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Journal Article

H2AX regulates meiotic telomere clustering

MPS-Authors

Liebe,  Bodo
Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons50515

Scherthan,  Harry
Dept. of Human Molecular Genetics (Head: Hans-Hilger Ropers), Max Planck Institute for Molecular Genetics, Max Planck Society;

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Citation

Fernandez-Capetillo, O., Liebe, B., Scherthan, H., & Nussenzweig, A. (2003). H2AX regulates meiotic telomere clustering. Journal of Cell Biology, 163(1), 15-20.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0010-8984-E
Abstract
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.