Friden P, Tsui P, Okamoto K, Freundlich M
Nucleic Acids Res. 1984 Nov 12;12(21):8145-60. doi: 10.1093/nar/12.21.8145.
DNase and restriction site protection studies show that cAMP and its receptor protein (CRP) bind to the promoter of the ilvB operon at approximately position -44 to -82. This region contains sequences that are homologous to those found in other CRP-dependent promoters. In vitro transcription from the ilvB promoter was markedly increased by the addition of cAMP and CRP. This stimulation was not found when the ilvB template lacked the proposed CRP binding site. cAMP-CRP did not alter the extent of transcription termination within the ilvB leader suggesting that this regulatory system may be independent of the attenuation mechanism involved in the negative control of this operon. The results of restriction enzyme site protection studies and experiments with altered promoter fragments indicate that the mechanism for CRP stimulation of the ilvB operon may be similar to a model recently proposed for lac.
脱氧核糖核酸酶(DNase)和限制酶切位点保护研究表明,环磷酸腺苷(cAMP)及其受体蛋白(CRP)在ilvB操纵子启动子上大约-44至-82位处结合。该区域包含与其他CRP依赖性启动子中发现的序列同源的序列。通过添加cAMP和CRP,ilvB启动子的体外转录显著增加。当ilvB模板缺乏假定的CRP结合位点时,未发现这种刺激作用。cAMP-CRP并未改变ilvB前导区内转录终止的程度,这表明该调节系统可能独立于参与该操纵子负调控的衰减机制。限制酶切位点保护研究结果以及对改变的启动子片段进行的实验表明,CRP刺激ilvB操纵子的机制可能类似于最近提出的lac操纵子模型。