Rockwell P, Gottesman M E
Institute of Cancer Research, College of Physicians and Surgeons of Columbia University, New York, NY 10032.
J Mol Biol. 1991 Nov 20;222(2):189-96. doi: 10.1016/0022-2836(91)90205-k.
The Escherichia coli rpoB636 mutant is defective in the transcription of lac and other catabolite-sensitive operons. The lac promoter variant, UV5, which is independent of cyclic AMP and the cyclic AMP receptor protein, CRP, was also defective in rpoB636 mutants. The activity of the lac UV5 promoter was restored to wild-type levels by deletion of cya (adenylate cyclase) or crp. Cyclic AMP and CRP apparently act as inhibitors of the rpoB636 RNA polymerase.
大肠杆菌rpoB636突变体在乳糖操纵子和其他对分解代谢物敏感的操纵子的转录过程中存在缺陷。乳糖启动子变体UV5独立于环腺苷酸（cAMP）和环腺苷酸受体蛋白（CRP），在rpoB636突变体中也存在缺陷。通过缺失cya（腺苷酸环化酶）或crp，乳糖UV5启动子的活性恢复到野生型水平。环腺苷酸和CRP显然作为rpoB636 RNA聚合酶的抑制剂起作用。
