SPONTANEOUS AND UV-INDUCED MUTATIONS IN ESCHERICHIA-COLI K-12 STRAINS WITH ALTERED OR ABSENT DNA-POLYMERASE-I
SPONTANEOUS AND UV-INDUCED MUTATIONS IN ESCHERICHIA-COLI K-12 STRAINS WITH ALTERED OR ABSENT DNA-POLYMERASE-I
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DOI：
10.1128/jb.171.5.2480-2484.1989
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发表时间：
1989-05-01
影响因子：
3.2
通讯作者：
RADMAN, M
中科院分区：
文献类型：
--
作者：
BATES, H;RANDALL, SK;RADMAN, M
在紫外线照射后，在通过polA基因（Δ polA）携带缺失的细菌中发生对缬氨酸抗性和利福平抗性的突变诱导，表明DNA聚合酶I（PolI）不是该过程的必需酶。PolI缺失菌株的自发突变频率比野生型高7- 10倍。在缺失菌株中存在5“→F“附加体上的3”核酸外切酶片段导致自发突变频率额外增加10倍，导致突变频率比野生型高约50至100倍。与5 ″ →在携带umuC突变的细菌中，3“外切核酸酶基因片段连同归因于polA缺失的大部分效应被阻断。因此，增变因子活性似乎反映了组成型SOS诱导。切除熟练的polA缺失菌株表现出对UV光的致死作用的敏感性增加，这仅部分地通过F“附加体上的polA+的存在而改善。UV诱导的利福平抗性突变率在Δ polA细菌中略低于携带polA+等位基因的细菌。这种效应不太可能是由PolI依赖性诱变途径的存在引起的，可能是由切除修复模式的改变引起的间接效应，因为它没有发生在切除缺陷（uvrA）细菌中。切除缺陷型polA缺失菌株具有与在F“附加体上携带polA+的同基因菌株相似的UV敏感性，表明在不存在切除修复的情况下，PolI的功能对于复制后修复是不需要的。我们的数据没有提供证据的紫外线诱变依赖于PolI的途径，虽然它仍然是一个悬而未决的问题，是否PolI是能够参与时，它是存在的。
The induction of mutations to valine resistance and to rifampin resistance occurs after UV irradiation in bacteria carrying a deletion through the polA gene (.DELTA.polA), showing that DNA polymerase I (PolI) is not an essential enzyme for this process. The PolI deletion strain showed a 7- to 10-fold-higher spontaneous mutation frequency than the wild type. The presence in the deletion strain of the 5'' .fwdarw. 3'' exonuclease fragment on an F'' episome caused an additional 10-fold increase in spontaneous mutation frequency, resulting in mutation frequencies on the order of 50- to 100-fold greater than wild type. The mutator effect associated with the 5'' .fwdarw. 3'' exonuclease gene fragment together with much of the effect attributable to the polA deletion was blocked in bacteria carrying a umuC mutation. The mutator activity therefore appears to reflect constitutive SOS induction. Excision-proficient polA deletion strains exhibited increased sensitivity to the lethal effect of UV light which was only partially ameliorated by the presence of polA+ on an F'' episome. The UV-induced mutation rate to rifampin resistance was marginally lower in .DELTA.polA bacteria than in bacteria carrying the polA+ allele. This effect is unlikely to be caused by the existence of a PolI-dependent mutagenic pathway and is probably an indirect effect caused by an alteration in the pattern of excision repair, since it did not occur in excision-deficient (uvrA) bacteria. An excision-deficient polA deletion strain possessed UV sensitivity similar to that of an isogenic strain carrying polA+ on an F'' episome, showing that none of the functions of PolI are needed for postreplication repair in the absence of excision repair. Our data provide no evidence for a pathway of UV mutagenesis dependent on PolI, although it remains an open question whether PolI is able to participate when it is present.