Open AccessFur Regulates Expression of the Salmonella Pathogenicity Island 1 Type III Secretion System through HilD
Author(s) -
Jeremy R. Ellermeier,
James M. Slauch
Publication year - 2008
Publication title -
journal of bacteriology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.652
H-Index - 246
eISSN - 1067-8832
pISSN - 0021-9193
DOI - 10.1128/jb.00926-07
Subject(s) - biology , pathogenicity island , repressor , salmonella enterica , secretion , regulator , type three secretion system , microbiology and biotechnology , salmonella , genetics , transcription factor , gene , bacteria , virulence , biochemistry
The invasion of intestinal epithelial cells bySalmonella enterica serovar Typhimurium is mediated by a type III secretion system (T3SS) encoded onSalmonella 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 activatehilA , which encodes the direct regulator of the SPI1 structural genes. Expression ofhilC ,hilD , andrtsA 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 activateshilA 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 theSalmonella ortholog and paralog of RyhB that control expression ofsodB . 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.