Bankaitis V A, Kline E L
J Bacteriol. 1981 Aug;147(2):500-8. doi: 10.1128/jb.147.2.500-508.1981.
A spontaneous lac+ revertant of an adenylate cyclase deletion strain of Escherichia coli K-12 was isolated and characterized. This revertant, designated strain KC20, exhibited a pleiotropic suppression of the adenylate cyclase defect, with the crp locus being the site of the suppressor mutation. Cyclic adenosine 3',5'-monophosphate at an exogenous concentration of 1 mM severely inhibited the growth of strain KC20 in minimal media. Lower concentrations of the cyclic nucleotide elicited less pronounced effects. Studies on araBAD and lacZYA expression showed that cyclic adenosine 3',5'-monophosphate elicited an initial dose-dependent hyperinduction of these systems. Hyperinduction of araBAD, in L-arabinose grown cultures of strain KC20, resulted in accumulation of inhibitory concentrations of methylglyoxal. Hyperinduction of lacZYA in lactose-grown cultures of strain KC20 did not result in any such methylglyoxal production.
分离并鉴定了大肠杆菌K-12腺苷酸环化酶缺失菌株的一个自发乳糖利用阳性回复突变体。这个回复突变体命名为KC20菌株，它对腺苷酸环化酶缺陷表现出多效性抑制，其中crp基因座是抑制突变的位点。外源浓度为1 mM的3',5'-环腺苷酸严重抑制了KC20菌株在基本培养基中的生长。较低浓度的环核苷酸产生的影响不那么明显。对araBAD和lacZYA表达的研究表明，3',5'-环腺苷酸引发了这些系统的初始剂量依赖性超诱导。在KC20菌株的L-阿拉伯糖生长培养物中，araBAD的超诱导导致了抑制浓度的甲基乙二醛的积累。在KC20菌株的乳糖生长培养物中，lacZYA的超诱导没有导致任何此类甲基乙二醛的产生。
