Impact of the RNA Chaperone Hfq on the Fitness and Virulence Potential of Uropathogenic Escherichia coli

Division of Cell Biology and Immunology, Pathology Department, University of Utah, Salt Lake City, Utah 84112-0565, USA

^* To whom correspondence should be addressed. Email: mulvey{at}path.utah.edu.

	Abstract

Hfq is a bacterial RNA chaperone involved in post-transcriptional regulation of many stress-inducible genes via small non-coding RNAs. Here we show that Hfq is critical for the uropathogenic Escherichia coli (UPEC) isolate UTI89 to effectively colonize the bladder and kidneys in a murine urinary tract infection model system. Disruption of hfq did not affect bacterial adherence to or invasion of host cells, but did limit the development of intracellular microcolonies by UTI89 within the terminally differentiated epithelial cells that line the lumen of the bladder. In vitro, the hfq mutant was significantly impaired in its ability to handle the antibacterial cationic peptide polymyxin B, reactive nitrogen and oxygen radicals, and growth in acidic medium (pH 5.0). Relative to the wild type strain, the hfq mutant also had a substantially reduced migration rate on motility agar and was less prone to form biofilms. Hfq activities are known to impact the regulation of both the stationary phase sigma factor RpoS (^S) and the envelope stress response sigma factor RpoE (^E). Although we saw similarities among hfq, rpoS, and rpoE deletion mutants in our assays, the rpoE and hfq mutants were phenotypically most alike. Cumulatively, our data indicate that Hfq likely affects UPEC virulence-related phenotypes primarily by modulating membrane homeostasis and envelope stress response pathways.