Malan T P, McClure W R
Cell. 1984 Nov;39(1):173-80. doi: 10.1016/0092-8674(84)90203-4.
The control of transcription initiation at the lactose operon promoter was investigated in vitro. We found that an upstream promoter (termed lac P2) interfered with RNA polymerase binding at the principal promoter (termed lac P1). The start site for lac P2 was located at base pair position -22 relative to the P1 start site. The addition of cAMP receptor protein and cAMP was shown to repress lac P2 and to activate lac P1. Abortive initiation reactions for both promoters were used to investigate the coordinate repression-activation elicited by CRP-cAMP. The effects of lac promoter mutations (L8, Ps, and UV5) were consistent with an important RNA polymerase positioning role for CRP-cAMP in the activation of lac operon expression.
我们在体外研究了乳糖操纵子启动子处转录起始的控制。我们发现一个上游启动子(称为lac P2)干扰了RNA聚合酶在主要启动子(称为lac P1)处的结合。lac P2的起始位点相对于P1起始位点位于碱基对位置-22处。已证明添加cAMP受体蛋白和cAMP可抑制lac P2并激活lac P1。利用两个启动子的流产起始反应来研究由CRP-cAMP引发的协同抑制-激活作用。lac启动子突变(L8、Ps和UV5)的影响与CRP-cAMP在激活乳糖操纵子表达中对RNA聚合酶定位的重要作用一致。