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首页> 外文期刊>Molecular and Cellular Biology >Saccharomyces cerevisiae Rrm3p DNA Helicase Promotes Genome Integrity by Preventing Replication Fork Stalling: Viability of rrm3 Cells Requires the Intra-S-Phase Checkpoint and Fork Restart Activities
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Saccharomyces cerevisiae Rrm3p DNA Helicase Promotes Genome Integrity by Preventing Replication Fork Stalling: Viability of rrm3 Cells Requires the Intra-S-Phase Checkpoint and Fork Restart Activities

机译：酿酒酵母Rrm3p DNA解旋酶通过防止复制叉停转促进基因组完整性：rrm3细胞的活力需要S阶段内关卡和叉重新启动活动

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Rrm3p is a 5′-to-3′ DNA helicase that helps replication forks traverse protein-DNA complexes. Its absence leads to increased fork stalling and breakage at over 1,000 specific sites located throughout the Saccharomyces cerevisiae genome. To understand the mechanisms that respond to and repair rrm3-dependent lesions, we carried out a candidate gene deletion analysis to identify genes whose mutation conferred slow growth or lethality on rrm3 cells. Based on synthetic phenotypes, the intra-S-phase checkpoint, the SRS2 inhibitor of recombination, the SGS1/TOP3 replication fork restart pathway, and the MRE11/RAD50/XRS2 (MRX) complex were critical for viability of rrm3 cells. DNA damage checkpoint and homologous recombination genes were important for normal growth of rrm3 cells. However, the MUS81/MMS4 replication fork restart pathway did not affect growth of rrm3 cells. These data suggest a model in which the stalled and broken forks generated in rrm3 cells activate a checkpoint response that provides time for fork repair and restart. Stalled forks are converted by a Rad51p-mediated process to intermediates that are resolved by Sgs1p/Top3p. The rrm3 system provides a unique opportunity to learn the fate of forks whose progress is impaired by natural impediments rather than by exogenous DNA damage.
机译：Rrm3p是一种5'至3'DNA解旋酶，可帮助复制叉穿越蛋白质-DNA复合物。它的缺失会导致整个酿酒酵母基因组中超过1000个特定位点的叉子停滞和断裂增加。为了了解应答和修复 rrm3 依赖性病变的机制，我们进行了候选基因缺失分析，以鉴定其突变赋予 rrm3 细胞缓慢生长或致死性的基因。基于合成表型，S阶段内检查点， SRS2 重组抑制剂， SGS1 / TOP3 复制叉重新启动途径和 MRE11 / RAD50 / XRS2 （MRX）复合物对于 rrm3 细胞的生存能力至关重要。 DNA损伤检查点和同源重组基因对于 rrm3 细胞的正常生长很重要。但是， MUS81 / MMS4 复制叉重启途径不会影响 rrm3 细胞的生长。这些数据表明了一个模型，在该模型中，在 rrm3 单元中生成的停滞和折断的叉子会激活一个检查点响应，从而为叉子的修复和重新启动提供了时间。摊叉通过Rad51p介导的过程转换为Sgs1p / Top3p解析的中间体。 rrm3 系统提供了一个独特的机会来学习叉子的命运，这些叉子的前进受到自然障碍而不是外源DNA损害的影响。

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