Malik S, Zalenskaya K, Goldfarb A
Department of Microbiology, Columbia University College of Physicians and Surgeons, New York, NY 10032.
Nucleic Acids Res. 1987 Oct 26;15(20):8521-30. doi: 10.1093/nar/15.20.8521.
The switch of RNA polymerase specificity from early to late promoters of bacteriophage T4 is achieved by substitution of host sigma factor, sigma 70, with the T4 induced factor, sigma gp55. However, overproduction of sigma gp55 from an expression vector is not detrimental to Escherichia coli growth. Direct competition binding assays demonstrate that sigma 70 readily displaces sigma gp55 from RNA polymerase and thereby reverses the promoter specificity of the enzyme. The displacement also occurs with the core enzyme modified by bacteriophage T4 infection. We postulate that an antagonist of sigma 70 should be formed in T4-infected cells to aid sigma gp55 in the early/late switch.
噬菌体T4早期启动子到晚期启动子的RNA聚合酶特异性转换是通过用T4诱导因子σgp55替代宿主σ因子σ70来实现的。然而,从表达载体过量产生σgp55对大肠杆菌的生长并无损害。直接竞争结合试验表明,σ70能轻易地将σgp55从RNA聚合酶上置换下来,从而逆转该酶的启动子特异性。这种置换在被噬菌体T4感染修饰的核心酶中也会发生。我们推测,在T4感染的细胞中应该形成一种σ70的拮抗剂,以帮助σgp55进行早期/晚期转换。