Mutations in SID2, a novel gene in Saccharomyces cerevisiae, cause synthetic lethality with sic1 deletion and may cause a defect during S phase.
Mutations in SID2, a novel gene in Saccharomyces cerevisiae, cause synthetic lethality with sic1 deletion and may cause a defect during S phase.
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SID2 是酿酒酵母中的一种新基因，其突变会导致 sic1 缺失导致合成致死，并可能导致 S 期缺陷。
DOI：
10.1093/genetics/159.1.17
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发表时间：
2001
期刊：
影响因子：
3.3
通讯作者：
Vallen,EA
中科院分区：
文献类型：
--
作者：
Jacobson,MD;Muñoz,CX;Knox,KS;Williams,BE;Lu,LL;Cross,FR;Vallen,EA
SIC 1编码一种非必需的B型细胞周期蛋白/CDK抑制剂，在G1/S转换和退出有丝分裂中发挥作用。为了更全面地理解这些转换的调节，分离了引起sic 1 Δ合成致死性的突变。SID 2是一个新基因，编码一种DNA复制或修复所必需的蛋白质。SID 2 -1 sic 1 Δ菌株和SID 2 - 2 - 1温度敏感菌株在分裂前期表现为单核、短纺锤体、含~2C DNA的大芽细胞; RAD 9是DNA损伤检查点所必需的，在细胞分裂后期前阻滞过程中，用场反转凝胶电泳分析小鼠2 - 21细胞的染色体，发现在染色体停滞处存在复制叉和复制泡。删除两个S期细胞周期蛋白CLB 5和CLB 6，实质上抑制了β 2 -1 sic 1 Δ细胞的失活，而稳定Clb 5蛋白则加剧了β 2 -1 sic 1 Δ细胞的缺陷。在同步化的突变株中，复制的开始似乎正常，但DNA合成的完成被延迟。突变株对羟基脲敏感，表明突变株可能遭受DNA损伤，当与额外的损伤结合时，导致活力下降。与这一假设相一致的是，即使SIC 1被表达，RAD 2 -1 rad 9细胞也是死亡的或生长非常缓慢的。
SIC1encodes a nonessential B-type cyclin/CDK inhibitor that functions at the G1/S transition and the exit from mitosis. To understand more completely the regulation of these transitions, mutations causing synthetic lethality withsic1Δ were isolated. In this screen, we identified a novel gene,SID2, which encodes an essential protein that appears to be required for DNA replication or repair.sid2-1 sic1Δ strains andsid2-21temperature-sensitive strains arrest preanaphase as large-budded cells with a single nucleus, a short spindle, and an ~2C DNA content.RAD9, which is necessary for the DNA damage checkpoint, is required for the preanaphase arrest ofsid2-1 sic1Δ cells. Analysis of chromosomes in mutantsid2-21cells by field inversion gel electrophoresis suggests the presence of replication forks and bubbles at the arrest. Deleting the two S phase cyclins,CLB5andCLB6, substantially suppresses thesid2-1 sic1Δ inviability, while stabilizing Clb5 protein exacerbates the defects ofsid2-1 sic1Δ cells. In synchronizedsid2-1mutant strains, the onset of replication appears normal, but completion of DNA synthesis is delayed.sid2-1mutants are sensitive to hydroxyurea indicating thatsid2-1cells may suffer DNA damage that, when combined with additional insult, leads to a decrease in viability. Consistent with this hypothesis,sid2-1 rad9cells are dead or very slow growing even whenSIC1is expressed.
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影响因子：
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作者：
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作者：
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DOI：
10.1093/emboj/17.2.498
发表时间：
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期刊：
The EMBO Journal
影响因子：
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作者：
Kate M. Kramer;D. Fesquet;A. Johnson;L. Johnston
通讯作者：
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影响因子：
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作者：
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通讯作者：
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