{"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":null,"pages":null},"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}
引用次数: 3
Abstract
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.