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Human Molecular Genetics, 2001, Vol. 10, No. 23 2651-2660
© 2001 Oxford University Press

Fanconi anemia protein, FANCA, associates with BRG1, a component of the human SWI/SNF complex

Tetsuya Otsuki, Yusuke Furukawa1, Keiko Ikeda2, Hitoshi Endo3, Takayuki Yamashita4, Azusa Shinohara5, Akihiko Iwamatsu5, Keiya Ozawa and Johnson M. Liu6,+

Department of Hematology, 1Center for Molecular Medicine, 2Department of Biology and 3Department of Biochemistry, Jichi Medical School, Yakushiji 3311-1, Minamikawachi, kawachi, Tochigi 329-0498, Japan, 4Division of Genetic Diagnosis, Institute of Medical Science, University of Tokyo, Sirokanedai 4-6-1, Minato-ku, Tokyo 108, Japan, 5Section of Protein Chemistry, Central Laboratories for Key Technology, Kirin Brewery Co. Ltd, Fukuura 1-13-5, Kanazawa-ku, Yokohama-shi, Kanagawa 236-0004, Japan and 6Hematology Branch, National Heart, Lung and Blood Institute, Building 10, Room 7C103, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD 20892, USA

Fanconi anemia (FA) is a genetic disorder that predisposes to hematopoietic failure, birth defects and cancer. We identified an interaction between the FA protein, FANCA and brm-related gene 1 (BRG1) product. BRG1 is a subunit of the SWI/SNF complex, which remodels chromatin structure through a DNA-dependent ATPase activity. FANCA was demonstrated to associate with the endogenous SWI/SNF complex. We also found a significant increase in the molecular chaperone, glucose-regulated protein 94 (GRP94) among BRG1-associated factors isolated from a FANCA-mutant cell line, which was not seen in either a normal control cell line or the mutant line complemented by wild-type FANCA. Despite this specific difference, FANCA did not appear to be absolutely required for in vitro chromatin remodeling. Finally, we demonstrated co-localization in the nucleus between transfected FANCA and BRG1. The physiological action of FANCA on the SWI/SNF complex remains to be clarified, but our work suggests that FANCA may recruit the SWI/SNF complex to target genes, thereby enabling coupled nuclear functions such as transcription and DNA repair.

+ To whom correspondence should be addressed. Tel: +1 301 496 2452; Fax: +1 301 496 8396; Email: liuj@nhlbi.nih.gov


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