Abstract
The RNA chaperone, Hfq, plays a diverse role in bacterial physiology beyond its original role as a host factor required for replication of Qβ RNA bacteriophage. In this study, we show that Hfq is involved in the expression and secretion of virulence factors in the facultative intracellular pathogen, Salmonella typhimurium. A Salmonella hfq deletion strain is highly attenuated in mice after both oral and intraperitoneal infection, and shows a severe defect in invasion of epithelial cells and a growth defect in both epithelial cells and macrophages in vitro. Surprisingly, we find that these phenotypes are largely independent of the previously reported requirement of Hfq for expression of the stationary phase sigma factor, RpoS. Our results implicate Hfq as a key regulator of multiple aspects of virulence including regulation of motility and outer membrane protein (OmpD) expression in addition to invasion and intracellular growth. These pleiotropic effects are suggested to involve a network of regulatory small non-coding RNAs, placing Hfq at the centre of post-transcriptional regulation of virulence gene expression in Salmonella. In addition, the hfq mutation appears to cause a chronic activation of the RpoE-mediated envelope stress response which is likely due to a misregulation of membrane protein expression.
Highlights
The bacterial Sm-like protein, Hfq, has been increasingly recognized as a post-transcriptional regulator of globalAccepted 19 October, 2006. *For correspondence
The RNA chaperone, Hfq, plays a diverse role in bacterial physiology beyond its original role as a host factor required for replication of Qb RNA bacteriophage
We show that Hfq is involved in the expression and secretion of virulence factors in the facultative intracellular pathogen, Salmonella typhimurium
Summary
The bacterial Sm-like protein, Hfq, has been increasingly recognized as a post-transcriptional regulator of globalAccepted 19 October, 2006. *For correspondence. The bacterial Sm-like protein, Hfq, has been increasingly recognized as a post-transcriptional regulator of global. (+49) 30 28460 265; Fax (+49) 30 28460 244. Re-use of this article is permitted in accordance with the Creative Commons Deed, Attribution 2.5, which does not permit commercial exploitation. Several recent studies addressed a potential role of Hfq in the virulence of pathogenic bacteria. A Brucella abortus hfq mutant displayed significantly reduced survival in cultured murine macrophages, and attenuated virulence in a mouse model (Robertson and Roop, 1999). Hfq was reported to be essential for the virulence of Vibrio cholerae (Ding et al, 2004).
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