Veyrat A, Monedero V, Pérez-Martínez G
Instituto de Agroquímica y Tecnología de Alimentos (CSIC), Valencia, Spain.
Microbiology (Reading). 1994 May;140 ( Pt 5):1141-9. doi: 10.1099/13500872-140-5-1141.
A 2-deoxy-D-glucose-resistant mutant of a pLZ15-cured derivative of Lactobacillus casei ATCC 393 was isolated on agar medium containing 10 mM 2-deoxy-D-glucose and 5 g lactose I-1. The mutant was impaired in the main glucose transport mechanism, a PTSman-type system. Additionally a proton-motive-force-dependent glucose permease was detected. The growth response and the sugar consumption rates of the wild-type and the PTSman-deficient mutant suggested that the mutated element of the complex IIABCman was, in the wild-type, responsible for a strong repression by glucose and mannose of the lactose and ribose assimilation genes, while assimilation of galactose was only weakly repressed. It is postulated that they are regulated by a different mechanism of catabolite repression.
在含有10 mM 2-脱氧-D-葡萄糖和5 g乳糖I-1的琼脂培养基上，分离出了干酪乳杆菌ATCC 393的pLZ15治愈衍生物的2-脱氧-D-葡萄糖抗性突变体。该突变体的主要葡萄糖转运机制（一种PTSman型系统）受损。此外，还检测到一种质子动力势依赖性葡萄糖通透酶。野生型和PTSman缺陷型突变体的生长反应和糖消耗率表明，在野生型中，复合物IIABCman的突变元件负责葡萄糖和甘露糖对乳糖和核糖同化基因的强烈抑制，而半乳糖的同化仅受到微弱抑制。据推测，它们受不同的分解代谢物阻遏机制调控。
