The AfaR small RNA controls expression of the AfaD-VIII invasin in pathogenic Escherichia coli strains
The AfaR small RNA controls expression of the AfaD-VIII invasin in pathogenic Escherichia coli strains
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DOI：
10.1093/nar/gkt208
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发表时间：
2013-05-01
影响因子：
14.9
通讯作者：
Le Bouguenec, Chantal
中科院分区：
文献类型：
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作者：
Pichon, Christophe;du Merle, Laurence;Le Bouguenec, Chantal
携带afa-8基因簇的致病性大肠杆菌菌株经常与人类和动物的肠外感染相关。afa-8A至E基因决定在细菌细胞表面形成由AfaD-VIII侵袭素和AfaE-VIII粘附素组成的无伞粘附鞘。这种结构被认为是宿主定殖所必需的。我们表征了编码小RNA AfaR的新基因，其在afaD-afaE顺反子间区域内从afaD信使RNA的3'非翻译区的互补链顺式转录。AfaR是一种反式作用的Hfq依赖性反义小RNA，其结合afaD信使RNA的5'非翻译区，启动几种核糖核酸酶E依赖性切割，从而下调AfaD-VIII侵袭素的产生。AfaR转录依赖于Sigma（E），Sigma是细胞质外替代性σ因子的应激反应家族的成员。我们发现AfaR依赖性调节途径受温度控制，允许在37摄氏度以上的温度下产生AfaD-VIII侵袭素。我们的研究结果表明，afa-8阳性致病性E。大肠杆菌菌株进入上皮细胞的过程受到AfaR小RNA的严格调控。
Pathogenic Escherichia coli strains carrying the afa-8 gene cluster are frequently associated with extra-intestinal infections in humans and animals. The afa-8 A to E genes determine the formation of an afimbrial adhesive sheath consisting of the AfaD-VIII invasin and the AfaE-VIII adhesin at the bacterial cell surface. This structure is thought to be required for host colonization. We characterized a new gene encoding the small RNA AfaR, which is transcribed in cis from the complementary strand of the 3' untranslated region of the afaD messenger RNA, within the afaD-afaE intercistronic region. AfaR is a trans-acting Hfq-dependent antisense small RNA that binds the 5' untranslated region of the afaD messenger RNA, initiating several ribonuclease E-dependent cleavages, thereby downregulating production of the AfaD-VIII invasin. AfaR transcription is dependent on Sigma(E), a member of the stress response family of extracytoplasmic alternative sigma factors. We found that the AfaR-dependent regulatory pathway was controlled by temperature, allowing the production of the AfaD-VIII invasin at temperatures above 37 degrees C. Our findings suggest that the entry of afa-8-positive pathogenic E. coli strains into epithelial cells is tightly regulated by the AfaR small RNA.