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首页> 外文期刊>Journal of bacteriology >Ultraviolet light protection, enhancement of ultraviolet light mutagenesis, and mutator effect of plasmid R46 in Salmonella typhimurium.
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Ultraviolet light protection, enhancement of ultraviolet light mutagenesis, and mutator effect of plasmid R46 in Salmonella typhimurium.

机译：紫外线防护，紫外线诱变的增强以及鼠伤寒沙门氏菌中质粒R46的诱变作用。

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摘要

Plasmid R46 partially protected Salmonella typhimurium, wild type or uvrB or polA, against the lethal effect of ultraviolet (UV) irradiation, but did not protect recA mutants. The plasmid also increased frequency of UV-induced reversion to His+ in all tested his point mutants (wild type for UV sensitivity), including amber, ochre, UGA, missense, and frame-shift mutants. Plasmid R46 also increased UV-induced reversion to His+ in uvrB and polA strains, but no UV mutagenic effect was detected in R- or R46-carrying recA derivatives of a his (amber) mutant. The spontaneous reversion frequency of his nonsense mutants of all classes, and of some his missense mutants, was increased about 10-fold when the strains carried R46, but the plasmid had no effect on the spontaneous reversion frequency of some other his missense mutations or of reversion rate of his frame-shift mutants (except for two uvrB derivatives of one single-base insertion mutant). The plasmid increased the ability of wild-type, polA, and uvrB hosts to support plaque production by UV-irradiated phage, and made strain LT2 hisG46 less sensitive to methyl methane sulfonate and to X rays and more responsive to the mutagenic effect of visible-light irradiation. R46 increased spontaneous reversion frequency of a his (amber) rec+ strain, but had no such effect in its recA sublines. Since the plasmid in the absence of host recA function fails to produce its mutator effect, or to confer UV protection or to enhance UV mutagenesis, these three effects may be produced via some mechanism involved in recA-dependent deoxyribonucleic acid repair, perhaps by an increase in activity of the "error prone" component of the inducible repair pathway.
机译：质粒R46部分保护鼠伤寒沙门氏菌，野生型或uvrB或polA，使其免受紫外线（UV）的致死作用，但不保护recA突变体。该质粒还在所有测试的他的点突变体（对紫外线敏感的野生型）中，包括琥珀色，色，UGA，错义和移码突变体，也增加了紫外线诱导的向His +还原的频率。质粒R46还增加了uvrB和polA菌株中UV诱导的向His +的回复，但在带有His（琥珀色）突变体的R-或R46的recA衍生物中未检测到UV诱变作用。当携带R46的菌株时，他所有类型的无义突变体和某些他的错义突变体的自发回复频率增加了约10倍，但该质粒对他的其他一些错义突变或自发突变的自发回复频率没有影响。移码突变体的回复率（一个单碱基插入突变体的两个uvrB衍生物除外）。该质粒提高了野生型，polA和uvrB宿主支持通过紫外线辐射的噬菌体产生噬菌斑的能力，并使LT2 hissG46菌株对甲烷磺酸甲酯和X射线的敏感性降低，并对可见-可见诱变作用的反应更强光照射。 R46增加了his（琥珀色）rec +菌株的自发逆转频率，但在recA子系中没有这种作用。由于没有宿主recA功能的质粒无法产生其突变效应，或无法提供紫外线保护或增强紫外线诱变作用，因此这三种作用可能是通过参与recA依赖性脱氧核糖核酸修复的某些机制产生的，可能是通过增加诱导修复途径中“易错”成分的活性。

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