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首页> 外文期刊>Journal of bacteriology >The tib Adherence Locus of Enterotoxigenic Escherichia coli Is Regulated by Cyclic AMP Receptor Protein
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The tib Adherence Locus of Enterotoxigenic Escherichia coli Is Regulated by Cyclic AMP Receptor Protein

机译：产肠毒素大肠杆菌的tib粘附位点受环AMP受体蛋白的调节。

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Enterotoxigenic Escherichia coli (ETEC) is a Gram-negative enteric pathogen that causes profuse watery diarrhea through the elaboration of heat-labile and/or heat-stable toxins. Virulence is also dependent upon the expression of adhesive pili and afimbrial adhesins that allow the pathogen to adhere to the intestinal epithelium or mucosa. Both types of enterotoxins are regulated at the level of transcription by cyclic AMP (cAMP) receptor protein (CRP). To further our understanding of virulence gene regulation, an in silico approach was used to identify putative CRP binding sites in the genome of H10407 (O78:H11), an ETEC strain that was originally isolated from the stool of a Bangledeshi patient with cholera-like symptoms circa 1971. One of the predicted binding sites was located within an intergenic region upstream of tibDBCA. TibA is an autotransporter and afimbrial adhesin that is glycosylated by TibC. Expression of the TibA glycoprotein was abolished in an H10407 crp mutant and restored when crp was provided in trans. TibA-dependent aggregation was also abolished in a cyaA::kan strain and restored by addition of exogenous cAMP to the growth medium. DNase I footprinting confirmed that the predicted site upstream of tibDBCA is bound by CRP. Point mutations within the CRP binding site were found to abolish or significantly impair CRP-dependent activation of the tibDB promoter. Thus, these studies demonstrate that CRP positively regulates the expression of the glycosylated afimbrial adhesin TibA through occupancy of a binding site within tibDBp.
机译：产肠毒素的大肠埃希菌（ETEC）是革兰氏阴性肠病原体，其通过精心设计对热不稳定和/或对热稳定的毒素导致大量腹泻。毒力还取决于允许病原体粘附到肠上皮或粘膜的粘附菌毛和房室粘附素的表达。两种类型的肠毒素均受环状AMP（cAMP）受体蛋白（CRP）调控转录水平。为了进一步了解毒力基因调控，使用了一种 in silico 方法来鉴定H10407（O78：H11）基因组中推定的CRP结合位点，该基因最初是从大肠杆菌的粪便中分离出来的一位患有霍乱样症状的Bangledeshi患者，大约在1971年。预测的结合位点之一位于 tibDBCA 上游的一个基因间区域内。 TibA是被TibC糖基化的自转运体和辅助粘附素。在H10407 crp 突变体中，TibA糖蛋白的表达被消除，并且在 trans 中提供 crp 时，TibA糖蛋白的表达得以恢复。 TibA依赖的聚集体在 cyaA :: kan 菌株中也被消除，并通过向生长培养基中添加外源性cAMP来恢复。 DNase I足迹确认了 tibDBCA 上游的预测位点受CRP约束。发现CRP结合位点内的点突变消除或显着削弱 tibDB 启动子的CRP依赖性激活。因此，这些研究表明，CRP通过占据 tibDBp 中的结合位点来正向调节糖基化的房室粘附素TibA的表达。

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