This Article Full Text Full Text (PDF) Other Versions of this Article: JB.00926-07v1 190/2/476    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 Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Ellermeier, J. R. Articles by Slauch, J. M. Search for Related Content PubMed PubMed Citation Articles by Ellermeier, J. R. Articles by Slauch, J. M.

 Previous Article  |  Next Article 

Journal of Bacteriology, January 2008, p. 476-486, Vol. 190, No. 2
0021-9193/08/$08.00+0     doi:10.1128/JB.00926-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Fur Regulates Expression of the Salmonella Pathogenicity Island 1 Type III Secretion System through HilD

Department of Microbiology,¹ College of Medicine, University of Illinois, Urbana, Illinois 61801²

Received 12 June 2007/ Accepted 26 October 2007

The invasion of intestinal epithelial cells by Salmonella enterica serovar Typhimurium is mediated by a type III secretion system (T3SS) encoded on Salmonella pathogenicity island 1 (SPI1). Expression of the SPI1 T3SS is tightly regulated by the combined action of HilC, HilD, and RtsA, three AraC family members that can independently activate hilA, which encodes the direct regulator of the SPI1 structural genes. Expression of hilC, hilD, and rtsA is controlled by a number of regulators that respond to a variety of environmental signals. In this work, we show that one such signal is iron mediated by Fur (ferric uptake regulator). Fur activates hilA transcription in a HilD-dependent manner. Fur regulation of HilD does not appear to be simply at the transcriptional or translational level but rather requires the presence of the HilD protein. Fur activation of SPI1 is not mediated through the Fur-regulated small RNAs RfrA and RfrB, which are the Salmonella ortholog and paralog of RyhB that control expression of sodB. Fur regulation of HilD is also not mediated through the known SPI1 repressor HilE or the CsrABC system. Although understanding the direct mechanism of Fur action on HilD requires further analysis, this work is an important step toward elucidating how various global regulatory systems control SPI1.

Published ahead of print on 9 November 2007.