The virR/virS locus regulates the transcription of genes encoding extracellular toxin production in Clostridium perfringens
The virR/virS locus regulates the transcription of genes encoding extracellular toxin production in Clostridium perfringens
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DOI：
10.1128/jb.178.9.2514-2520.1996
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发表时间：
1996-05-01
影响因子：
3.2
通讯作者：
Shimizu, T
中科院分区：
文献类型：
--
作者：
BaThein, W;Lyristis, M;Shimizu, T
产气荚膜梭菌胞外毒素的产生受双组分调控基因virR和virS的正调控，用来自野生型菌株13和同基因virR和virS突变体TS 133和JIR 4000的RNA制备物进行的北方（RNA）印迹显示，virR和virS基因组成操纵子并转录为单个2，1-kb mRNA分子，引物延伸分析鉴定了virR上游的两个启动子。突变体及其互补衍生物的杂交分析表明，virR/virS系统正调控α-毒素的产生（或磷脂酶C），θ-毒素（产气荚膜梭菌溶素O）和κ毒素然而，这些基因的调控模式显示出不同。θ毒素结构基因pfoA具有主要和非常次要的启动子，编码κ毒素的coLA基因具有两个主要启动子，其中只有一个是依赖于virR/virS的。相比之下，α-毒素结构基因，馅饼，只有一个启动子，这表明是由virR和virS基因部分调控。virR/virS依赖的启动子的比较分析没有发现任何共同的序列基序，可以代表VirR结合位点。得出的结论是，要么virR/virS系统通过对每个毒素结构基因特异性的二级调控基因调节其作用，要么VirR蛋白不具有单一的共有结合序列。
Extracellular toxin production in Clostridium perfringens is positively regulated by the two-component regulatory genes virR and virS, Northern (RNA) blots carried out with RNA preparations from the wild-type strain 13 and the isogenic virR and virS mutants TS133 and JIR4000 showed that the virR and virS genes composed an operon and were transcribed as a single 2,1-kb mRNA molecule, Primer extension analysis led to the identification of two promoters upstream of virR, Hybridization analysis of the mutants and their complemented derivatives showed that the virR/virS system positively regulated the production of alpha-toxin (or phospholipase C), theta-toxin (perfringolysin O), and kappa-toxin (collagenase) at the transcriptional level, However, the modes of regulation of these genes were shown to differ, The theta-toxin structural gene, pfoA, had both a major and a very minor promoter, with the major promoter being virR/virS dependent, The coLA gene, which encodes the kappa-toxin, had two major promoters, only one of which was virR/virS-dependent. In contrast, the alpha-toxin structural gene, pie, had only one promoter, which was shown to be partially regulated by the virR and virS genes. Comparative analysis of the virR/virS-dependent promoters did not reveal any common sequence motifs that could represent VirR-binding sites. It was concluded that either the virR/virS system modulates its effects via secondary regulatory genes that are specific for each toxin structural gene or the VirR protein does not have a single consensus binding sequence.