TY - JOUR
T1 - OmpR coordinates the expression of virulence factors of Enterohemorrhagic Escherichia coli in the alimentary tract of Caenorhabditis elegans
AU - Wang, Sin Tian
AU - Kuo, Cheng Ju
AU - Huang, Chih Wen
AU - Lee, Tzer Min
AU - Chen, Jenn Wei
AU - Chen, Chang Shi
N1 - Funding Information:
We thank the Caenorhabditis Genetics Center (CGC), which is supported by the National Institutes of Health (United States) Office of Research Infrastructure Programs (P40 OD010440), for the C. elegans N2 strain. We thank Ken Sato (Gunma University, Japan) for the mCherry::ACT-5 worm. We are grateful for the assistance from the Taiwan C. elegans core facility (CECF), funded by the Minister of Science and Technology (MOST 108-2319-B-002-004-) Taiwan. We thank Miranda Loney for editing the manuscript. This work is supported by the Ministry of Science and Technology (MOST) grants (105-2321-B-006-011-, 106-2321-B-006-005-, 107-2628-B-006-003-, and 108-2628-B-006-005-) to CSC. The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript, and there were no potential conflicts of interest to be disclosed.
Funding Information:
We thank the Caenorhabditis Genetics Center (CGC), which is supported by the National Institutes of Health (United States) Office of Research Infrastructure Programs (P40 OD010440), for the N2 strain. We thank Ken Sato (Gunma University, Japan) for the mCherry::ACT‐5 worm. We are grateful for the assistance from the Taiwan core facility (CECF), funded by the Minister of Science and Technology (MOST 108‐2319‐B‐002‐004‐) Taiwan. We thank Miranda Loney for editing the manuscript. This work is supported by the Ministry of Science and Technology (MOST) grants (105‐2321‐B‐006‐011‐, 106‐2321‐B‐006‐005‐, 107‐2628‐B‐006‐003‐, and 108‐2628‐B‐006‐005‐) to CSC. The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript, and there were no potential conflicts of interest to be disclosed. C. elegans C. elegans
Publisher Copyright:
© 2021 John Wiley & Sons Ltd
PY - 2021/7
Y1 - 2021/7
N2 - Enterohemorrhagic Escherichia coli (EHEC), an enteropathogen that colonizes in the intestine, causes severe diarrhea and hemorrhagic colitis in humans by the expression of the type III secretion system (T3SS) and Shiga-like toxins (Stxs). However, how EHEC can sense and respond to the changes in the alimentary tract and coordinate the expression of these virulence genes remains elusive. The T3SS-related genes are known to be regulated by the locus of enterocyte effacement (LEE)-encoded regulators, such as Ler, as well as non-LEE-encoded regulators in response to different environmental cues. Herein, we report that OmpR, which participates in the adaptation of E. coli to osmolarity and pH alterations, is required for EHEC infection in Caenorhabditis elegans. OmpR protein was able to directly bind to the promoters of ler and stx1 (Shiga-like toxin 1) and regulate the expression of T3SS and Stx1, respectively, at the transcriptional level. Moreover, we demonstrated that the expression of ler in EHEC is in response to the intestinal environment and is regulated by OmpR in C. elegans. Taken together, we reveal that OmpR is an important regulator of EHEC which coordinates the expression of virulence factors during gastrointestinal infection in vivo.
AB - Enterohemorrhagic Escherichia coli (EHEC), an enteropathogen that colonizes in the intestine, causes severe diarrhea and hemorrhagic colitis in humans by the expression of the type III secretion system (T3SS) and Shiga-like toxins (Stxs). However, how EHEC can sense and respond to the changes in the alimentary tract and coordinate the expression of these virulence genes remains elusive. The T3SS-related genes are known to be regulated by the locus of enterocyte effacement (LEE)-encoded regulators, such as Ler, as well as non-LEE-encoded regulators in response to different environmental cues. Herein, we report that OmpR, which participates in the adaptation of E. coli to osmolarity and pH alterations, is required for EHEC infection in Caenorhabditis elegans. OmpR protein was able to directly bind to the promoters of ler and stx1 (Shiga-like toxin 1) and regulate the expression of T3SS and Stx1, respectively, at the transcriptional level. Moreover, we demonstrated that the expression of ler in EHEC is in response to the intestinal environment and is regulated by OmpR in C. elegans. Taken together, we reveal that OmpR is an important regulator of EHEC which coordinates the expression of virulence factors during gastrointestinal infection in vivo.
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U2 - 10.1111/mmi.14698
DO - 10.1111/mmi.14698
M3 - Article
C2 - 33567149
AN - SCOPUS:85101878164
SN - 0950-382X
VL - 116
SP - 168
EP - 183
JO - Molecular Microbiology
JF - Molecular Microbiology
IS - 1
ER -