Shanabruch W G, Walker G C
Mol Gen Genet. 1980;179(2):289-97. doi: 10.1007/BF00425456.
Twenty Tn5 insertion mutants of the drug resistance plasmid pKM101 have been isolated that are unable to enhance mutagenesis with ultraviolet (UV) irradiation or methyl methanesulfonate. By restriction mapping, the Tn5 insertion in each of these pKM101 mutants was shown to be within a 1.9 kb region of the plasmid genome. We have termed this segment of the pKM101 map the muc (mutagenesis: UV and chemical) gene(s). Characterization of these mutants indicated that any Tn5 insertion within the muc gene(s) abolished the ability of pKM101 to: (a) enhance spontaneous, UV and chemical mutagenesis, (b) increase host survival following UV-irradiation, (c) increase the survival of UV-irradiated phage plated on irradiated or unirradiated cells, and (d) suppress the repair and mutagenesis deficiencies of a umuC- mutant. Possible models to explain the role of the pKM101 muc gene(s) in mutagenesis and repair are discussed.
已分离出20个耐药质粒pKM101的Tn5插入突变体，它们无法通过紫外线（UV）照射或甲磺酸甲酯增强诱变作用。通过限制性图谱分析，这些pKM101突变体中每个的Tn5插入都显示在质粒基因组的1.9 kb区域内。我们将pKM101图谱的这一片段称为muc（诱变：紫外线和化学）基因。对这些突变体的表征表明，muc基因内的任何Tn5插入都会消除pKM101的以下能力：（a）增强自发、紫外线和化学诱变作用，（b）增加紫外线照射后的宿主存活率，（c）增加在照射或未照射细胞上平板培养的紫外线照射噬菌体的存活率，以及（d）抑制umuC突变体的修复和诱变缺陷。文中讨论了解释pKM101 muc基因在诱变和修复中作用的可能模型。
