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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Listeria monocytogenes regulates flagellar motility gene expression through MogR, a transcriptional repressor required for virulence
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Listeria monocytogenes regulates flagellar motility gene expression through MogR, a transcriptional repressor required for virulence

机译：单核细胞增生李斯特菌通过MogR调节鞭毛运动基因的表达，MogR是毒力所需的转录阻遏物

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摘要

Previous studies have shown that Listeria monocytogenes flagellar motility genes, including flaA, encoding flagellin, are transcriptionally down-regulated at 37degreesC. For some L. monocytogenes strains, temperature-dependent motility gene expression is less stringent. By using flaA-lacZ transcriptional fusions, we identified regions upstream of the -35/-10 promoter elements that are necessary for temperature-dependent expression of flaA in L, monocytogenes strain EGDe. Whereas the sequence of the flaA promoter region was identical in L. monocytogenes strain 10403S, transcriptional activity was only partially down-regulated at 37degreesC in 10403S. This finding suggested that a transacting regulatory protein with differential expression or activity in EGDe might be involved in temperature-dependent transcription of flaA. Indeed, a protein factor capable of specifically binding to the flaA promoter region was identified in cytoplasmic extracts of EGDe by using affinity purification and MS. Deletion of the factor-encoding gene (Imo0674) resulted in loss of temperature-dependent flaA expression and an increase in flaA promoter activity. Expression of other motility genes was also deregulated in the Imo0674 deletion. We have designated Imo0674 as mogR, indicating its role as a motility gene repressor. In tissue culture models, MogR repression of flaA during intracellular infection was independent of temperature and a deletion of mogR reduced the capacity for cell-to-cell spread. During in vivo infection, a deletion of mogR resulted in a 250-fold decrease in virulence. These studies indicate that regulation of flagellar motility gene expression and/or other genes controlled by MogR is required for full virulence of L. monocytogenes.
机译：以前的研究表明，单核细胞增多性李斯特菌鞭毛运动基因，包括编码鞭毛蛋白的flaA，在37℃转录下调。对于某些单核细胞增生李斯特菌菌株，温度依赖性运动基因的表达不太严格。通过使用flaA-lacZ转录融合，我们确定了-35 / -10启动子元件上游的区域，这些区域对于L单核细胞增生李斯特菌EGDe的flaA的温度依赖性表达是必需的。尽管在单核细胞增生李斯特氏菌菌株10403S中flaA启动子区域的序列是相同的，但在10403S中在37℃下转录活性仅被部分下调。该发现表明，在EGDe中具有差异表达或活性的交易调节蛋白可能与flaA的温度依赖性转录有关。实际上，通过使用亲和纯化和MS在EGDe的细胞质提取物中鉴定出能够特异性结合flaA启动子区域的蛋白质因子。删除编码因子的基因（Imo0674）导致温度依赖性flaA表达的丧失和flaA启动子活性的增加。 Imo0674删除中其他运动基因的表达也被下调。我们将Imo0674指定为mogR，表明其作为运动基因阻遏物。在组织培养模型中，细胞内感染过程中对flaA的MogR抑制与温度无关，而mogR的缺失会降低细胞间扩散的能力。在体内感染期间，mogR的缺失导致毒力降低了250倍。这些研究表明，鞭毛运动基因表达和/或由MogR控制的其他基因的调控对于单核细胞增生李斯特菌的完全毒力是必需的。

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