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

Ji Hye Park, Eun Jung Park, Han Sae Lee, So Jung Kim, Shin Kyoung Hur, Anthony N. Imbalzano, Jongbum Kwon

Research output: Contribution to journalArticlepeer-review

224 Scopus citations


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.

Original languageEnglish
Pages (from-to)3986-3997
Number of pages12
JournalEMBO Journal
Issue number17
StatePublished - 6 Sep 2006


  • ATP-dependent chromatin remodeling
  • DNA double-strand break repair
  • Radiosensitivity
  • SWI/SNF complex
  • γ-H2AX


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