{"title":"在酿酒酵母中,紫外线或γ射线诱导的rho -突变体与核重组修复途径无关","authors":"Martine Heude","doi":"10.1016/0167-8817(88)90017-X","DOIUrl":null,"url":null,"abstract":"<div><p>In order to discover whether the nuclear recombinational repair pathway also acts on lesions induced in mitochondrial DNA (mtDNA), the possible role of the <em>RAD50, −51, −52, −55</em> and <em>−56</em> genes on the induction of <em>rho</em><sup>−</sup> mutants by radiations was studied. Such induction appeared to be independent of this pathway. Nevertheless, an efficient induction of respiration-deficient mutants was observed in γ-irradiated <em>rad52</em> diploids. We demonstrate that these mutants do not result from a lack of mtDNA repair, but from chromosome losses induced by γ-rays. Such an impairment of the respiratory ability of diploids by chromosome losses was effectively observed in the aneuploid progeny of unirradiated <em>RAD<sup>+</sup> cdc6</em> diploids incubated at the restrictive temperature.</p></div>","PeriodicalId":100936,"journal":{"name":"Mutation Research/DNA Repair Reports","volume":"194 2","pages":"Pages 151-163"},"PeriodicalIF":0.0000,"publicationDate":"1988-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0167-8817(88)90017-X","citationCount":"3","resultStr":"{\"title\":\"The induction of rho− mutants by UV or γ-rays is independent of the nuclear recombinational repair pathway in Saccharomyces cerevisiae\",\"authors\":\"Martine Heude\",\"doi\":\"10.1016/0167-8817(88)90017-X\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>In order to discover whether the nuclear recombinational repair pathway also acts on lesions induced in mitochondrial DNA (mtDNA), the possible role of the <em>RAD50, −51, −52, −55</em> and <em>−56</em> genes on the induction of <em>rho</em><sup>−</sup> mutants by radiations was studied. Such induction appeared to be independent of this pathway. Nevertheless, an efficient induction of respiration-deficient mutants was observed in γ-irradiated <em>rad52</em> diploids. We demonstrate that these mutants do not result from a lack of mtDNA repair, but from chromosome losses induced by γ-rays. Such an impairment of the respiratory ability of diploids by chromosome losses was effectively observed in the aneuploid progeny of unirradiated <em>RAD<sup>+</sup> cdc6</em> diploids incubated at the restrictive temperature.</p></div>\",\"PeriodicalId\":100936,\"journal\":{\"name\":\"Mutation Research/DNA Repair Reports\",\"volume\":\"194 2\",\"pages\":\"Pages 151-163\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1988-09-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1016/0167-8817(88)90017-X\",\"citationCount\":\"3\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Mutation Research/DNA Repair Reports\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/016788178890017X\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Mutation Research/DNA Repair Reports","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/016788178890017X","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
The induction of rho− mutants by UV or γ-rays is independent of the nuclear recombinational repair pathway in Saccharomyces cerevisiae
In order to discover whether the nuclear recombinational repair pathway also acts on lesions induced in mitochondrial DNA (mtDNA), the possible role of the RAD50, −51, −52, −55 and −56 genes on the induction of rho− mutants by radiations was studied. Such induction appeared to be independent of this pathway. Nevertheless, an efficient induction of respiration-deficient mutants was observed in γ-irradiated rad52 diploids. We demonstrate that these mutants do not result from a lack of mtDNA repair, but from chromosome losses induced by γ-rays. Such an impairment of the respiratory ability of diploids by chromosome losses was effectively observed in the aneuploid progeny of unirradiated RAD+ cdc6 diploids incubated at the restrictive temperature.