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大肠杆菌中λ样原噬菌体诱导的RecA非依赖途径。

RecA-independent pathways of lambdoid prophage induction in Escherichia coli.

作者信息

Rozanov D V, D'Ari R, Sineoky S P

机构信息

State Scientific Research Institute of Genetics and Selection of Industrial Microorganisms, Moscow 113545, Russia.

出版信息

J Bacteriol. 1998 Dec;180(23):6306-15. doi: 10.1128/JB.180.23.6306-6315.1998.

Abstract

Two Escherichia coli genes, expressed from multicopy plasmids, are shown to cause partial induction of prophage lambda in recA mutant lysogens. One is rcsA, which specifies a positive transcriptional regulator of the cps genes, which are involved in capsular polysaccharide synthesis. The other is dsrA, which specifies an 85-nucleotide RNA that relieves repression of the rcsA gene by histone-like protein H-NS. Genetic contexts known to increase Cps expression also cause RecA-independent lambda induction: the rcsC137 mutation, which causes constitutive Cps expression, and the lon and rcsA3 mutations, which stabilize RcsA. Lambdoid phages 21, phi80, and 434 are also induced by RcsA and DsrA overexpression in recA lysogens. Excess lambda cI repressor specifically blocks lambda induction, suggesting that induction involves repressor inactivation rather than repressor bypass. RcsA-mediated induction requires RcsB, the known effector of the cps operon, whereas DsrA-mediated induction is RcsB independent in stationary phase, pointing to the existence of yet another RecA-independent pathway of prophage induction.

摘要

从多拷贝质粒表达的两个大肠杆菌基因被证明可在recA突变溶原菌中引起原噬菌体λ的部分诱导。一个是rcsA,它指定了参与荚膜多糖合成的cps基因的正转录调节因子。另一个是dsrA,它指定了一种85个核苷酸的RNA,可缓解组蛋白样蛋白H-NS对rcsA基因的抑制。已知增加Cps表达的遗传背景也会导致RecA非依赖性的λ诱导:导致Cps组成型表达的rcsC137突变,以及稳定RcsA的lon和rcsA3突变。在recA溶原菌中,RcsA和DsrA的过表达也会诱导类λ噬菌体21、phi80和434。过量的λcI阻遏物特异性地阻断λ诱导,这表明诱导涉及阻遏物失活而非阻遏物旁路。RcsA介导的诱导需要RcsB,即cps操纵子的已知效应物,而DsrA介导的诱导在稳定期是RcsB非依赖性的,这表明存在另一种RecA非依赖性的原噬菌体诱导途径。

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