Kuan C T, Tessman I
Department of Biological Sciences, Purdue University, West Lafayette, Indiana 47907.
J Bacteriol. 1991 Oct;173(20):6406-10. doi: 10.1128/jb.173.20.6406-6410.1991.
The LexA protein of Escherichia coli represses expression of a variety of genes that, by definition, constitute the SOS regulon. Genetic evidence suggests that Tn5 transposition is also regulated by the product of the lexA gene (C.-T. Kuan, S.-K. Liu, and I. Tessman, Genetics 128:45-57, 1991). We now show that the LexA protein represses expression of the tnp gene, located in the IS50R component of Tn5, which encodes a transposase, and that LexA does not repress expression of the IS50R inh gene, which encodes an inhibitor of transposition. Elimination of LexA resulted in increased expression of the tnp gene by a factor of 2.7 +/- 0.4, as indicated by the activity of a lacZ gene fused to the tnp gene. LexA protein retarded the electrophoretic movement of a 101-bp segment of IS50R DNA that contained a putative LexA protein-binding site in the tnp promoter; the interaction between the LexA repressor and the promoter region of the tnp gene appears to be relatively weak. These features show that the IS50R tnp gene is a member of the SOS regulon.
大肠杆菌的LexA蛋白可抑制多种基因的表达,根据定义,这些基因构成了SOS调节子。遗传学证据表明,Tn5转座也受lexA基因产物的调控(C.-T. 关、S.-K. 刘和I. 特斯曼,《遗传学》128:45 - 57, 1991)。我们现在证明,LexA蛋白可抑制位于Tn5的IS50R组件中的tnp基因的表达,该基因编码一种转座酶,且LexA并不抑制编码转座抑制剂的IS50R inh基因的表达。如与tnp基因融合的lacZ基因的活性所示,去除LexA导致tnp基因的表达增加了2.7 +/- 0.4倍。LexA蛋白使IS50R DNA的一个101碱基对片段的电泳迁移率减慢,该片段在tnp启动子中含有一个假定的LexA蛋白结合位点;LexA阻遏物与tnp基因启动子区域之间的相互作用似乎相对较弱。这些特征表明,IS50R tnp基因是SOS调节子的一个成员。