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Nat Struct Mol Biol. 2009 Aug;16(8):814-8. doi: 10.1038/nsmb.1640. Epub 2009 Jul 26.

Role of mammalian Mre11 in classical and alternative nonhomologous end joining.

Author information

1
Department of Medicine, Harvard Medical School and Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA. axie@bidmc.harvard.edu

Abstract

The mammalian Mre11-Rad50-Nbs1 (MRN) complex coordinates double-strand break signaling with repair by homologous recombination and is associated with the H2A.X chromatin response to double-strand breaks, but its role in nonhomologous end joining (NHEJ) is less clear. Here we show that Mre11 promotes efficient NHEJ in both wild-type and Xrcc4(-/-) mouse embryonic stem cells. Depletion of Mre11 reduces the use of microhomology during NHEJ in Xrcc4(+/+) cells and suppresses end resection in Xrcc4(-/-) cells, revealing specific roles for Mre11 in both classical and alternative NHEJ. The NHEJ function of Mre11 is independent of H2A.X. We propose a model in which both enzymatic and scaffolding functions of Mre11 cooperate to support mammalian NHEJ.

PMID:
19633669
PMCID:
PMC2730592
DOI:
10.1038/nsmb.1640
[Indexed for MEDLINE]
Free PMC Article

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