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BAF53 is critical for focus formation of γ?H2AX in response to DNA damage

Animal Cells and Systems 2009년 13권 4호 p.405 ~ 409
박판규, 강동현, 권혁만,
소속 상세정보
박판규 ( Park Pan-Kyu ) - Hankuk University of Foreign Studies Department of Bioscience and Biotechnology
강동현 ( Kang Dong-Hyun ) - Hankuk University of Foreign Studies Department of Bioscience and Biotechnology
권혁만 ( Kwon Hyock-Man ) - Hankuk University of Foreign Studies Department of Bioscience and Biotechnology

Abstract


When DNA double?strand breaks (DSBs) were induced in mammalian cells, many DNA damage response proteins are accumulated at damage sites to form nuclear foci called IR?induced foci. Although the formation of foci has been shown to promote repair efficiency, the structural organization of chromatin in foci remains obscure. BAF53 is an actin?related protein which is required for maintenance of chromosome territory. In this study, we show that the formation of IR?induced foci by γ?H2AX and 53BP1 were reduced when BAF53 is depleted, while DSB? activated ATM pathway and the phosphorylation of H2AX remains intact after DNA damage in BAF53 knockdown cells. We also found that DSB repair efficiency was largely compromised in BAF53 knockdown cells. These results indicate that BAF53 is critical for formation of foci by γ?H2AX decorated chromatin at damage sites and the structural organization of chromatin in foci is an important factor to achieve the maximum efficiency of DNA repair.

키워드

BAF53; IR-induced foci; γ-H2AX; chromosomal subdomain

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