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Enterohemorrhagic Escherichia coli (EHEC) is an important foodborne pathogen that infects humans by colonizing the large intestine. The genome of EHEC O157:H7 contains 177 unique O islands (OIs). Certain OIs significantly contribute to the heightened virulence and pathogenicity exhibited by EHEC O157:H7. However, the function of most OI genes remains unknown. We demonstrated here that EHEC O157:H7 adherence to and colonization of the mouse large intestine are both dependent on OI-97. Z3495, which is annotated as a LysR-type transcriptional regulator and encoded in OI-97, contributes to this phenotype. Z3495 activated the locus of enterocyte effacement (LEE) gene expression, promoting bacterial adherence. Deletion of z3495 significantly decreased the transcription of ler and other LEE genes, the ability to adhere to the host cells, and colonization in the mouse large intestine. Furthermore, the ChIP-seq results confirmed that Z3495 can directly bind to the promoter region of rcsF, which is a well-known activator of Ler, and increase LEE gene expression. Finally, phylogenetic analysis revealed that Z3495 is a widespread transcriptional regulator in enterohemorrhagic and enteropathogenic Escherichia coli. As a result of this study, we have gained a deeper understanding of how bacteria control their virulence and provide another example of a laterally acquired regulator that regulates LEE gene expression in bacteria. [ABSTRACT FROM AUTHOR]

Vibrio cholerae (V. cholerae) is an aquatic bacterium responsible for acute and fatal cholera outbreaks worldwide. When V. cholerae is ingested, the bacteria colonize the epithelium of the small intestine and stimulate the Paneth cells to produce large amounts of cationic antimicrobial peptides (CAMPs). Human defensin 5 (HD-5) is the most abundant CAMPs in the small intestine. However, the role of the V. cholerae response to HD-5 remains unclear. Here we show that HD-5 significantly upregulates virulence gene expression. Moreover, a two-component system, CarSR (or RstAB), is essential for V. cholerae virulence gene expression in the presence of HD-5. Finally, phosphorylated CarR can directly bind to the promoter region of TcpP, activating transcription of tcpP, which in turn activates downstream virulence genes to promote V. cholerae colonization. In conclusion, this study reveals a virulence-regulating pathway, in which the CarSR two-component regulatory system senses HD-5 to activate virulence genes expression in V. cholerae. The antimicrobial peptide human defensin-5 (HD-5) is found to upregulate Vibrio cholera virulence genes in a manner dependent on the two-component system, CarSR, providing insights into how the cholera pathogen responds to intestinal HD-5. [ABSTRACT FROM AUTHOR]

Summary: Epigenetic modifications have emerged as an important mechanism underlying plant defence against pathogens. We examined the role of JMJ14, a Jumonji (JMJ) domain‐containing H3K4 demethylase, in local and systemic plant immune responses in Arabidopsis.The function of JMJ14 in local or systemic defence response was investigated by pathogen growth assays and by analysing expression and H3K4me3 enrichments of key defence genes using qPCR and ChIP‐qPCR. Salicylic acid (SA) and pipecolic acid (Pip) levels were quantified and function of JMJ14 in SA‐ and Pip‐mediated defences was analysed in Col‐0 and jmj14 plants.jmj14 mutants were compromised in both local and systemic defences. JMJ14 positively regulates pathogen‐induced H3K4me3 enrichment and expression of defence genes involved in SA‐ and Pip‐mediated defence pathways. Consequently, loss of JMJ14 results in attenuated defence gene expression and reduced Pip accumulation during establishment of systemic acquired resistance (SAR). Exogenous Pip partially restored SAR in jmj14 plants, suggesting that JMJ14 regulated Pip biosynthesis and other downstream factors regulate SAR in jmj14 plants.JMJ14 positively modulates defence gene expressions and Pip levels in Arabidopsis. [ABSTRACT FROM AUTHOR]