Palmer B R, Marinus M G
Department of Pharmacology, University of Massachusetts Medical School, Worcester 01655.
Mutat Res. 1991 Sep;264(1):15-23. doi: 10.1016/0165-7992(91)90040-b.
We have shown previously that dam mutants of Escherichia coli have a weak mutator phenotype which generates mostly transition mutations in the P22 mnt gene. In contrast, in mutD5 cells, which have a strong mutator phenotype, transversion mutations were the most prevalent. A dam-16 mutD5 strain, defective in both DNA polymerase III associated-proofreading and Dam-directed mismatch repair exhibits a strong mutator phenotype but, surprisingly, its mutation spectrum is similar to that of the dam rather than the mutD parent. The most likely explanation is that Dam-directed mismatch repair in the mutD5 strain corrects most of the potential transition mutations (therefore yielding transversions) in the newly synthesised strand. When the dam-16 allele is present together with mutD5 a reduced efficiency of repair as well as loss of strand discrimination and misdirected repair results in the appearance of transition mutations at high frequency.
我们之前已经表明，大肠杆菌的dam突变体具有较弱的诱变表型，主要在P22 mnt基因中产生转换突变。相比之下，具有强烈诱变表型的mutD5细胞中，颠换突变最为普遍。dam-16 mutD5菌株在与DNA聚合酶III相关的校对和Dam介导的错配修复方面均存在缺陷，表现出强烈的诱变表型，但令人惊讶的是，其突变谱与dam而非mutD亲本相似。最可能的解释是，mutD5菌株中Dam介导的错配修复纠正了新合成链中大多数潜在的转换突变（从而产生颠换）。当dam-16等位基因与mutD5同时存在时，修复效率降低以及链识别丧失和修复错误导致转换突变高频出现。
