Author:
Nanbu Tomoko,Takahashi Katsunori,Murray Johanne M.,Hirata Naoya,Ukimori Shinobu,Kanke Mai,Masukata Hisao,Yukawa Masashi,Tsuchiya Eiko,Ueno Masaru
Abstract
Protection of telomeres protein 1 (Pot1) binds to single-stranded telomere overhangs and protects chromosome ends. RecQ helicases regulate homologous recombination at multiple stages, including resection, strand displacement, and resolution. Fission yeastpot1and RecQ helicaserqh1double mutants are synthetically lethal, but the mechanism is not fully understood. Here, we show that the synthetic lethality ofpot1Δrqh1Δ double mutants is due to inappropriate homologous recombination, as it is suppressed by the deletion ofrad51+. The expression of Rad51 in thepot1Δrqh1Δrad51Δ triple mutant, which has circular chromosomes, is lethal. Reduction of the expression of Rqh1 in apot1disruptant with circular chromosomes caused chromosome missegregation, and this defect was partially suppressed by the deletion ofrad51+. Taken together, our results suggest that Rqh1 is required for the maintenance of circular chromosomes when homologous recombination is active. Crossovers between circular monomeric chromosomes generate dimers that cannot segregate properly inEscherichia coli. We propose that Rqh1 inhibits crossovers between circular monomeric chromosomes to suppress the generation of circular dimers.
Publisher
American Society for Microbiology
Subject
Cell Biology,Molecular Biology
Cited by
10 articles.
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