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Hfq is essential for Vibrio cholerae virulence and downregulates σ E expression
Author(s) -
Ding Yanpeng,
Davis Brigid M.,
Waldor Matthew K.
Publication year - 2004
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.1365-2958.2004.04142.x
Subject(s) - vibrio cholerae , biology , virulence , sigma factor , mutant , microbiology and biotechnology , virulence factor , gene , pathogenicity island , gene expression , genetics , promoter , bacteria
Summary Hfq is an RNA‐binding protein that interacts with both small untranslated RNAs (sRNAs) and mRNAs to modulate gene expression post‐transcriptionally. In Escherichia coli and Salmonella typhimurium , Hfq is required for efficient expression of the stationary phase sigma factor σ S , and consequently is critical for Salmonella virulence. We have found that Hfq is also essential for the virulence of Vibrio cholerae , as strains lacking hfq fail to colonize the suckling mouse intestine. Deletion of the V. cholerae hfq does not prevent production of σ S , nor does it prevent expression of TCP, V. cholerae 's primary colonization factor. The expression and activity of the alternative sigma factor σ E are dramatically increased in a V. cholerae hfq mutant. Comparison of the transcriptome of an hfq mutant with that of an rseA mutant, which also overexpresses σ E , revealed that σ E controls approximately half the genes found to be upregulated in the hfq mutant. However, increased σ E does not appear to account for this strain's reduced virulence. It is likely that sRNAs, in conjunction with Hfq, are critical regulators of V. cholerae pathogenicity.