Kirchner C E, Rudden M J
J Bacteriol. 1966 Nov;92(5):1453-6. doi: 10.1128/jb.92.5.1453-1456.1966.
Kirchner, Carl E. J. (Suffolk County Community College, Selden, N.Y.), and Matthew J. Rudden. Location of a mutator gene in Salmonella typhimurium by cotransduction. J. Bacteriol. 92:1453-1456. 1966.-The LT7 strain of Salmonella typhimurium has been shown to possess a mutator gene which is responsible for an increase in mutation frequency for most loci tested. Preliminary results suggested the gene might be responsible for the production of an abnormal purine or pyrimidine base. Phage prepared on the mutator strain were used to transduce selected purine and pyrimidine LT2 mutants that do not possess this gene. A high frequency (60%) of cotransduction was observed with mutants from only one locus, purA. Transduction of additional mutants from this region gave similar results, except for one mutant (purA1) which showed no transduction of the mutator gene or the purA1 region. The results show that the mutator gene is very closely linked to the purA locus and suggest that it might be part of it.
基尔希纳，卡尔·E.J.（纽约州塞尔登萨福克县社区学院），以及马修·J.鲁登。通过共转导确定鼠伤寒沙门氏菌中一个诱变基因的位置。《细菌学杂志》92:1453 - 1456。1966年。——已证明鼠伤寒沙门氏菌的LT7菌株拥有一个诱变基因，该基因导致大多数测试位点的突变频率增加。初步结果表明该基因可能负责产生异常的嘌呤或嘧啶碱基。用诱变菌株制备的噬菌体用于转导选定的不具有该基因的嘌呤和嘧啶LT2突变体。仅在一个位点purA的突变体中观察到高频率（60%）的共转导。来自该区域的其他突变体的转导产生了类似结果，但有一个突变体（purA1）未显示诱变基因或purA1区域的转导。结果表明诱变基因与purA位点紧密连锁，并表明它可能是其一部分。
