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首页> 外文期刊>Molecular and Cellular Biology >Opposing Effects of Ubiquitin Conjugation and SUMO Modification of PCNA on Replicational Bypass of DNA Lesions in Saccharomyces cerevisiae
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Opposing Effects of Ubiquitin Conjugation and SUMO Modification of PCNA on Replicational Bypass of DNA Lesions in Saccharomyces cerevisiae

机译：泛素结合和PCNA的SUMO修饰对酿酒酵母DNA损伤复制旁路的相反作用

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摘要

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 ζ (Polζ) and Polη and postreplicational repair mediated by the Mms2-Ubc13 ubiquitin-conjugating enzyme and Rad5. Here we report our studies with a proliferating cell nuclear antigen (PCNA) mutation, pol30-119, which results from a change of the lysine 164 residue to arginine. It has been shown recently that following treatment of yeast cells with DNA-damaging agents, the lysine 164 residue of PCNA becomes monoubiquitinated in a Rad6-Rad18-dependent manner and that subsequently this PCNA residue is polyubiquitinated via a lysine 63-linked ubiquitin chain in an Mms2-Ubc13-, Rad5-dependent manner. PCNA is also modified by SUMO conjugation at the lysine 164 residue. Our genetic studies with the pol30-119 mutation show that in addition to conferring a defect in Polζ-dependent UV mutagenesis and in Polη-dependent TLS, this PCNA mutation inhibits postreplicational repair of discontinuities that form in the newly synthesized strand across from UV lesions. In addition, we provide evidence for the activation of the RAD52 recombinational pathway in the pol30-119 mutant and we infer that SUMO conjugation at the lysine 164 residue of PCNA has a role in suppressing the Rad52-dependent postreplicational repair pathway.
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通过DNA损伤的复制，这些途径包括DNA聚合酶ζ（Polζ）和Polη的跨病变合成（TLS）以及由Saccharomyces cerevisiae介导的复制后修复。 Mms2-Ubc13泛素结合酶和Rad5。在这里，我们报告了我们的研究，其中涉及增殖细胞核抗原（PCNA）突变 pol30-119 ，该突变是由于赖氨酸164残基变为精氨酸而引起的。最近显示，在用DNA破坏剂处理酵母细胞后，PCNA的赖氨酸164残基以Rad6-Rad18依赖性方式被单泛素化，随后该PCNA残基通过赖氨酸63连接的泛素链被多泛素化。 Mms2-Ubc13-，Rad5依赖的方式。 PCNA也可以通过SUMO偶联在赖氨酸164残基上进行修饰。我们对 pol30-119 突变的遗传研究表明，除了赋予Polζ依赖的UV诱变和Polη依赖的TLS缺陷外，这种PCNA突变还抑制了新形成的不连续性的复制后修复。合成的链从紫外线损伤处穿过。此外，我们为 pol30-119 突变体中 RAD52 重组途径的激活提供了证据，并且我们推断PCNA赖氨酸164残基上的SUMO偶联具有一定作用。抑制Rad52依赖的复制后修复途径。

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