Csonka L N, Clark A J
Genetics. 1979 Oct;93(2):321-43. doi: 10.1093/genetics/93.2.321.
A negative regulatory gene for the srl operon (srlR) was recognized by the characteristics of an insertion mutation generated by the transposon Tn10 determining tetracycline resistance. This finding is discussed in light of previous hypotheses on the regulation of the srl genes, which mediate metabolism of glucitol (i.e., sorbitol). Mapping showed that the order of genes in this region is: srlR srlD srlC recA alaS. Using two different methods, five mutations of both srl and recA were detected. The phenotype conferred by these mutations, UV sensitivity and extreme recombination deficiency, is characteristic of standard recA point mutants. Three of the mutations were deletions that also removed the genes for tetracycline resistance of the nearby transposon. A fourth mutation ended at a distance from Tn10 sufficient to allow separation of the two by recombination following P1 transduction; our tests did not allow us to conclude whether this mutation was an inversion or a deletion. The fifth mutation was a deletion that seemed to end immediately adjacent to the boundary of Tn10, proximal to recA. Mechanisms for the generation of these srl recA mutations are discussed.
通过转座子Tn10产生的决定四环素抗性的插入突变特征,识别出了srl操纵子的一个负调控基因(srlR)。根据先前关于介导葡糖醇(即山梨醇)代谢的srl基因调控的假说,对这一发现进行了讨论。图谱分析表明,该区域基因顺序为:srlR、srlD、srlC、recA、alaS。使用两种不同方法,检测到了srl和recA的五个突变。这些突变赋予的表型,即紫外线敏感性和极端重组缺陷,是标准recA点突变体的特征。其中三个突变是缺失突变,它们还去除了附近转座子的四环素抗性基因。第四个突变在距Tn10一定距离处终止,足以通过P1转导后的重组将两者分开;我们的测试无法让我们得出该突变是倒位还是缺失的结论。第五个突变是一个缺失突变,似乎紧邻Tn10边界recA近端处终止。讨论了这些srl recA突变产生的机制。