Busby S, Spassky A, Chan B
Gene. 1987;53(2-3):145-52. doi: 10.1016/0378-1119(87)90002-3.
C to T:A transversion at bp position -19 in the gal operon promoter region relieves the dependence of galP1 promoter activity on the cAMP-CRP complex. Deletion analysis shows that expression from the promoter is decreased on replacement of the sequence between 49 and 54 bp upstream from the P1 start point. Moreover, protection experiments show that RNA polymerase interacts with this region in open complexes at P1. We propose that this contact is necessary for optimal P1 activity; point mutations in the gal promoter region can alter DNA flexibility and hence the strength of this contact; CRP factor activates P1 transcription by favouring formation of this contact; and the gal repressor blocks P1 activity by binding to this zone.
在半乳糖操纵子启动子区域第 -19 碱基对位置发生的 G:C 到 T:A 的颠换消除了半乳糖 P1 启动子活性对 cAMP - CRP 复合物的依赖性。缺失分析表明,在替换 P1 起始点上游 49 至 54 碱基对之间的序列时,启动子的表达会降低。此外,保护实验表明,RNA 聚合酶在 P1 的开放复合物中与该区域相互作用。我们提出,这种接触对于 P1 的最佳活性是必要的;半乳糖启动子区域的点突变可以改变 DNA 的柔韧性,从而改变这种接触的强度;CRP 因子通过促进这种接触的形成来激活 P1 转录;而半乳糖阻遏物通过结合到该区域来阻断 P1 活性。