Affiliation:
1. Department of Microbiology and Molecular Genetics, Michigan State University, East Lansing, Michigan 48824
Abstract
ABSTRACT
The virulence of yersiniae is promoted in part by shared ≈70-kb plasmids (pCD in
Yersinia pestis
and pYV in enteropathogenic
Yersinia pseudotuberculosis
and
Yersinia enterocolitica
) that mediate a low-calcium response. This phenotype is characterized at 37°C by either bacteriostasis in Ca
2+
-deficient medium with expression of pCD/pYV-encoded virulence effectors (Yops and LcrV) or vegetative growth and repression of Yops and LcrV with ≥2.5 mM Ca
2+
(Lcr
+
). Regulation of Yops and LcrV is well defined but little is known about bacteriostasis other than that Na
+
plus
l
-glutamate promotes prompt restriction of
Y. pestis
. As shown here,
l
-aspartate substituted for
l
-glutamate in this context but only Na
+
exacerbated the nutritional requirement for Ca
2+
. Bacteriostasis of
Y. pestis
(but not enteropathogenic yersiniae) was abrupt in Ca
2+
-deficient medium at neutral to slightly alkaline pH (7.0 to 8.0), although increasing the pH to 8.5 or 9.0, especially with added Na
+
(but not
l
-glutamate), facilitated full-scale growth. Added
l
-glutamate (but not Na
+
) favored Ca
2+
-independent growth at acidic pH (5.0 to 6.5). Yops and LcrV were produced in Ca
2+
-deficient media at pH 6.5 to 9.0 regardless of the presence of added Na
+
or
l
-glutamate, although their expression at alkaline pH was minimal. Resting Ca
2+
-starved Lcr
+
cells of
Y. pestis
supplied with
l
-glutamate first excreted and then destroyed
l
-aspartate. These findings indicate that expression of Yops and LcrV is necessary but not sufficient for bacteriostasis of Ca
2+
-starved yersiniae and suggest that abrupt restriction of
Y. pestis
requires Na
+
and the known absence of aspartate ammonia-lyase in this species.
Publisher
American Society for Microbiology
Subject
Infectious Diseases,Immunology,Microbiology,Parasitology
Cited by
34 articles.
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