缺乏甲基化指导的DNA错配修复的大肠杆菌突变体
Escherichia coli mutator mutants deficient in methylation-instructed DNA mismatch correction.
作者信息
Glickman B W, Radman M
出版信息
Proc Natl Acad Sci U S A. 1980 Feb;77(2):1063-7. doi: 10.1073/pnas.77.2.1063.
Abstract
Our approach to the isolation of DNA mismatch-correction-deficient mutants was based upon the isolation of 2-aminopurine-resistant second-site revertants of Escherichia coli dam- mutants. We isolated such second-site revertants which, when separated from the dam- mutation, have a mutator character of their own. These new mutators all mapped at three known mutator loci, mutH, mutL, and mutS, which exhibit the same mutagenic spectrum as the dam- mutator: increased levels of base substitution and frameshift mutations. The mutator potencies of double and triple mut- mutants suggest that these mutators are involved in the same general mismatch-repair pathway. All these mutations result in a hyper-recombination phenotype, but in four-factor crosses among lambda phages, a specific loss of intragenic recombination (Pam3 X Pam80) was found in mutL and mutS mutants, as would be predicted from the postulated role of mismatch correction in gene conversion and high negative interference phenomena.
摘要
我们分离DNA错配修复缺陷突变体的方法基于对大肠杆菌dam-突变体的2-氨基嘌呤抗性第二位点回复突变体的分离。我们分离出了这样的第二位点回复突变体，当它们与dam-突变分离时，具有自身的诱变特性。所有这些新的诱变剂都定位于三个已知的诱变剂位点，即mutH、mutL和mutS，它们表现出与dam-诱变剂相同的诱变谱：碱基替代和移码突变水平增加。双突变和三突变mut-突变体的诱变能力表明，这些诱变剂参与了相同的一般错配修复途径。所有这些突变都导致了高重组表型，但在λ噬菌体之间的四因子杂交中，在mutL和mutS突变体中发现了基因内重组（Pam3×Pam80）的特异性丧失，这与错配修复在基因转换和高负干扰现象中的假定作用所预测的一致。
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