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鼠伤寒沙门氏菌LT2中的诱变需要一条可诱导途径。

An inducible pathway is required for mutagenesis in Salmonella typhimurium LT2.

作者信息

Orrego C, Eisenstadt E

出版信息

J Bacteriol. 1987 Jun;169(6):2885-8. doi: 10.1128/jb.169.6.2885-2888.1987.

DOI:10.1128/jb.169.6.2885-2888.1987
PMID:3294811
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC212206/
Abstract

UV mutability of Salmonella typhimurium LT2 was eliminated in the presence of a multicopy plasmid carrying the Escherichia coli lexA+ gene. This result suggests that inducible, SOS-like functions are required for UV mutagenesis in S. typhimurium. S. typhimurium strains carrying either point or deletion mutations in topA had previously been shown to lose their mutability by UV or methyl methanesulfonate (K. Overbye and P. Margolin, J. Bacteriol. 146:170-178, 1981; K. Overbye, S. M. Basu, and P. Margolin, Cold Spring Harbor Symp. Quant. Biol. 47:785-791, 1983). Mitomycin C induction of the phi(mucB'-lacZ') fusion (a DNA damage-inducible locus carried on plasmid pSE205) in S. typhimurium topA was normal, suggesting that RecA is activated in topA mutants. These observations lead us to deduce that S. typhimurium has at least one DNA damage-inducible locus in addition to recA that is required for UV mutability.

摘要

在携带大肠杆菌lexA⁺基因的多拷贝质粒存在的情况下，鼠伤寒沙门氏菌LT2的紫外线可变性被消除。这一结果表明，鼠伤寒沙门氏菌的紫外线诱变需要诱导型的、类似SOS的功能。先前已表明，携带topA点突变或缺失突变的鼠伤寒沙门氏菌菌株会丧失其对紫外线或甲磺酸甲酯的可变性（K. Overbye和P. Margolin，《细菌学杂志》146:170 - 178，1981；K. Overbye，S. M. Basu和P. Margolin，《冷泉港定量生物学研讨会》47:785 - 791，1983）。在鼠伤寒沙门氏菌topA中，丝裂霉素C对phi(mucB'-lacZ')融合体（携带在质粒pSE205上的一个DNA损伤诱导位点）的诱导是正常的，这表明RecA在topA突变体中被激活。这些观察结果使我们推断，除了recA之外，鼠伤寒沙门氏菌至少还有一个DNA损伤诱导位点，它是紫外线可变性所必需的。

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