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A correction to this article has been published: J. Cell Biol. 163 (3) 673
Published online 6 October 2003. doi:10.1083/jcb.200305124
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© The Rockefeller University Press, 0021-9525/2003/10/15 $8.00
The Journal of Cell Biology, Volume 163, Number 1, 15-20

Report

H2AX regulates meiotic telomere clustering



Oscar Fernandez-Capetillo1, Bodo Liebe2, Harry Scherthan2 and André Nussenzweig1

1 Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892
2 Max-Planck-Institut für Molekulare Genetik, D-14195 Berlin, Germany

Address correspondence to André Nussenzweig, Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Tel.: (301) 435-6425. Fax: (301) 496-0887. email: andre_nussenzweig{at}nih.gov

The histone H2A variant H2AX is phosphorylated in response to DNA double-strand breaks originating from diverse origins, including dysfunctional telomeres. Here, we show that normal mitotic telomere maintenance does not require H2AX. Moreover, H2AX is dispensable for the chromosome fusions arising from either critically shortened or deprotected telomeres. However, H2AX has an essential role in controlling the proper topological distribution of telomeres during meiotic prophase I. Our results suggest that H2AX is a downstream effector of the ataxia telangiectasia–mutated kinase in controlling telomere movement during meiosis.

Key Words: DNA repair; genomic instability; meiosis; ATM; spermatocyte

The online version of this article includes supplemental material.

Abbreviations used in this paper: ATM, ataxia telangiectasia mutated; DSB, double-strand break; MEF, mouse embryonic fibroblast; SC, synaptonemal complex; Terc, RNA component of telomerase.


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