A requirement for recombinational repair in Saccharomyces cerevisiae is caused by DNA replication defects of mec1 mutants.

摘要: To examine the role of RAD52 recombinational repair pathway in compensating for DNA replication defects Saccharomyces cerevisiae, we performed a genetic screen to identify mutants that require Rad52p viability. We isolated 10 mec1 mutations display synthetic lethality with rad52. These (designated mec1-srf rad-fifty-two) simultaneously cause two types phenotypes: checkpoint function Mec1p and essential Mec1p. Velocity sedimentation alkaline sucrose gradients revealed accumulate small single-stranded synthesis intermediates, suggesting is required normal progression synthesis. sml1 suppressor suppress both accumulation intermediates requirement mutants, but they do not defect mutants. Thus, it appears be Rad52p. By using hydroxyurea introduce similar defects, found breaks frequently lead double-stranded are rapidly repaired rad52 Taken together, these data suggest prevent or caused by defective