogakou, E. P., Pilch, D. R., Orr, A. H., Ivanova, V. S. & Bonner, W. M. J. Biol. Chem. 273, 5858–5868 (1998).

    CAS  Article  Google Scholar 

  3. Fernandez-Capetillo, O., Lee, A., Nussenzweig, M. & Nussenzweig, A. DNA Repair 3, 959–967 (2004).

    CAS  Article  Google Scholar 

  4. Bartek, J. & Lukas, J. Curr. Opin. Cell Biol. 19, 238–245 (2007).

    CAS  Article  Google Scholar 

  5. Xiao, A. et al. Nature 457, 57–62 (2009).

    ADS  CAS  Article  Google Scholar 

  6. Cook, P. J. et al. Nature 458, 591–596 (2009).

    ADS  CAS  Article  Google Scholar 

  7. Poot, R. A. et al. Nature Cell Biol. 6, 1236–1244 (2004).

    CAS  Article  Google Scholar 

  8. Bozhenok, L., Wade, P. A. & Varga-Weisz, P. EMBO J. 21, 2231–2241 (2002).

    CAS  Article  Google Scholar 

  9. Stucki, M. et al. Cell 123, 1213–1226 (2005).

    CAS  Article  Google Scholar 

  10. Lukas, C. et al. EMBO J. 23, 2674–2683 (2004).

    CAS  Article  Google Scholar 

Download references

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Authors and Affiliations

  1. Jiri Lukas and Jiri Bartek are at the Institute of Cancer Biology and the Centre for Genotoxic Stress Research, Danish Cancer Society, Strandboulevarden 49, DK-2100 Copenhagen, Denmark. jil@cancer.dk; jb@cancer.dk,

    Jiri Lukas & Jiri Bartek

  2. jb@cancer.dk,

    Jiri Lukas & Jiri Bartek

Authors
  1. Jiri Lukas
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  2. Jiri Bartek
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Lukas, J., Bartek, J. New tales of an old tail. Nature 458, 581–583 (2009). https://doi.org/10.1038/458581a

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