Yeats S M, Schwarz T F, Ryan T P, Garner I, Hayward R S, McConnell D J
Mol Gen Genet. 1981;183(1):187-91. doi: 10.1007/BF00270160.
A spontaneous rifampicin-resistant mutant of E. coli, RpoB26, which inhibits the growth of bacteriophage T7, has been described in the accompanying paper (Schwarz et al.). The rifr mutation appears to increase the rate of transcriptional termination in a rho-deficient strain. T7 mutants with the ability to grow (Gor+) on the Rifr mutant were isolated, and some of their properties were investigated. One of these Gor+ mutants has a small deletion, located between nucleotides 9694 and 9820 of the T7 DNA sequence (Dunn and Studier 1980), which affects the size of the T7 single-stranded DNA binding protein (ssDBP), the product of gene 2.5 (p 2.5) (Dunn and Studier 1980). The Gor+ phenotype was also mapped to this region by genetic methods. Gor+ is recessive to the wild-type (Gor-) phenotype. This suggests that the T7 ssDBP may normally increase the frequency of transcriptional termination in the early region by binding to single-stranded nucleic acid configurations, and so affecting molecular conformations involved in the termination process. Excessive termination in RpoB26 could therefore be compensated for by alterations of the ssDBP.
大肠杆菌的一种自发利福平抗性突变体RpoB26，它能抑制噬菌体T7的生长，已在随附论文（施瓦茨等人）中有所描述。利福平抗性突变似乎会提高ρ因子缺陷菌株中的转录终止速率。分离出了能在利福平抗性突变体上生长（Gor+）的T7突变体，并对它们的一些特性进行了研究。其中一个Gor+突变体有一个小缺失，位于T7 DNA序列（邓恩和斯图迪尔，1980年）的核苷酸9694和9820之间，这影响了T7单链DNA结合蛋白（ssDBP）的大小，该蛋白是基因2.5（p2.5）的产物（邓恩和斯图迪尔，1980年）。通过遗传学方法也将Gor+表型定位到了该区域。Gor+相对于野生型（Gor-）表型是隐性的。这表明T7 ssDBP可能通常通过与单链核酸构型结合来增加早期区域的转录终止频率，从而影响终止过程中涉及的分子构象。因此，RpoB26中过度的终止可以通过ssDBP的改变来补偿。
