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pubmed-article:17417655pubmed:abstractTextHuman RAD51 and RAD54 are key players in homologous recombination, a process that requires homology recognition and strand invasion by a RAD51-single-stranded DNA (ssDNA) nucleoprotein filament and chromatin remodeling by RAD54. Here we use in vitro chromatin reconstitution systems to show that RAD51-ssDNA stimulates RAD54-dependent chromatin remodeling in a homology-dependent, polarity-independent manner. This stimulation was not seen with RAD54B or other remodelers. Chromatin remodeling by RAD54 enabled strand invasion by RAD51-ssDNA on nucleosomal templates, which was homology- and polarity-dependent. Three natural RAD54 mutants found in primary cancer cells showed specific defects in remodeling or in the RAD54-RAD51 interaction. We propose that RAD54 is recruited by RAD51-ssDNA filament to the chromatin of the intact chromosome and that it remodels that chromatin to facilitate accessibility for strand exchange.lld:pubmed
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pubmed-article:17417655pubmed:dateRevised2007-12-3lld:pubmed
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pubmed-article:17417655pubmed:articleTitleHomology-driven chromatin remodeling by human RAD54.lld:pubmed
pubmed-article:17417655pubmed:affiliationDepartment of Molecular Biology, Massachusetts General Hospital and Department of Genetics, Harvard Medical School, 185 Cambridge Street, Boston, Massachusetts 02114, USA.lld:pubmed
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