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Genomic instability in mice lacking histone H2AX

  1. Author:
    Celeste, A.
    Petersen, S.
    Romanienko, P. J.
    Fernandez-Capetillo, O.
    Chen, H. T.
    Sedelnikova, O. A.
    Reina-San-Martin, B.
    Coppola, V.
    Meffre, E.
    Difilippantonio, M. J.
    Redon, C.
    Pilch, D. R.
    Olaru, A.
    Eckhaus, M.
    Camerini-Otero, R. D.
    Tessarollo, L.
    Livak, F.
    Manova, K.
    Bonner, W. M.
    Nussenzweig, M. C.
    Nussenzweig, A.

  2. Author Address

    NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA NIDDKD, Genet & Biochem Branch, NIH, Bethesda, MD 20892 USA NIH, Mol Pharmacol Lab, Bethesda, MD 20892 USA Rockefeller Univ, Howard Hughes Med Inst, Lab Mol Immunol, New York, NY 10021 USA NIH, Mouse Canc Genet Program, Frederick, MD 20892 USA NCI, Dept Genet, NIH, Bethesda, MD 20892 USA Univ Maryland, Sch Med, Dept Microbiol & Immunol, Baltimore, MD 21201 USA NIH, Vet Resources Program, Natl Ctr Res Resources, Bethesda, MD 20892 USA Mem Sloan Kettering Canc Ctr, Mol Cytol Core Facil, New York, NY 10021 USA Mem Sloan Kettering Canc Ctr, Program Mol Biol, New York, NY 10021 USA Nussenzweig A NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA
    1. Year: 2002
  2. Journal: Science
    1. 296
    2. 5569
    3. Pages: 922-927
  4. Type of Article: Article
  1. Abstract:

    Higher order chromatin structure presents a barrier to the recognition and repair of DNA damage. Double-strand breaks (DSBs) induce histone H2AX phosphorylation, which is associated with the recruitment of repair factors to damaged DNA. To help clarify the physiological role of H2AX, we targeted H2AX in mice. Although H2AX is not essential for irradiation-induced cell-cycle checkpoints, H2AX(-/-) mice were radiation sensitive, growth retarded, and immune deficient, and mutant males were infertile. These pleiotropic phenotypes were associated with chromosomal instability, repair defects, and impaired recruitment of Nbs1, 53bp1, and Brca1, but not Rad51, to irradiation-induced foci. Thus, H2AX is critical for facilitating the assembly of specific DNA-repair complexes on damaged DNA.

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