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紫外线照射大肠杆菌后的暗修复过程。3. rec突变对大肠杆菌K-12切除缺陷型突变体恢复的影响。

Dark-recovery processes in Escherichia coli irradiated with ultraviolet light. 3. Effect of rec mutations on recovery of excision-deficient mutants of Escherichia coli K-12.

作者信息

Ganesan A K, Smith K C

出版信息

J Bacteriol. 1970 May;102(2):404-10. doi: 10.1128/jb.102.2.404-410.1970.

Abstract

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 (rec(-)uvr(+)) 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 rec(-)uvr(+) 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.

摘要

由于uvr突变而无法从其脱氧核糖核酸(DNA)中切除嘧啶二聚体的大肠杆菌K - 12突变体,在暴露于紫外线辐射后,接种在基本盐培养基上时比接种在含有酵母提取物的复杂培养基(如营养琼脂)上时具有更高的存活率。这种反应被称为基本培养基恢复(MMR)。uvr突变体的恢复可以在液体培养基以及固体培养基中发生,但在缓冲液中或在不允许细胞生长和正常DNA复制的氨基酸饥饿条件下则不会发生。因此,MMR可以与K - 12的重组缺陷型(rec(-)uvr(+))衍生物的恢复区分开来,后者可以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,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基因也控制K - 12中的重组。携带uvr突变以及recA13、recA56、recB21或recC22的细胞未能表现出MMR,并且比它们的rec(+)uvr(-)或rec(-)uvr(+)亲本对紫外线辐射更敏感。通过转导或回复从recA uvr(-)菌株获得的rec(+)uvr(-)衍生物恢复了MMR能力。我们的结果表明,recA、recB或recC这三个基因中的任何一个失活都会阻止细胞表现出MMR。

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