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首页> 外文期刊>Journal of bacteriology >A Distinct Regulatory Sequence Is Essential for the Expression of a Subset of nle Genes in Attaching and Effacing Escherichia coli
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A Distinct Regulatory Sequence Is Essential for the Expression of a Subset of nle Genes in Attaching and Effacing Escherichia coli

机译：不同的调控序列对于在附着和表面修饰的大肠杆菌中表达nle基因子集至关重要。

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Enteropathogenic Escherichia coli uses a type III secretion system (T3SS), encoded in the locus of enterocyte effacement (LEE) pathogenicity island, to translocate a wide repertoire of effector proteins into the host cell in order to subvert cell signaling cascades and promote bacterial colonization and survival. Genes encoding type III-secreted effectors are located in the LEE and scattered throughout the chromosome. While LEE gene regulation is better understood, the conditions and factors involved in the expression of effectors encoded outside the LEE are just starting to be elucidated. Here, we identified a highly conserved sequence containing a 13-bp inverted repeat (IR), located upstream of a subset of genes coding for different non-LEE-encoded effectors in A/E pathogens. Site-directed mutagenesis and deletion analysis of the nleH1 and nleB2 regulatory regions revealed that this IR is essential for the transcriptional activation of both genes. Growth conditions that favor the expression of LEE genes also facilitate the activation of nleH1 and nleB2; however, their expression is independent of the LEE-encoded positive regulators Ler and GrlA but is repressed by GrlR and the global regulator H-NS. In contrast, GrlA and Ler are required for nleA expression, while H-NS silences it. Consistent with their role in the regulation of nleA, purified Ler and H-NS bound to the regulatory region of nleA upstream of its promoter. This work shows that at least two modes of regulation control the expression of effector genes in attaching and effacing (A/E) pathogens, suggesting that a subset of effector functions may be coordinately expressed in a particular niche or time during infection.
机译：肠致病性大肠杆菌使用在肠上皮细胞侵染（LEE）致病岛位置编码的III型分泌系统（T3SS）将大量效应蛋白转移到宿主细胞中，从而破坏细胞信号级联并促进细菌定殖和生存。编码III型分泌效应子的基因位于LEE中，并散布在整个染色体中。尽管人们对LEE基因的调控有了更好的了解，但人们刚刚开始阐明与LEE外编码的效应子表达有关的条件和因素。在这里，我们确定了一个高度保守的序列，该序列包含一个13 bp的反向重复序列（IR），位于A / E病原体中编码不同的非LEE编码效应子的基因子集的上游。对 nleH1 和 nleB2 调控区的定点诱变和缺失分析表明，该IR对于两个基因的转录激活都是必不可少的。有利于LEE基因表达的生长条件也促进了 nleH1 和 nleB2 的激活。但是，它们的表达独立于LEE编码的正调控子Ler和GrlA，但受到GrlR和全局调控子H-NS的抑制。相反， nleA 表达需要GrlA和Ler，而H-NS使它沉默。与其在 nleA 调控中的作用一致，纯化的Ler和H-NS与其启动子上游的 nleA 调控区结合。这项工作表明，至少有两种调节模式可以控制效应基因在附着和消失病原体中的表达，这表明在感染过程中，效应子功能的一个子集可以在特定的环境或时间中协同表达。

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