Shuster C W, Rundell K
J Bacteriol. 1969 Oct;100(1):103-9. doi: 10.1128/jb.100.1.103-109.1969.
A class of galactose-resistant mutants has been derived from strains of Salmonella typhimurium which are defective in uridine diphosphoglucose-4-epimerase. Resistant strains are phenotypically similar to parent organisms but do not lyse in the presence of galactose. Low levels of functional epimerase can be detected in induced cells grown at 20 C but not at 37 C, and acid is not produced from galactose. Sufficient galactose is synthesized at reduced temperatures to fabricate smooth lipopolysaccharide and acceptor sites for phage P22 from galactose-deficient media. The leaky nature of these mutants may account for resistance to galactose death by maintaining galactose metabolites at a subcritical level. Glucose protects sensitive strains by control of levels of toxic metabolites by catabolite repression.
一类半乳糖抗性突变体源自鼠伤寒沙门氏菌菌株，这些菌株在尿苷二磷酸葡萄糖-4-表异构酶方面存在缺陷。抗性菌株在表型上与亲本生物体相似，但在半乳糖存在的情况下不会裂解。在20℃生长的诱导细胞中可检测到低水平的功能性表异构酶，但在37℃时则检测不到，并且半乳糖不会产生酸。在降低的温度下合成了足够的半乳糖，以从缺乏半乳糖的培养基中制造光滑的脂多糖和噬菌体P22的受体位点。这些突变体的渗漏特性可能通过将半乳糖代谢物维持在亚临界水平来解释对半乳糖致死的抗性。葡萄糖通过分解代谢阻遏控制有毒代谢物的水平来保护敏感菌株。
