J Bacteriol, May 1998, p. 2409-2417, Vol. 180, No. 9
0021-9193/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Department of Microbiology and Immunology, College of Medicine, University of South Alabama, Mobile, Alabama 36688
Received 6 November 1997/Accepted 27 February 1998
The acid tolerance response enables Salmonella
typhimurium to survive exposures to potentially lethal acidic
environments. The acid stress imposed in a typical assay for acid
tolerance (log-phase cells in minimal glucose medium) was shown to
comprise both inorganic (i.e., low pH) and organic acid components. A
gene previously determined to affect acid tolerance, atbR,
was identified as pgi, the gene encoding
phosphoglucoisomerase. Mutations in pgi were shown to
increase acid tolerance by preventing the synthesis of organic acids.
Protocols designed to separate the stresses of inorganic from organic
acids revealed that the regulators
38 (RpoS), Fur, and
Ada have major effects on tolerance to organic acid stress but only
minor effects on inorganic acid stress. In contrast, the two-component
regulatory system PhoP (identified as acid shock protein ASP29) and
PhoQ proved to be important for tolerance to organic acid stress but
had little effect against organic acid stress. PhoP mutants also failed
to induce four ASPs, confirming a role for this regulator in acid
tolerance. Acid shock induction of PhoP appears to occur at the
transcriptional level and requires the PhoPQ system. Furthermore,
induction by acid occurs even in the presence of high concentrations of
magnesium, the ion known to be sensed by PhoQ. These results suggest
that PhoQ can sense both Mg2+ and pH. Since
phoP mutants are avirulent, the low pH activation of this
system has important implications concerning the pathogenesis of
S. typhimurium. The involvement of four regulators,
two of which are implicated in virulence, underscores the complexity of
the acid tolerance stress response and further suggests that features of acid tolerance and virulence are interwoven.
Present address: Department of Pathology and Laboratory Medicine,
University of California at Los Angeles, Los Angeles, CA 90095-1713.
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