Hagen D C, Gerson S L, Magasanik B
J Bacteriol. 1975 Feb;121(2):583-93. doi: 10.1128/jb.121.2.583-593.1975.
Two super-repressor mutations in the histidine utilization (hut) operons of Salmonella typhimurium are described. Cells bearing either of these mutations have levels of hut enzymes that do not increase above the uninduced levels when growth is in the presence of either histidine or the gratuitous inducer imidazole propionate. Both mutations lie in the region of the gene for the hut repressor, hutC, and reverse mutations of both are to the constitutive (repressor-negative) rather than to the inducible (wild type) phenotype. In hybrid merodiploid strains the super-repressor mutations are dominant over either wild-type (hutC+) or repressor-negative (hutC-) alleles. Whereas both super-repressor mutations cause the uninducible synthesis of hut enzymes, the degree of repression is different. One mutation causes repression of enzyme synthesis in one of the two hut operons to a level below the basal, uninduced level of wild-type cells. The other mutation causes repression to a lesser degree than in wild-type cells, so that the hut enzymes are present at a level above the normal basal level; this partially constitutive synthesis is greater for the enzymes of one of the hut operons than for the enzymes of the other. Thus, both mutations apparently result in repressors with altered operator-binding properties, in addition to altered inducer-binding properties.
本文描述了鼠伤寒沙门氏菌组氨酸利用（hut）操纵子中的两种超级阻遏物突变。携带这两种突变之一的细胞，在组氨酸或 gratuitous 诱导物咪唑丙酸存在下生长时，其 hut 酶水平不会高于未诱导水平。这两种突变均位于 hut 阻遏物基因 hutC 的区域，并且两者的回复突变均导致组成型（阻遏物阴性）而非诱导型（野生型）表型。在杂交部分二倍体菌株中，超级阻遏物突变相对于野生型（hutC +）或阻遏物阴性（hutC -）等位基因均占主导。虽然两种超级阻遏物突变都导致 hut 酶的不可诱导合成，但阻遏程度不同。一种突变导致两个 hut 操纵子之一中的酶合成被阻遏到低于野生型细胞基础未诱导水平的程度。另一种突变导致的阻遏程度低于野生型细胞，因此 hut 酶的水平高于正常基础水平；这种部分组成型合成对于其中一个 hut 操纵子的酶比另一个 hut 操纵子的酶更大。因此，除了诱导物结合特性改变外，这两种突变显然还导致阻遏物的操纵子结合特性发生改变。
