Grossman A D, Ullmann A, Burgess R R, Gross C A
J Bacteriol. 1984 Apr;158(1):110-4. doi: 10.1128/jb.158.1.110-114.1984.
An immediate 12-fold inhibition in the rate of beta-galactosidase synthesis occurs in Escherichia coli cells containing the mutant sigma allele rpoD800 after a shift to 42 degrees C. In the present study we characterize the nature of the inhibition. The severe inhibition of beta-galactosidase synthesis was partly relieved by cyclic AMP (cAMP). We inferred that the inhibition might be mediated by a decreased intracellular concentration of cAMP. Consistent with this inference, the rate of cAMP accumulation in mutant cells after a temperature upshift was depressed relative to that in wild-type cells. Glucose and chloramphenicol, two agents known to inhibit differentially beta-galactosidase mRNA synthesis, caused a similar inhibition in the rate of cAMP accumulation. Thus, three diverse stimuli, glucose, chloramphenicol, and a temperature-sensitive sigma mutation, appear to affect beta-galactosidase synthesis by regulating the synthesis of cAMP.
在含有突变型σ等位基因rpoD800的大肠杆菌细胞中,温度转移至42℃后,β-半乳糖苷酶合成速率立即出现12倍的抑制。在本研究中,我们对这种抑制的本质进行了表征。环磷酸腺苷(cAMP)可部分缓解β-半乳糖苷酶合成的严重抑制。我们推断,这种抑制可能是由细胞内cAMP浓度降低介导的。与这一推断一致,温度升高后突变细胞中cAMP的积累速率相对于野生型细胞有所降低。葡萄糖和氯霉素这两种已知可差异抑制β-半乳糖苷酶mRNA合成的物质,对cAMP的积累速率产生了类似的抑制作用。因此,三种不同的刺激因素,即葡萄糖、氯霉素和温度敏感型σ突变,似乎通过调节cAMP的合成来影响β-半乳糖苷酶的合成。