LysR-type transcriptional regulator OvrB encoded in O island 9 drives enterohemorrhagic Escherichia coli O157:H7 virulence
LysR-type transcriptional regulator OvrB encoded in O island 9 drives enterohemorrhagic Escherichia coli O157:H7 virulence
复制标题
O岛9编码的LysR型转录调节因子OvrB驱动肠出血性大肠杆菌O157:H7毒力
DOI：
10.1080/21505594.2019.1661721
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发表时间：
2019-01-01
期刊：
影响因子：
5.2
通讯作者：
Yang, Bin
中科院分区：
文献类型：
--
作者：
Liu, Yutao;Liu, Bin;Yang, Bin
肠出血性大肠杆菌（EHEC）O 157：H7（O 157）是一种主要的食源性致病菌，在世界范围内引起严重的人类疾病。O 157的基因组包含177个基因组岛，称为O岛（OI），包括滋贺毒素转化位点（OI-45和OI-93）和肠上皮细胞消失位点（LEE）致病岛（OI-148）。然而，OIs中的大多数基因是未表征的，并且编码未知的功能。在这项研究中，我们首次证明了OI-9编码一种新的转录激活因子Z 0346（命名为OvrB），它是细菌粘附宿主细胞和O 157中LEE基因表达所必需的。OvrB直接与LEE 1的启动子区结合，激活ler（编码LEE基因的主调节因子）的转录，进而激活LEE 1 -5基因，促进O 157粘附。此外，小鼠口腔感染试验表明，OvrB促进O 157在小鼠肠道中的定殖。最后，OvrB被证明是一个广泛的转录激活因子的毒力基因在其他肠出血性和肠致病性大肠杆菌血清型。我们的工作大大扩展了对细菌毒力控制的理解，并提供了新的证据表明，水平转移的调节基因介导LEE基因的表达。
ABSTRACT Enterohemorrhagic Escherichia coli (EHEC) O157:H7 (O157) is a major foodborne pathogen that causes severe illness in humans worldwide. The genome of O157 contains 177 genomic islands known as O islands (OIs), including Shiga toxin-converting phages (OI-45 and OI-93) and the locus for enterocyte effacement (LEE) pathogenicity island (OI-148). However, most genes in OIs are uncharacterized and code for unknown functions. In this study, we demonstrated, for the first time, that OI-9 encodes a novel transcriptional activator, Z0346 (named OvrB), which is required for bacterial adherence to host cells and LEE gene expression in O157. OvrB directly binds to the promoter region of LEE1 and activates the transcription of ler (encoding a master regulator of LEE genes), which in turn activates LEE1–5 genes to promote O157 adherence. Furthermore, mouse oral infection assays showed that OvrB promotes O157 colonization in the mouse intestine. Finally, OvrB is shown to be a widespread transcriptional activator of virulence genes in other enterohemorrhagic and enteropathogenic Escherichia coli serotypes. Our work significantly expands the understanding of bacterial virulence control and provides new evidence suggesting that horizontally transferred regulator genes mediate LEE gene expression.