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Journal of Bacteriology, May 2001, p. 2733-2745, Vol. 183, No. 9
0021-9193/01/$04.00+0   DOI: 10.1128/JB.183.9.2733-2745.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Roles of hilC and hilD in Regulation of hilA Expression in Salmonella enterica Serovar Typhimurium

Robin L. Lucas and Catherine A. Lee*

Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts 02115

Received 11 December 2000/Accepted 2 February 2001

Sequences between -332 and -39 upstream of the hilA promoter are required for repression of hilA. An unidentified repressor is thought to bind these upstream repressing sequences (URS) to inhibit hilA expression. Two AraC-like transcriptional regulators encoded on Salmonella pathogenicity island 1 (SPI1), HilC and HilD, bind to the URS to counteract the repression of hilA. The URS is required for regulation of hilA by osmolarity, oxygen, PhoP/PhoQ, and SirA/BarA. Here, we show that FadD, FliZ, PhoB, and EnvZ/OmpR also require the URS to regulate hilA. These environmental and regulatory factors may affect hilA expression by altering the expression or activity of HilC, HilD, or the unknown repressor. To begin investigating these possibilities, we tested the effects of environmental and regulatory factors on hilC and hilD expression. We also examined hilA regulation when hilC or hilD was disrupted or expressed to a high level. Although hilC is regulated by all environmental conditions and regulatory factors that modulate hilA expression, hilC is not required for the regulation of hilA by any conditions or factors except EnvZ/OmpR. In contrast, hilD is absolutely required for hilA expression, but environmental conditions and regulatory factors have little or no effect on hilD expression. We speculate that EnvZ/OmpR regulates hilA by altering the expression and/or activity of hilC, while all other regulatory conditions and mutations regulate hilA by modulating hilD posttranscriptionally. We also discuss models in which the regulation of hilA expression is mediated by modulation of the expression or activity of one or more repressors.

* Corresponding author. Mailing address: Department of Microbiology and Molecular Genetics, Harvard Medical School, 200 Longwood Ave., Boston, MA 02115. Phone: (617) 432-4988. Fax: (617) 738-7664. E-mail: clee{at}hms.harvard.edu.

Journal of Bacteriology, May 2001, p. 2733-2745, Vol. 183, No. 9
0021-9193/01/$04.00+0   DOI: 10.1128/JB.183.9.2733-2745.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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