Regulation of LiaRS-dependent gene expression in Bacillus subtilis:: Identification of inhibitor proteins, regulator binding sites, and target genes of a conserved cell envelope stress-sensing two-component system

Regulation of LiaRS-dependent gene expression in Bacillus subtilis:: Identification of inhibitor proteins, regulator binding sites, and target genes of a conserved cell envelope stress-sensing two-component system
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DOI:
10.1128/jb.00310-06
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发表时间:
2006-07-01
影响因子:
3.2
通讯作者:
Mascher, Thorsten
Mascher, Thorsten
中科院分区:
生物学3区
文献类型:
--
作者:
Jordan, Sina;Junker, Anja;Mascher, Thorsten

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枯草芽孢杆菌细胞膜应激反应的调控网络涉及胞质外功能因子和双组分信号转导系统。一个这样的系统,LiaRS,响应于干扰十一肾上腺素循环的细胞壁抗生素和细胞质膜的扰动。它由liaIHGFSR基因座的最后两个基因编码。在这里,我们分析了两个LiaR依赖性操纵子liaIHGFSR和yhcYZ-yhd,4的表达,并表征了LiaR依赖性激活所需的回文序列。由于强liaI启动子的诱导导致liaIH和liaIHGFRS转录物,LiaR被正向自动调节。lia 1操纵子的系统缺失分析表明,LiaF是一个有效的负调控LiaR依赖的基因表达:非极性liaF缺失导致组成型激活的两个特征LiaR依赖的启动子。liaF基因在革兰氏阳性细菌的厚壁菌门组中在序列和基因组背景下都是保守的,直接位于liaSR直系同源物的上游。LiaH是大肠杆菌噬菌体休克蛋白A的同源物,在负调节来自LiaR依赖性启动子的杆菌肽诱导型表达中也起着更微妙的作用。我们的研究结果支持一个模型,其中LiaFRS模块集成了正反馈和负反馈回路,以抑制细胞的包络应力信号。
The regulatory network of the cell envelope stress response in Bacillus subtilis involves both extracytoplasmic function or-factors and two-component signal transducing systems. One such system, LiaRS, responds to cell wall antibiotics that interfere with the undecaprenol cycle and to perturbation of the cytoplasmic membrane. It is encoded by the last two genes of the liaIHGFSR locus. Here, we analyzed the expression of two LiaR-dependent operons, liaIHGFSR and yhcYZ-yhd,4, and characterized a palindromic sequence required for LiaR-dependent activation. Since induction of the strong liaI promoter leads to both liaIH and liaIHGFRS transcripts, LiaR is positively autoregulated. Systematic deletion analysis of the lia1 operon revealed that LiaF is a potent negative regulator of LiaR-dependent gene expression: a nonpolar liaF deletion led to constitutive activation of both characterized LiaR-dependent promoters. The liaF gene is conserved in both sequence and genomic context in the Firmicutes group of gram-positive bacteria, located directly upstream of liaSR orthologs. LiaH, a homolog of Escherichia coli phage shock protein A, also plays a more subtle role in negatively modulating the bacitracin-inducible expression from LiaR-dependent promoters. Our results support a model in which the LiaFRS module integrates both positive and negative feedback loops to transduce cell envelope stress signals.