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Journal of Bacteriology, May 1999, p. 3096-3104, Vol. 181, No. 10
0021-9193/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

A HilA-Independent Pathway to Salmonella typhimurium Invasion Gene Transcription

Jennifer L. Rakeman,1 Heather R. Bonifield,1,2 and Samuel I. Miller1,2,*

Departments of Microbiology1 and Medicine,2 University of Washington, Seattle, Washington 98195

Received 23 December 1998/Accepted 4 March 1999

Salmonella typhimurium invasion of nonphagocytic cells requires the expression of a type III secretion system (TTSS) encoded within Salmonella pathogenicity island 1 (SPI1). TTSS gene transcription is activated in response to environmental signals and requires transcriptional regulators encoded within (HilA) and outside (SirA) SPI1. Two unique loci, sirB and sirC, which contribute to SPI1 gene transcription were defined. sirC is an SPI1-encoded transcription factor of the AraC family that contributes to the invasive phenotype. sirB is required for maximal expression of sirC and consists of two open reading frames located near kdsA, a gene involved in lipopolysaccharide biosynthesis. sirC expression, unlike expression of other SPI1 genes, does not require HilA. Overexpression of sirC or sirA restores expression of a subset of SPI1 genes, including invF and sspC, in the absence of HilA. These data define roles for SirC and SirA as part of a HilA-independent pathway to SPI1 gene expression. We postulate that HilA-independent activation of inv expression is important for efficient assembly and function of the SPI1 TTSS.

* Corresponding author. Mailing address: Departments of Medicine and Microbiology, University of Washington, Health Sciences Building, Box 357710, Seattle, WA 98195. Phone: (206) 616-5107. Fax: (206) 616-4295. E-mail: millersi{at}u.washington.edu.

Journal of Bacteriology, May 1999, p. 3096-3104, Vol. 181, No. 10
0021-9193/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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