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首页> 外文期刊>Molecular and Cellular Biology >Mms2-Ubc13-Dependent and -Independent Roles of Rad5 Ubiquitin Ligase in Postreplication Repair and Translesion DNA Synthesis in Saccharomyces cerevisiae
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Mms2-Ubc13-Dependent and -Independent Roles of Rad5 Ubiquitin Ligase in Postreplication Repair and Translesion DNA Synthesis in Saccharomyces cerevisiae

机译：Mms2-Ubc13依赖性和非依赖性Rad5泛素连接酶在酿酒酵母中的复制后修复和转移DNA合成中的作用。

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The Rad6-Rad18 ubiquitin-conjugating enzyme complex of Saccharomyces cerevisiae promotes replication through DNA lesions via three separate pathways that include translesion synthesis (TLS) by DNA polymerases η and ζ and postreplicational repair (PRR) of discontinuities that form in the newly synthesized DNA opposite from DNA lesions, mediated by the Mms2-Ubc13 ubiquitin-conjugating enzyme and Rad5. Rad5 is an SWI/SNF family ATPase, and additionally, it functions as a ubiquitin ligase in the ubiquitin conjugation reaction. To decipher the roles of these Rad5 activities in lesion bypass, here we examine the effects of mutations in the Rad5 ATPase and ubiquitin ligase domains on the PRR of UV-damaged DNA and on UV-induced mutagenesis. Even though the ATPase-defective mutation confers only a modest degree of UV sensitivity whereas the ubiquitin ligase mutation causes a high degree of UV sensitivity, we find that both of these mutations produce the same high level of PRR defect as that conferred by the highly UV-sensitive rad5Δ mutation. From these studies, we infer a requirement of the Rad5 ATPase and ubiquitin ligase activities in PRR, and based upon the effects of different rad5 mutations on UV mutagenesis, we suggest a role for Rad5 in affecting the efficiency of lesion bypass by the TLS polymerases. In contrast to the role of Rad5 in PRR, however, where its function is coupled with that of Mms2-Ubc13, Rad5 function in TLS would be largely independent of this ubiquitin-conjugating enzyme complex.
机译：酿酒酵母的Rad6-Rad18泛素结合酶复合物通过三种途径促进DNA损伤的复制，这些途径包括DNA聚合酶η和ζ的跨病变合成（TLS）和不连续点的复制后修复（PRR）， Mms2-Ubc13泛素结合酶和Rad5介导的新合成DNA中与DNA损伤相反的形式。 Rad5是SWI / SNF家族的ATPase，此外，它在泛素结合反应中起泛素连接酶的作用。为了解释这些Rad5活性在病变旁路中的作用，在这里我们检查Rad5 ATPase和泛素连接酶结构域中的突变对UV损伤的DNA的PRR和对UV诱导的诱变的影响。即使ATPase缺陷突变仅赋予中等程度的UV敏感性，而遍在蛋白连接酶突变引起高度的UV敏感性，我们发现这两种突变均产生与高UV引起的相同水平的PRR缺陷敏感的 rad5 Δ突变。从这些研究中，我们推断出PRR中Rad5 ATPase和泛素连接酶活性的需求，并基于不同的 rad5 突变对紫外线诱变的影响，我们建议Rad5在影响UV诱变效率中的作用。 TLS聚合酶可绕过病灶。但是，与Rad5在PRR中的作用相反，Rad5的功能与Mms2-Ubc13的作用相反，TLS中的Rad5的功能将在很大程度上独立于这种泛素结合酶复合物。

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