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出芽酵母的Mms4与Rad52上位性相关,且Mms4的功能可被一种细菌霍利迪连接体解离酶替代。

Budding yeast mms4 is epistatic with rad52 and the function of Mms4 can be replaced by a bacterial Holliday junction resolvase.

作者信息

Odagiri Nao, Seki Masayuki, Onoda Fumitoshi, Yoshimura Akari, Watanabe Sei, Enomoto Takemi

机构信息

Molecular Cell Biology Laboratory, Graduate School of Pharmaceutical Sciences, Tohoku University, Aoba, Aramaki, Aoba-ku, Sendai 980-8578, Japan.

出版信息

DNA Repair (Amst). 2003 Mar 1;2(3):347-58. doi: 10.1016/s1568-7864(02)00234-3.

Abstract

MMS4 of Saccharomyces cerevisiae was originally identified as the gene responsible for one of the collection of methyl methanesulfonate (MMS)-sensitive mutants, mms4. Recently it was identified as a synthetic lethal gene with an SGS1 mutation. Epistatic analyses revealed that MMS4 is involved in a pathway leading to homologous recombination requiring Rad52 or in the recombination itself, in which SGS1 is also involved. MMS sensitivity of mms4 but not sgs1, was suppressed by introducing a bacterial Holliday junction (HJ) resolvase, RusA. The frequencies of spontaneously occurring unequal sister chromatid recombination (SCR) and loss of marker in the rDNA in haploid mms4 cells and interchromosomal recombination between heteroalleles in diploid mms4 cells were essentially the same as those of wild-type cells. Although UV- and MMS-induced interchromosomal recombination was defective in sgs1 diploid cells, hyper-induction of interchromosomal recombination was observed in diploid mms4 cells, indicating that the function of Mms4 is dispensable for this type of recombination.

摘要

酿酒酵母的MMS4最初被鉴定为负责甲磺酸甲酯(MMS)敏感突变体集合之一的基因,即mms4。最近它被鉴定为与SGS1突变具有合成致死性的基因。上位性分析表明,MMS4参与了一条通向需要Rad52的同源重组的途径或SGS1也参与的重组本身。通过引入细菌Holliday连接(HJ)解离酶RusA,可抑制mms4而非sgs1的MMS敏感性。单倍体mms4细胞中rDNA自发发生的不等姐妹染色单体重组(SCR)和标记丢失的频率以及二倍体mms4细胞中异等位基因间的染色体间重组频率与野生型细胞基本相同。虽然紫外线和MMS诱导的染色体间重组在sgs1二倍体细胞中存在缺陷,但在二倍体mms4细胞中观察到染色体间重组的超诱导,这表明Mms4的功能对于这种类型的重组是可有可无的。

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