Double-strand break repair: are Rad51/RecA-DNA joints barriers to DNA replication?

被引:29
作者
Aguilera, A [1 ]
机构
[1] Univ Sevilla, Fac Biol, Dept Genet, E-41012 Seville, Spain
关键词
D O I
10.1016/S0168-9525(01)02309-5
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
The central step of homologous recombination is the DNA strand exchange reaction catalyzed by bacterial RecA or eukaryotic Rad51. Besides Rad51-mediated synthesis-dependent strand annealing (SDSA), DNA ends can promote replication in Escherichia coli(recombination-dependent replication, RDR) and yeast (break-induced replication, BIR). However, what causes a DNA end to be repaired via SDSA or via BIR/RDR? I propose that Rad51/RecA-DNA plectonemic joints act as barriers to DNA replication and that BIR/RDR is only possible when the DNA polymerase that synthesizes DNA from the invading 3' end does not encounter RecA/Rad51-DNA joints in its path.
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页码:318 / 321
页数:4
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