JCB logo
Accuri Cytometers
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents
A correction to this article has been published: J. Cell Biol. 163 (3) 673
Published online 6 October 2003. doi:10.1083/jcb.200305124
This Article
Right arrow Full Text
Right arrow Full Text (PDF, 209K)
Right arrow PPT slides of all figures
Right arrow Supplemental Material Index
Right arrow Correction (v163,p673)
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JCB
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Fernandez-Capetillo, O.
Right arrow Articles by Nussenzweig, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Fernandez-Capetillo, O.
Right arrow Articles by Nussenzweig, A.
Right arrowPubmed/NCBI databases
*Gene*GEO Profiles
*HomoloGene*OMIM
*Protein*UniGene
*Substance via MeSH
Related Collections
Right arrowRelated Article
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

© 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.


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?

Related Article

Choreographing telomeres
Nicole LeBrasseur
J. Cell Biol. 2003 163: 11. [Full Text] [PDF]



This article has been cited by other articles:



  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents