Recovery from checkpoint-mediated arrest after repair of a double-strand break requires Srs2 helicase

被引:274
作者
Vaze, MB
Pellicioli, A
Lee, SE
Ira, G
Liberi, G
Arbel-Eden, A
Foiani, M
Haber, JE [1 ]
机构
[1] Brandeis Univ, Rosenstiel Ctr, Waltham, MA 02454 USA
[2] Brandeis Univ, Dept Biol, Waltham, MA 02454 USA
[3] Univ Milan, Dipartimento Genet & Biol Microrganismi, I-20133 Milan, Italy
[4] Ist FIRC Oncol Mol, I-20133 Milan, Italy
[5] Nicholas Copernicus Univ, Inst Gen & Mol Biol, PL-87100 Torun, Poland
关键词
D O I
10.1016/S1097-2765(02)00593-2
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
In Saccharomyces strains in which homologous recombination is delayed sufficiently to activate the DNA damage checkpoint, Rad53p checkpoint kinase activity appears 1 hr after DSB induction and disappears soon after completion of repair. Cells lacking Srs2p helicase fail to recover even though they apparently complete DNA repair; Rad53p kinase remains activated. srs2A cells also fail to adapt when DSB repair is prevented. The recovery defect of srs2A is suppressed in mec1Delta strains lacking the checkpoint or when DSB repair occurs before checkpoint activation. Permanent preanaphase arrest of srs2Delta cells is reversed by the addition of caffeine after cells have arrested. Thus, in addition to its roles in recombination, Srs2p appears to be needed to turn off the DNA damage checkpoint.
引用
收藏
页码:373 / 385
页数:13
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