期刊
MOLECULAR AND CELLULAR BIOLOGY
卷 21, 期 6, 页码 2048-2056出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/MCB.21.6.2048-2056.2001
关键词
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资金
- NIGMS NIH HHS [GM20056, R37 GM020056, R01 GM053738, R01 GM020056, GM53738] Funding Source: Medline
Broken chromosomes can be repaired by several homologous recombination mechanisms, including gene conversion and break-induced replication (BIR). In Saccharomyces cerevisiae, an HO endonuclease-induced double-strand break (DSB) is normally repaired by gene conversion. Previously, we have shown that in the absence of RAD52, repair is nearly absent and diploid cells lose the broken chromosome; however, in cells lacking RAD51, gene conversion is absent but cells can repair the DSB by BIR. We now report that gene conversion is also abolished when RAD54, RAD55, and RAD57 are deleted but BIR occurs, as with rad51 Delta cells. DSB-induced gene conversion is not significantly affected when RAD50, RAD59, TID1 (RDH54), SRS2, or SGS1 is deleted. Various double mutations largely eliminate both gene conversion and BIR, including rad51 Delta rad50 Delta, rad51 Delta rad59 Delta, and rad54 Delta tid1 Delta. These results demonstrate that there is a RAD51- and RAD54-independent BIR pathway that requires RAD59, TID1, RAD50, and presumably MRE11 and XRS2. The similar genetic requirements for BIR and telomere maintenance in the absence of telomerase also suggest that these two professes proceed by similar mechanisms.
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