{"title":"大肠杆菌rep-38与mmrA1突变的比较","authors":"Rakesh C. Sharma , Kendric C. Smith","doi":"10.1016/0167-8817(87)90032-0","DOIUrl":null,"url":null,"abstract":"<div><p>The <em>rep-38</em> and <em>mmrA1</em> mutations are located very close to each other (∼85 min), and have been suggested to be allelic. To address this question we have compared the phenotypes of the <em>mmrA1</em> and <em>rep-38</em> mutants. Both the <em>mmrA1</em> and <em>rep-38</em> mutations blocked the enhanced killing and inhibition of postreplication repair by rich growth medium that occurs in UV-irradiated <em>Escherichia coli</em> K-12 <em>uvrA</em> cells, i.e., the <em>mmrA1</em> and <em>rep-38</em> strains did not show minimal medium recovery (MMR). However, ΦX174 bacteriophage propagated well in <em>mmrA1</em> strains, but not in <em>rep-38</em> strains; a <em>rep</em> mutation sensitized a <em>uvrA</em> strain to UV irradiation, but a <em>mmrA</em> mutation did not. During chloramphenicol treatment, the <em>rep-38</em> strain showed a larger amount of residual DNA synthesis than observed in the <em>mmrA1</em> strain. The <em>mmrA1</em> mutation appears to be a dominant mutation. This was determined by the failure of either plasmid pLC44-7 or episome F′KLF11, both of which carry the <em>mmrA</em><sup>+</sup> gene, to complement the Mmr<sup>−</sup> phenotype of a <em>uvrA mmrA</em> strain. Plasmid pLC44-7 is known to complement the <em>rep-38</em> mutation, suggesting that <em>rep-38</em> is a recessive mutation. Although certain of the phenotypes of the <em>rep</em> and <em>mmrA</em> mutants are similar, a number are quite different. These differences suggest that these two mutations are not allelic.</p></div>","PeriodicalId":100936,"journal":{"name":"Mutation Research/DNA Repair Reports","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"1987-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/0167-8817(87)90032-0","citationCount":"3","resultStr":"{\"title\":\"Comparison of the rep-38 and mmrA1 mutations of Escherichia coli\",\"authors\":\"Rakesh C. Sharma , Kendric C. Smith\",\"doi\":\"10.1016/0167-8817(87)90032-0\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>The <em>rep-38</em> and <em>mmrA1</em> mutations are located very close to each other (∼85 min), and have been suggested to be allelic. To address this question we have compared the phenotypes of the <em>mmrA1</em> and <em>rep-38</em> mutants. Both the <em>mmrA1</em> and <em>rep-38</em> mutations blocked the enhanced killing and inhibition of postreplication repair by rich growth medium that occurs in UV-irradiated <em>Escherichia coli</em> K-12 <em>uvrA</em> cells, i.e., the <em>mmrA1</em> and <em>rep-38</em> strains did not show minimal medium recovery (MMR). However, ΦX174 bacteriophage propagated well in <em>mmrA1</em> strains, but not in <em>rep-38</em> strains; a <em>rep</em> mutation sensitized a <em>uvrA</em> strain to UV irradiation, but a <em>mmrA</em> mutation did not. During chloramphenicol treatment, the <em>rep-38</em> strain showed a larger amount of residual DNA synthesis than observed in the <em>mmrA1</em> strain. The <em>mmrA1</em> mutation appears to be a dominant mutation. This was determined by the failure of either plasmid pLC44-7 or episome F′KLF11, both of which carry the <em>mmrA</em><sup>+</sup> gene, to complement the Mmr<sup>−</sup> phenotype of a <em>uvrA mmrA</em> strain. Plasmid pLC44-7 is known to complement the <em>rep-38</em> mutation, suggesting that <em>rep-38</em> is a recessive mutation. Although certain of the phenotypes of the <em>rep</em> and <em>mmrA</em> mutants are similar, a number are quite different. These differences suggest that these two mutations are not allelic.</p></div>\",\"PeriodicalId\":100936,\"journal\":{\"name\":\"Mutation Research/DNA Repair Reports\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1987-07-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1016/0167-8817(87)90032-0\",\"citationCount\":\"3\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Mutation Research/DNA Repair Reports\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/0167881787900320\",\"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/0167881787900320","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Comparison of the rep-38 and mmrA1 mutations of Escherichia coli
The rep-38 and mmrA1 mutations are located very close to each other (∼85 min), and have been suggested to be allelic. To address this question we have compared the phenotypes of the mmrA1 and rep-38 mutants. Both the mmrA1 and rep-38 mutations blocked the enhanced killing and inhibition of postreplication repair by rich growth medium that occurs in UV-irradiated Escherichia coli K-12 uvrA cells, i.e., the mmrA1 and rep-38 strains did not show minimal medium recovery (MMR). However, ΦX174 bacteriophage propagated well in mmrA1 strains, but not in rep-38 strains; a rep mutation sensitized a uvrA strain to UV irradiation, but a mmrA mutation did not. During chloramphenicol treatment, the rep-38 strain showed a larger amount of residual DNA synthesis than observed in the mmrA1 strain. The mmrA1 mutation appears to be a dominant mutation. This was determined by the failure of either plasmid pLC44-7 or episome F′KLF11, both of which carry the mmrA+ gene, to complement the Mmr− phenotype of a uvrA mmrA strain. Plasmid pLC44-7 is known to complement the rep-38 mutation, suggesting that rep-38 is a recessive mutation. Although certain of the phenotypes of the rep and mmrA mutants are similar, a number are quite different. These differences suggest that these two mutations are not allelic.