Gemmill R M, Tripp M, Friedman S B, Calvo J M
J Bacteriol. 1984 Jun;158(3):948-53. doi: 10.1128/jb.158.3.948-953.1984.
Two mutations that affect expression of the Salmonella typhimurium leu operon were investigated. leu operon DNA from these mutant strains was cloned, and nucleotide sequences of the leu control regions were determined. leu-500, which eliminates expression of all four leu genes simultaneously, is a point mutation in the -10 region of the leu promoter. leu-2012 is a point mutation within the -35 region of the leu promoter. leu-2012 suppressed leucine auxotrophy caused by leu-500 only when the medium contained a carbon source that does not cause catabolite repression. A cya mutation (adenylate cyclase deficiency) introduced into the leu-500 leu-2012 strain caused leu enzymes to be made only if cAMP was supplied exogenously. A leu-500 leu-2012 strain containing a crp mutation (cAMP receptor protein deficiency), on the other hand, could not make leu enzymes even in the presence of cAMP. In vitro transcription experiments demonstrated that the leu-2012 mutation created a new transcription initiation site. RNA polymerase utilized this site in vitro in the absence of added cAMP receptor protein and cAMP.
对影响鼠伤寒沙门氏菌亮氨酸操纵子表达的两种突变进行了研究。从这些突变菌株中克隆了亮氨酸操纵子DNA,并测定了亮氨酸控制区的核苷酸序列。leu-500能同时消除所有四个亮氨酸基因的表达,它是亮氨酸启动子-10区的一个点突变。leu-2012是亮氨酸启动子-35区内的一个点突变。仅当培养基含有不引起分解代谢物阻遏的碳源时,leu-2012才能抑制由leu-500引起的亮氨酸营养缺陷型。导入leu-500 leu-2012菌株的cya突变(腺苷酸环化酶缺陷)导致只有在外源提供cAMP时才能产生亮氨酸酶。另一方面,含有crp突变(cAMP受体蛋白缺陷)的leu-500 leu-2012菌株即使在有cAMP的情况下也不能产生亮氨酸酶。体外转录实验表明,leu-2012突变产生了一个新的转录起始位点。在没有添加cAMP受体蛋白和cAMP的情况下,RNA聚合酶在体外利用了这个位点。