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Hfq negatively regulates type III secretion in EHEC and several other pathogens
Author(s) -
Shakhnovich Elizabeth A.,
Davis Brigid M.,
Waldor Matthew K.
Publication year - 2009
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.2009.06856.x
Subject(s) - biology , effector , secretion , virulence , gene , pathogenicity island , genetics , chaperone (clinical) , type three secretion system , microbiology and biotechnology , transcription (linguistics) , regulation of gene expression , transcriptional regulation , mutant , escherichia coli , gene expression , biochemistry , medicine , linguistics , philosophy , pathology
Summary Hfq is a conserved RNA‐binding protein that regulates diverse cellular processes through post‐transcriptional control of gene expression, often by functioning as a chaperone for regulatory sRNAs. Here, we explored the role of Hfq in enterohaemorrhagic Escherichia coli (EHEC), a group of non‐invasive intestinal pathogens. EHEC virulence is dependent on a Type III secretion system encoded in the LEE pathogenicity island. The abundance of transcripts for all 41 LEE genes and more than half of confirmed non‐LEE‐encoded T3 effectors were elevated in an EHEC hfq deletion mutant. Thus, Hfq promotes co‐ordinated expression of the LEE‐encoded T3S apparatus and both LEE‐ and non‐LEE‐encoded effectors. Increased transcript levels led to the formation of functional secretion complexes capable of secreting high quantities of effectors into the supernatant. The increase in LEE‐derived transcripts and proteins was dependent on Ler, the LEE‐encoded transcriptional activator, and the ler transcript appears to be a direct target of Hfq‐mediated negative regulation. Finally, we found that Hfq contributes to the negative regulation of T3SSs in several other pathogens, suggesting that Hfq, potentially along with species‐specific sRNAs, underlies a common means to prevent unfettered expression of T3SSs.