首页> 美国卫生研究院文献>Journal of Bacteriology >Dark-Recovery Processes in Escherichia coli Irradiated with Ultraviolet Light III. Effect of rec Mutations on Recovery of Excision-Deficient Mutants of Escherichia coli K-12
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Dark-Recovery Processes in Escherichia coli Irradiated with Ultraviolet Light III. Effect of rec Mutations on Recovery of Excision-Deficient Mutants of Escherichia coli K-12

机译:用紫外线III照射的大肠杆菌中的黑暗恢复过程。 rec突变对大肠杆菌K-12缺乏表达突变株的恢复的影响

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摘要

Mutants of Escherichia coli K-12 unable to excise pyrimidine dimers from their deoxyribonucleic acid (DNA) because of a uvr mutation show a higher survival when plated on a minimal salts medium after exposure to ultraviolet radiation than when plated on a complex medium such as nutrient agar containing yeast extract. This response has been called minimal medium recovery (MMR). Recovery of uvr mutants can take place in liquid as well as on solid medium, but not in buffer or under conditions of amino acid starvation that do not permit cell growth and normal DNA replication. MMR can thus be distinguished from the recovery of recombination-deficient (recuvr+) derivatives of K-12 which can occur under conditions where growth is not possible. Because MMR is characteristic of excision-defective mutants, it evidently reflects a type of repair independent of excision. We have obtained genetic evidence that MMR is determined by the rec genes, which also control recombination in K-12. Cells carrying a uvr mutation together with recA13, recA56, recB21, or recC22 failed to show MMR and were more sensitive to ultraviolet radiation than either their rec+uvr or recuvr+ parents. The rec+uvr derivatives obtained from recA uvr strains by transduction or by reversion regained the capacity for MMR. Our results indicate that inactivation of any one of the three genes, recA, recB, or recC, prevents cells from showing MMR.
机译:大肠杆菌K-12突变体由于uvr突变而无法从其脱氧核糖核酸(DNA)中切除嘧啶二聚体,因此在紫外线照射后接种于最小盐分培养基上比在营养物质等复杂培养基上接种时,其存活率更高。含有酵母提取物的琼脂。此响应称为最小介质恢复(MMR)。 uvr突变体的回收既可以在液体中也可以在固体培养基中进行,但不能在缓冲液中或不允许细胞生长和正常DNA复制的氨基酸饥饿条件下进行。因此,可以将MMR与K-12的重组缺陷(rec - uvr + )衍生物的回收区别开来,后者可能在无法生长的条件下发生。因为MMR是切除缺陷型突变体的特征,所以它显然反映了一种独立于切除的修复类型。我们已经获得了遗传证据,表明MMR是由rec基因决定的,rec基因还控制着K-12的重组。带有uvr突变以及recA13,recA56,recB21或recC22的细胞均无法显示MMR,并且比rec + uvr -或rec < sup>- uvr + 父母。通过转导或逆转从recA uvr -菌株获得的rec + uvr -衍生物重新获得了MMR的能力。我们的结果表明, recA,recB recC 这三个基因中的任何一个失活都会阻止细胞显示MMR。

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