Choy H E, Hanger R R, Aki T, Mahoney M, Murakami K, Ishihama A, Adhya S
Department of Molecular Biology, Odense University, Denmark.
J Mol Biol. 1997 Sep 26;272(3):293-300. doi: 10.1006/jmbi.1997.1221.
By binding to the DNA site OE at position -60.5 in the gal operon, the GalR protein activates transcription from the P2 promoter located on the opposite face of DNA (position -5) and represses transcription from the P1 promoter located on the same face (position +1). GalR increases RNA polymerase binding at P2 and inhibits isomerization at P1 by forming a GalR-DNA-RNA polymerase ternary complex in each case. The specific effect of GalR at one promoter is independent of the presence of the other promoter. The enhancement or repression is also not the intrinsic property of a promoter; the regulation can be reversed by switching the angular orientation of the promoters relative to OE. Both enhancement and repression appear to require the same interaction between RNA polymerase alpha-subunit and GalR and/or the same interaction between RNA polymerase alpha-subunit and DNA in the ternary complexes. We have discussed how GalR might exert opposite effects in the steps involved in the formation of the open complex from free RNA polymerase and DNA.
通过与半乳糖操纵子中位置为-60.5的DNA位点OE结合，GalR蛋白激活位于DNA相对面（位置-5）的P2启动子的转录，并抑制位于同一面（位置+1）的P1启动子的转录。GalR通过在每种情况下形成GalR-DNA-RNA聚合酶三元复合物来增加RNA聚合酶在P2处的结合，并抑制P1处的异构化。GalR在一个启动子上的特定作用与另一个启动子的存在无关。增强或抑制也不是启动子的固有特性；通过改变启动子相对于OE的角度方向，调控作用可以逆转。增强和抑制似乎都需要RNA聚合酶α亚基与GalR之间相同的相互作用和/或三元复合物中RNA聚合酶α亚基与DNA之间相同的相互作用。我们已经讨论了GalR如何在从游离RNA聚合酶和DNA形成开放复合物的过程中发挥相反的作用。
