Budding yeast Mms22 and Mms1 regulate homologous recombination induced by replisome blockage
Budding yeast Mms22 and Mms1 regulate homologous recombination induced by replisome blockage
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DOI：
10.1016/j.dnarep.2008.01.007
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发表时间：
2008-05-03
期刊：
影响因子：
3.8
通讯作者：
Rouse, John
中科院分区：
文献类型：
--
作者：
Duro, Eris;Vaisica, Jessica A.;Rouse, John
缺乏MMS22或MMS1的酵母细胞对干扰复制体进程的药物高度敏感，但这些基因的细胞功能尚不清楚。在这项研究中，我们研究了发芽酵母MMS22和MMS1在同源重组(HR)中的作用。在缺乏MMS22或MMS1的细胞中，由阻断复制体的试剂诱导的姐妹染色单体之间或同源染色体之间的重组是严重缺陷的。相反，双链断裂诱导的HR不受这些基因缺失的影响。在缺乏cullin RTT101和组蛋白乙酰转移酶RTT109的细胞以及缺乏组蛋白伴侣ASF1的细胞中，也观察到MMS诱导的HR的主要缺陷，所有这些都与MMS22和MMS1存在遗传上的相互作用。最后，我们发现缺乏MMS22或MMS1的细胞在从MMS诱导的复制体停滞中恢复方面是有缺陷的。这些结果表明MMS22和MMS1为S期特异性重组促进因子。(C)2008爱思唯尔B.V.保留所有权利。
Yeast cells lacking MMS22 or MMS1 are hypersensitive to agents that perturb replisome progression but the cellular functions of these genes are unknown. In this study we investigate the involvement of budding yeast MMS22 and MMS1 in homologous recombination (HR). Recombination between sister chromatids or between homologous chromosomes induced by agents that block replisomes was severely defective in cells lacking MMS22 or MMS1. In contrast, HR induced by double-strand breaks was not affected by the absence of these genes. Major defects in MMS-induced HR were also observed in cells lacking the cullin RTT101, the histone acetyltransferase RTT109 and in cells lacking the histone chaperone ASF1, all of which interact genetically with MMS22 and MMS1. Finally, we show that cells lacking either MMS22 or MMS1 are defective in recovery from MMS-induced replisome stalling. These results identify Mms22 and Mms1 as S-phase specific recombination-promoting factors. (c) 2008 Elsevier B.V. All rights reserved.