NDLI: Mammalian SWI/SNF complexes facilitate DNA double-strand break repair by promoting γ-H2AX induction

Content Provider	PubMed Central
Author	Park, Ji-hye Park, Eun-jung Lee, Han-sae Kim, So Jung Hur, Shin-kyoung Imbalzano, Anthony N. Kwon, Jongbum
Copyright Year	2006
Abstract	Although mammalian SWI/SNF chromatin remodeling complexes have been well established to play important role in transcription, their role in DNA repair has remained largely unexplored. Here we show that inactivation of the SWI/SNF complexes and downregulation of the catalytic core subunits of the complexes both result in inefficient DNA double-strand break (DSB) repair and increased DNA damage sensitivity as well as a large defect in H2AX phosphorylation (γ-H2AX) and nuclear focus formation after DNA damage. The expression of most DSB repair genes remains unaffected and DNA damage checkpoints are grossly intact in the cells inactivated for the SWI/SNF complexes. Although the SWI/SNF complexes do not affect the expression of ATM, DNA-PK and ATR, or their activation and/or recruitment to DSBs, they rapidly bind to DSB-surrounding chromatin via interaction with γ-H2AX in the manner that is dependent on the amount of DNA damage. Given the crucial role for γ-H2AX in efficient DSB repair, these results suggest that the SWI/SNF complexes facilitate DSB repair, at least in part, by promoting H2AX phosphorylation by directly acting on chromatin.
Related Links	http://dx.doi.org/10.1038/sj.emboj.7601291
Ending Page	3997
Page Count	12
Starting Page	3986
File Format	PDF
ISSN	02614189
e-ISSN	14602075
Journal	The EMBO Journal
Issue Number	17
Volume Number	25
Language	English
Publisher Date	2006-09-06
Access Restriction	Open
Subject Keyword	Biochemistry, Genetics and Molecular Biology(all) Immunology and Microbiology(all) Neuroscience(all) Molecular Biology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Neuroscience Immunology and Microbiology Medicine Molecular Biology

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