Choy H E, Park S W, Aki T, Parrack P, Fujita N, Ishihama A, Adhya S
Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-4255, USA.
EMBO J. 1995 Sep 15;14(18):4523-9. doi: 10.1002/j.1460-2075.1995.tb00131.x.
Gal or Lac repressor binding to an upstream DNA segment, in the absence of DNA looping, represses the P1 promoter located on the same face and activates the P2 promoter situated on the opposite face of the DNA helix in the gal operon. Both inhibition and stimulation of transcription requires the physical presence of the C-terminal domain of the alpha subunit of RNA polymerase although the latter is not required for transcription itself. We propose that Gal and Lac repressors inhibit or stimulate transcription initiation by disabling or stimulating RNA polymerase activity at a post-binding step by directly or indirectly altering the C-terminal alpha domain to an unfavorable state at P1 or a more favorable state at P2, respectively.
在缺乏DNA环化的情况下，半乳糖或乳糖阻遏物与上游DNA片段结合，会抑制位于同一条链上的P1启动子，并激活位于半乳糖操纵子中DNA螺旋相反链上的P2启动子。转录的抑制和刺激都需要RNA聚合酶α亚基C末端结构域的实际存在，尽管转录本身并不需要它。我们提出，半乳糖和乳糖阻遏物通过在结合后步骤中直接或间接将C末端α结构域分别改变为P1处的不利状态或P2处的更有利状态，从而使RNA聚合酶活性失活或激活，进而抑制或刺激转录起始。
