High-throughput transposon sequencing identifies HprR as a key regulator of the LEE operon and virulence in E. coli O157:H7.

Authors

Miaomiao Liu, Pan Wu, Tao Luo, Linxing Li, Yuchen Wang, Jingliang Qin, Dan Liu, Xiaoya Li, Binbin Xiang, Yuanyuan Niu, Lu Wang, Bin Liu

Published in

Virulence. Volume 17. Issue 1. Pages 2653855. Epub Apr 07, 2026.

Abstract

Enterohemorrhagic Escherichia coli (EHEC) comprises a prominent group of extracellular human pathogens that specifically colonize the colonic epithelium, leading to severe gastrointestinal diseases and representing a significant global public health threat. During infection, EHEC O157:H7-the most prevalent serotype - tightly adheres to intestinal epithelial cells and induces the formation of characteristic attaching and effacing (A/E) lesions. However, the molecular mechanisms governing this close interaction remain incompletely understood. In this study, we employed transposon-directed insertion-site sequencing (TraDIS) to conduct a genome-wide screen for genes essential for EHEC O157:H7 adherence. Among the identified candidates, disruption of hprR (encoding the response regulator of the HprS/HprR two-component system) resulted in markedly reduced epithelial colonization. Subsequent mechanistic analyses revealed that HprR positively regulates expression of genes within the locus of enterocyte effacement (LEE) pathogenicity island in a Ler-dependent manner, thereby promoting type III secretion system (T3SS) activity and epithelial colonization. Additionally, during luminal survival, HprR was found to directly bind to the promoter region of hiuH, a gene encoding a transthyretin-like protein, thereby enhancing bacterial resistance to oxidative stress and promoting persistence in the colonic lumen. Collectively, this study defines a comprehensive genomic framework for understanding EHEC O157:H7 colonization and identifies HprR as a dual-function regulatory protein that coordinates both epithelial adherence and luminal survival, thereby shaping host-pathogen interactions.

PMID:
41947494
Bibliographic data and abstract were imported from PubMed on 12 Sep 2026.

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