ISOLATION, CHARACTERIZATION, AND GENETIC ANALYSIS OF MUTATOR GENES IN ESCHERICHIA-COLI B AND K-12
ISOLATION, CHARACTERIZATION, AND GENETIC ANALYSIS OF MUTATOR GENES IN ESCHERICHIA-COLI B AND K-12
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DOI：
10.1128/jb.104.1.363-375.1970
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发表时间：
1970-01-01
影响因子：
3.2
通讯作者：
BRYSON, V
中科院分区：
文献类型：
--
作者：
LIBERFARB, RM;BRYSON, V
大肠杆菌B（B/UV）和K-12（JC 355）经诱变处理后，获得21株Mut突变株。这些Mut菌株的特征在于突变为链霉素抗性和T期抗性的比率显著高于亲本（Mut+）比率。12个菌株的突变基因已定位在E. colichromosome：1个靠近leu位点，5个靠近purA位点，6个靠近cysC位点。此外，还从弗罗姆中分离到8株突变株。coliB/UV仍然未映射。人们做了一些努力来推断增变基因的作用方式。已检查这些分离株的脱氧核糖核酸修复机制（紫外线损伤的暗修复、宿主细胞再活化、重组能力、丝裂霉素C损伤的修复）中可能存在的缺陷。通过使用转导分析，发现NTG 119的紫外敏感性和其增变因子性质是由两个独立但紧密连锁的突变引起的。接受NTG 119或NTG 35突变的PurA+转导子对丝裂霉素C的敏感性均高于PurA受体。除非转导选择敏感性，一个可能的解释是，丝裂霉素C诱导的损伤的修复缺陷与这些转导子和供体中突变的作用方式有关。嘌呤合成异常可能与某些菌株的突变性有关，突变子正确和purA共转导（NTG 119 100%共转导）。三个突变体是重组缺陷型的，并且在重组修复中可能具有缺陷步骤。一个定位在cysC附近的三个基因附近。
Twenty-one Mut mutants were obtained fromEscherichia coliB (B/UV) and K-12 (JC355) after treatment with mutagens. These Mut strains are characterized by rates of mutation to streptomycin resistance and T-phase resistance which are significantly higher than the parental (Mut+) rates. Mutator genes in 12 strains have been mapped at three locations on theE. colichromosome: one close to theleulocus; five close to thepurAlocus; and six close tocysC. In addition, eight mutator strains derived fromE. coliB/UV are still unmapped. Some effort was made to deduce the mode of action of the mutator genes. These isolates have been examined for possible defects in deoxyribonucleic acid repair mechanisms (dark repair of ultraviolet damage, host-cell reactivation, recombination ability, repair of mitomycin C damage). By using transductional analysis, it was found that the ultraviolet sensitivity of NTG119 and its mutator property results from two separate but closely linked mutations. PurA+transductants that receivemutfrom NTG119 or NTG35 are all more sensitive to mitomycin C than is the PurA recipient. Unless transduction selects for sensitivity, a probable interpretation is that defective repair of mitomycin C-induced damage is related to the mode of action ofmutin these transductants and the donor. Abnormal purine synthesis may be involved in the mutability of some strains with cotransduction of the mutator properly andpurA(100% cotransduction for NTG119). Three mutators are recombination-deficient and may have a defective step in recombination repair. One maps near threerecgenes close tocysC.