Rad51/Dmc1 paralogs and mediators oppose DNA helicases to limit hybrid DNA formation and promote crossovers during meiotic recombination

摘要: During meiosis programmed DNA double-strand breaks (DSBs) are repaired by homologous recombination using the sister chromatid or chromosome (homolog) as a template. This repair results in crossover (CO) and non-crossover (NCO) recombinants. Only CO formation between homologs provides physical linkages guiding correct segregation, which essential to produce healthy gametes. The factors that determine CO/NCO decision still poorly understood. Using Schizosaccharomyces pombe model we show Rad51/Dmc1-paralog complexes Rad55-Rad57 Rdl1-Rlp1-Sws1 together with Swi5-Sfr1 play major role antagonizing both FANCM-family helicase/translocase Fml1 RecQ-type helicase Rqh1 limit hybrid promote Mus81-Eme1-dependent COs. A common attribute of these protein is an ability stabilize Rad51/Dmc1 nucleoprotein filament, propose it this property imposes constraints on enzymes gain access intermediate, thereby controlling manner processed resolved.