作者: R. Prakash , D. Satory , E. Dray , A. Papusha , J. Scheller
DOI: 10.1101/GAD.1737809
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摘要: Eukaryotes possess mechanisms to limit crossing over during homologous recombination, thus avoiding possible chromosomal rearrangements. We show here that budding yeast Mph1, an ortholog of human FancM helicase, utilizes its helicase activity suppress spontaneous unequal sister chromatid exchanges and DNA double-strand break-induced chromosome crossovers. Since the efficiency kinetics break repair are unaffected, Mph1 appears channel intermediates into a noncrossover pathway. Importantly, works independently two other helicases-Srs2 Sgs1-that also attenuate over. By chromatin immunoprecipitation, we find targeting breaks in cells. Purified binds D-loop structures is particularly adept at unwinding these structures. but not helicase-defective variant, dissociates Rad51-made D-loops. Overall, results from our analyses suggest new role promoting breaks.