The available SRL3 deletion strain of Saccharomyces cerevisiae contains a truncation of DNA damage tolerance protein Mms2: Implications for Srl3 and Mms2 functions.

Eunmi Kim, Wolfram Siede
{"title":"The available <i>SRL3</i> deletion strain of <i>Saccharomyces cerevisiae</i> contains a truncation of DNA damage tolerance protein Mms2: Implications for Srl3 and Mms2 functions.","authors":"Eunmi Kim,&nbsp;Wolfram Siede","doi":"10.5580/42c","DOIUrl":null,"url":null,"abstract":"<p><p>A screen of the commercially available collection of haploid deletion mutants of <i>Saccharomyces cerevisiae</i> for spontaneous mutator mutants newly identified a deletion of <i>SRL3</i>. This gene had been previously isolated as a suppressor of lethality of checkpoint kinase deletions if overexpressed. We found DNA damage sensitivity and extended checkpoint arrests to be associated with this strain. However, when crossed to wild-type, a mutant gene conferring these phenotypes was found to segregate from the <i>SRL3</i> deletion. The mutation was identified as a C-terminal truncation of Mms2, an E2 ubiquitin conjugating enzyme involved in error-free replicative bypass of lesions. This confirmed an earlier report that Mms2 may be required to restrain error-prone polymerase ζ activity and underscored that residues of the C-terminus are necessary for Mms2 function. Srl3, on the other hand, does not appear to influence DNA damage sensitivity or spontaneous mutability if deleted. However, the absence of these phenotypes does not contradict its likely role as a positive regulator of dNTP levels.</p>","PeriodicalId":22514,"journal":{"name":"The Internet journal of microbiology","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4008323/pdf/nihms238834.pdf","citationCount":"1","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"The Internet journal of microbiology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.5580/42c","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 1

Abstract

A screen of the commercially available collection of haploid deletion mutants of Saccharomyces cerevisiae for spontaneous mutator mutants newly identified a deletion of SRL3. This gene had been previously isolated as a suppressor of lethality of checkpoint kinase deletions if overexpressed. We found DNA damage sensitivity and extended checkpoint arrests to be associated with this strain. However, when crossed to wild-type, a mutant gene conferring these phenotypes was found to segregate from the SRL3 deletion. The mutation was identified as a C-terminal truncation of Mms2, an E2 ubiquitin conjugating enzyme involved in error-free replicative bypass of lesions. This confirmed an earlier report that Mms2 may be required to restrain error-prone polymerase ζ activity and underscored that residues of the C-terminus are necessary for Mms2 function. Srl3, on the other hand, does not appear to influence DNA damage sensitivity or spontaneous mutability if deleted. However, the absence of these phenotypes does not contradict its likely role as a positive regulator of dNTP levels.

酿酒酵母SRL3缺失菌株含有DNA损伤耐受蛋白Mms2的截断:对SRL3和Mms2功能的影响。
通过对商业上可获得的酿酒酵母单倍体缺失突变体的筛选,发现了SRL3的缺失。该基因先前被分离出来,作为过度表达的检查点激酶缺失的致死率的抑制因子。我们发现DNA损伤敏感性和延长检查点逮捕与该菌株有关。然而,当与野生型杂交时,发现具有这些表型的突变基因从SRL3缺失中分离出来。该突变被鉴定为Mms2的c端截断,Mms2是一种E2泛素偶联酶,参与病变的无错误复制旁路。这证实了早先的一篇报道,即Mms2可能需要抑制容易出错的聚合酶ζ活性,并强调了c端残基对于Mms2的功能是必要的。另一方面,Srl3如果被删除,似乎不会影响DNA损伤敏感性或自发易变性。然而,这些表型的缺失并不与它作为dNTP水平的积极调节因子的可能作用相矛盾。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信