Biochemistry, Department of

 

Document Type

Article

Date of this Version

2000

Citation

Journal of Bacteriology, Apr. 2000, p. 1872–1882 Vol. 182, No. 7

Comments

Copyright © 2000, American Society for Microbiology. All Rights Reserved.

Abstract

HilA activates the expression of Salmonella enterica serovar Typhimurium invasion genes. To learn more

about regulation of hilA, we isolated Tn5 mutants exhibiting reduced hilA and/or invasion gene expression. In

addition to expected mutations, we identified Tn5 insertions in pstS, fadD, flhD, flhC, and fliA. Analysis of the

pstS mutant indicates that hilA and invasion genes are repressed by the response regulator PhoB in the absence

of the Pst high-affinity inorganic phosphate uptake system. This system is required for negative control of the

PhoR-PhoB two-component regulatory system, suggesting that hilA expression may be repressed by PhoRPhoB

under low extracellular inorganic phosphate conditions. FadD is required for uptake and degradation of

long-chain fatty acids, and our analysis of the fadD mutant indicates that hilA is regulated by a FadDdependent,

FadR-independent mechanism. Thus, fatty acid derivatives may act as intracellular signals to

regulate hilA expression. flhDC and fliA encode transcription factors required for flagellum production,

motility, and chemotaxis. Complementation studies with flhC and fliA mutants indicate that FliZ, which is

encoded in an operon with fliA, activates expression of hilA, linking regulation of hilA with motility. Finally,

epistasis tests showed that PhoB, FadD, FliZ, SirA, and EnvZ act independently to regulate hilA expression and

invasion. In summary, our screen has identified several distinct pathways that can modulate S. enterica serovar

Typhimurium’s ability to express hilA and invade host cells. Integration of signals from these different

pathways may help restrict invasion gene expression during infection.

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