Description:
<jats:title>Abstract</jats:title><jats:p>In <jats:italic>Enterobacteriaceae</jats:italic>, the RNA chaperone Hfq mediates the interaction of small RNAs with target mRNAs, thereby modulating transcript stability and translation. This post-transcriptional control helps bacteria adapt quickly to changing environmental conditions. Our previous mutational analysis showed that Hfq is involved in metabolism and stress survival in the enteropathogen <jats:italic>Yersinia enterocolitica</jats:italic>. In this study we demonstrate that Hfq is essential for virulence in mice and influences production of surface pathogenicity factors, in particular lipopolysaccharide and adhesins mediating interaction with host tissue. Hfq inhibited the production of Ail, the Ail-like protein OmpX and the MyfA pilin post-transcriptionally. In contrast Hfq promoted production of two major autotransporter adhesins YadA and InvA. While protein secretion <jats:italic>in vitro</jats:italic> was not affected, <jats:italic>hfq</jats:italic> mutants exhibited decreased protein translocation by the type III secretion system into host cells, consistent with decreased production of YadA and InvA. The influence of Hfq on YadA resulted from a complex interplay of transcriptional, post-transcriptional and likely post-translational effects. Hfq regulated <jats:italic>invA</jats:italic> by modulating the expression of the transcriptional regulators <jats:italic>rovA</jats:italic>, <jats:italic>phoP</jats:italic> and <jats:italic>ompR</jats:italic>. Therefore, Hfq is a global coordinator of surface virulence determinants in <jats:italic>Y. enterocolitica</jats:italic> suggesting that it constitutes an attractive target for developing new antimicrobial strategies.</jats:p>