Regulation of natural competence by the orphan two-component system sensor kinase ChiS involves a non-canonical transmembrane regulator in Vibrio cholerae
Regulation of natural competence by the orphan two-component system sensor kinase ChiS involves a non-canonical transmembrane regulator in Vibrio cholerae
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DOI：
10.1111/mmi.12462
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发表时间：
2014-01-01
影响因子：
3.6
通讯作者：
Izumiya, Hidemasa
中科院分区：
文献类型：
--
作者：
Yamamoto, Shouji;Mitobe, Jiro;Izumiya, Hidemasa
在霍乱弧菌中，41个甲壳素诱导基因，包括参与DNA摄取的天然能力的基因，由孤儿双组分系统(TCS)传感器激酶CHI控制。然而，CHIS控制这些基因表达的机制目前尚不清楚。在这里，我们报告了一种名为TFOS‘的新转录因子参与了这一过程。TFOS是一种跨膜蛋白，含有一个大的周质结构域和一个细胞质的AraC型DNA结合域，但缺乏TCS标志域。TFOS的失活消除了自然感受态，以及编码甲壳素诱导的小RNA的tfor基因的转录，这种小RNA是感受态基因表达所必需的。一个TFOS片段，包含与tfor启动子特异结合并激活其转录的DNA结合域。细胞内TFOS水平不受CHIS干扰和TFOS和CHIS共表达的影响，表明TFOS在转录激活过程中受到CHIS的翻译后调控；然而，当CHIS的典型磷酸传递残基发生突变时，这种调节仍然存在。这些结果表明，CHIS通过TFOS调控甲壳素诱导的非典型信号转导通路，导致TFOR的转录激活。
In Vibrio cholerae, 41 chitin-inducible genes, including the genes involved in natural competence for DNA uptake, are governed by the orphan two-component system (TCS) sensor kinase ChiS. However, the mechanism by which ChiS controls the expression of these genes is currently unknown. Here, we report the involvement of a novel transcription factor termed TfoS' in this process. TfoS is a transmembrane protein that contains a large periplasmic domain and a cytoplasmic AraC-type DNA-binding domain, but lacks TCS signature domains. Inactivation of tfoS abolished natural competence as well as transcription of the tfoR gene encoding a chitin-induced small RNA essential for competence gene expression. A TfoS fragment containing the DNA-binding domain specifically bound to and activated transcription from the tfoR promoter. Intracellular TfoS levels were unaffected by disruption of chiS and coexpression of TfoS and ChiS in Escherichia coli recovered transcription of the chromosomally integrated tfoR::lacZ gene, suggesting that TfoS is post-translationally modulated by ChiS during transcriptional activation; however, this regulation persisted when the canonical phosphorelay residues of ChiS were mutated. The results presented here suggest that ChiS operates a chitin-induced non-canonical signal transduction cascade through TfoS, leading to transcriptional activation of tfoR.