Journal
GENES & DEVELOPMENT
Volume 23, Issue 1, Pages 67-79Publisher
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.1737809
Keywords
Genome instability; recombination; DNA helicase; crossing over; Fanconi anemia
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Funding
- NIH [GM80600, GM20056, ES07061, GM57814, GM53738]
- Wellcome Trust [GR076476]
- EMBO/HHMI [ME888]
- Deutsche Forschungsgemeinschaft [Kr 914/6-1]
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [R01ES007061] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM020056, R37GM020056, R01GM076020, R01GM053738, R01GM057814, R01GM080600] Funding Source: NIH RePORTER
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Eukaryotes possess mechanisms to limit crossing over during mitotic homologous recombination, thus avoiding possible chromosomal rearrangements. We show here that budding yeast Mph1, an ortholog of human FancM helicase, utilizes its helicase activity to suppress spontaneous unequal sister chromatid exchanges and DNA double-strand break-induced chromosome crossovers. Since the efficiency and kinetics of break repair are unaffected, Mph1 appears to channel repair intermediates into a noncrossover pathway. Importantly, Mph1 works independently of two other helicases-Srs2 and Sgs1-that also attenuate crossing over. By chromatin immunoprecipitation, we find targeting of Mph1 to double-strand breaks in cells. Purified Mph1 binds D-loop structures and is particularly adept at unwinding these structures. Importantly, Mph1, but not a helicase-defective variant, dissociates Rad51-made D-loops. Overall, the results from our analyses suggest a new role of Mph1 in promoting the noncrossover repair of DNA double-strand breaks.
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