Requirement of RAD52 group genes for postreplication repair of UV-damaged DNA in Saccharomyces cerevisiae
Requirement of RAD52 group genes for postreplication repair of UV-damaged DNA in Saccharomyces cerevisiae
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DOI：
10.1128/mcb.01331-07
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发表时间：
2007-11-01
影响因子：
5.3
通讯作者：
Prakash, Louise
中科院分区：
文献类型：
--
作者：
Gangavarapu, Venkateswarlu;Prakash, Satya;Prakash, Louise
在酿酒酵母中，通过DNA损伤的复制由Rad 6-Rad 18依赖性过程促进，所述过程包括通过DNA聚合酶-eta和zeta的跨损伤合成和Rad 5-Mms 2-Ubc 13控制的复制后修复（PRR）途径，所述途径修复新合成的DNA中的不连续性，所述不连续性与模板链上的DNA损伤相对形成。在这里，我们研究的贡献的RAD 51，RAD 52，和RAD 54基因和RAD 50和XRS 2基因的紫外线损伤的DNA的PRR。我们发现，RAD 51，RAD 52和RAD 54基因的缺失损害PRR的效率，并且几乎所有的PRR在没有Rad 5和Rad 52的情况下都被抑制。我们建议Rad 5通路的作用时，病变位于前导链模板和Rad 52通路时，病变位于滞后链模板。我们推测这两种途径都以非重组方式运作，Rad 5通过其DNA解旋酶活性介导复制叉回归和模板转换，Rad 52通过合成依赖性链退火模式。此外，我们的研究结果表明Rad 50和Xrs 2蛋白的作用，从而为MRX复合物通过Rad 5和Rad 52途径促进PRR。
In Saccharomyces cerevisiae, replication through DNA lesions is promoted by Rad6-Rad18-dependent processes that include translesion synthesis by DNA polymerases -eta and zeta and a Rad5-Mm s2-Ubc13-control led postreplicational repair (PRR) pathway which repairs the discontinuities in the newly synthesized DNA that form opposite from DNA lesions on the template strand. Here, we examine the contributions of the RAD51, RAD52, and RAD54 genes and of the RAD50 and XRS2 genes to the PRR of UV-damaged DNA. We find that deletions of the RAD51, RAD52, and RAD54 genes impair the efficiency of PRR and that almost all of the PRR is inhibited in the absence of both Rad5 and Rad52. We suggest a role for the Rad5 pathway when the lesion is located on the leading strand template and for the Rad52 pathway when the lesion is located on the lagging strand template. We surmise that both of these pathways operate in a nonrecombinational manner, Rad5 by mediating replication fork regression and template switching via its DNA helicase activity and Rad52 via a synthesis-dependent strand annealing mode. In addition, our results suggest a role for the Rad50 and Xrs2 proteins and thereby for the MRX complex in promoting PRR via both the Rad5 and Rad52 pathways.