Bächi B, Kornberg H L
J Gen Microbiol. 1975 Oct;90(2):321-35. doi: 10.1099/00221287-90-2-321.
The isolation and properties of a mutant of Escherichia coli K12 that is totally unable to take up and utilize gluconate are described. Genetical analysis shows this phenotype to be associated with two lesions. One phenotype, designated GntM-, is the result of a mutation in a gene co-transducible with malA; the other, designated GNTS-, is the result of a mutation in a gene (GntS) co-transducible with fdp. The GntS--phenotype differs little from that of wild-type cells, but GntM- GntS+ organisms grow on gluconate only after a prolonged lag and form a gluconate uptake system that is strongly repressed by pyruvate. Moreover, such GntM- mutants readily give rise to further mutants that form a gluconate uptake system, gluconate kinase and 6-phosphogluconate dehydratase consititutively; in partial diploids, this constitutivity is recessive to the inducible character. It is postulated that the GntM- phenotype is due to malfunction of a negative control gene gntR, and that gntS+ specifies the activity of a gluconate uptake system.
本文描述了一株完全无法摄取和利用葡萄糖酸盐的大肠杆菌K12突变体的分离及特性。遗传学分析表明，该表型与两个损伤有关。一种表型称为GntM-，是由一个与malA共转导的基因突变所致；另一种称为GNTS-，是由一个与fdp共转导的基因（GntS）突变所致。GNTS-表型与野生型细胞的表型差异不大，但GntM- GntS+生物体仅在长时间延迟后才能在葡萄糖酸盐上生长，并形成一个被丙酮酸强烈抑制的葡萄糖酸盐摄取系统。此外，这种GntM-突变体很容易产生进一步的突变体，这些突变体组成型地形成葡萄糖酸盐摄取系统、葡萄糖酸盐激酶和6-磷酸葡萄糖酸脱水酶；在部分二倍体中，这种组成型对诱导型是隐性的。据推测，GntM-表型是由于负调控基因gntR功能失调所致，而gntS+则决定了葡萄糖酸盐摄取系统的活性。
