Genomic island-encoded LmiA regulates acid resistance and biofilm formation in enterohemorrhagic O157:H7.

Enterohemorrhagic (EHEC) O157:H7 is an important intestinal pathogen that causes severe foodborne diseases. We previously demonstrated that the genomic island-encoded regulator LmiA activates the locus of enterocyte effacement (LEE) genes to promote EHEC O157:H7 adherence and colonization in the host intestine. However, whether LmiA is involved in the regulation of any other biological processes in EHEC O157:H7 remains largely unexplored. Here, we compared global gene expression differences between the EHEC O157:H7 wild-type strain and an mutant strain using RNA-seq technology. Genes whose expression was affected by LmiA were identified and classified using the Cluster of Orthologous Groups (COG) database. Specifically, the expression of acid resistance genes (including , , and ) was significantly downregulated, whereas the transcript levels of biofilm-related genes (including , , , and ) were increased, in the Δ mutant compared to the EHEC O157:H7 wild-type strain. Further investigation revealed that LmiA enhanced the acid resistance of EHEC O157:H7 by directly activating the transcription of and . In contrast, LmiA reduced EHEC O157:H7 biofilm formation by indirectly repressing the expression of biofilm-related genes. Furthermore, LmiA-mediated regulation of acid resistance and biofilm formation is highly conserved and widespread among EHEC and enteropathogenic (EPEC). Our findings provide essential insight into the regulatory function of LmiA in EHEC O157:H7, particularly its role in regulating acid resistance and biofilm formation.