This Article Full Text Full Text (PDF) Other Versions of this Article: JB.00178-07v1 189/13/4587    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Thijs, I. M. V. Articles by Vanderleyden, J. Search for Related Content PubMed PubMed Citation Articles by Thijs, I. M. V. Articles by Vanderleyden, J.

Delineation of the Salmonella enterica Serovar Typhimurium HilA Regulon through Genome-Wide Location and Transcript Analysis

Centre of Microbial and Plant Genetics, K. U. Leuven, Kasteelpark Arenberg 20, 3001 Leuven, Belgium,¹ ESAT-SCD, K. U. Leuven, Kasteelpark Arenberg 10, 3001 Leuven, Belgium,² Sidney Kimmel Cancer Center, 10835 Altman Row, San Diego, California 92121³

Received 2 February 2007/ Accepted 25 April 2007

The Salmonella enterica serovar Typhimurium HilA protein is the key regulator for the invasion of epithelial cells. By a combination of genome-wide location and transcript analysis, the HilA-dependent regulon has been delineated. Under invasion-inducing conditions, HilA binds to most of the known target genes and a number of new target genes. The sopB, sopE, and sopA genes, encoding effector proteins secreted by the type III secretion system on Salmonella pathogenicity island 1 (SPI-1), were identified as being both bound by HilA and differentially regulated in an HilA mutant. This suggests a cooperative role for HilA and InvF in the regulation of SPI-1-secreted effectors. Also, siiA, the first gene of SPI-4, is both bound by HilA and differentially regulated in an HilA mutant, thus linking this pathogenicity island to the invasion key regulator. Finally, the interactions of HilA with the SPI-2 secretion system gene ssaH and the flagellar gene flhD imply a repressor function for HilA under invasion-inducing conditions.

Published ahead of print on 4 May 2007.

This article has been cited by other articles:

• Main-Hester, K. L., Colpitts, K. M., Thomas, G. A., Fang, F. C., Libby, S. J. (2008). Coordinate Regulation of Salmonella Pathogenicity Island 1 (SPI1) and SPI4 in Salmonella enterica Serovar Typhimurium. Infect. Immun. 76: 1024-1035 [Abstract] [Full Text]  
• Lin, D., Rao, C. V., Slauch, J. M. (2008). The Salmonella SPI1 Type Three Secretion System Responds to Periplasmic Disulfide Bond Status via the Flagellar Apparatus and the RcsCDB System. J. Bacteriol. 190: 87-97 [Abstract] [Full Text]