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Not Keeping Up with Repairs

Replication of DNA or DNA damage processes can result in double-strand breaks, which in turn may lead to chromosomal translocation and an increased risk of malignancy. Celeste et al. tested the role of the DNA repair-associated protein, H2AX, in maintaining genomic stability. Cells from H2AX-deficient mice displayed several genetic abnormalities, including elevated sensitivity to irradiation-induced damage, chromosomal breakage, and an increased incidence of translocations. Male H2AX−/− mice were infertile due to defective spermatogenesis that resulted from failure of synapsis and meiotic arrest. T and B cell development was also diminished, and B cells displayed defects in switch recombination. Recruitment of DNA repair enzymes was severely affected in the absence of H2AX, confirming a central role for this protein in coordinating the response to DNA damage. A. Celeste, S. Petersen, P. J. Romanienko, O. Fernandez-Capetillo, H. T. Chen, O. A. Sedelnikova, B. Reina-San-Martin, V. Coppola, E. Meffre, M. J. Difilippantonio, C. Redon, D. R. Pilch, A. Olaru, M. Eckhaus, R. D. Camerini-Otero, L. Tessarollo, F. Livak, K. Manova, W. M. Bonner, M. C. Nussenzweig, A. Nussenzweig, Genomic instability in mice lacking histone H2AX. Science 296, 922-927 (2002). [Abstract] [Full Text]