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Influence of Na⁺, Dicarboxylic Amino Acids, and pH in Modulating the Low-Calcium Response of Yersinia pestis

Department of Microbiology and Molecular Genetics, Michigan State University, East Lansing, Michigan 48824

Received 10 January 2005/ Returned for modification 4 March 2005/ Accepted 11 April 2005

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 Ca²⁺-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 Ca²⁺ (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 Ca²⁺. Bacteriostasis of Y. pestis (but not enteropathogenic yersiniae) was abrupt in Ca²⁺-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 Ca²⁺-independent growth at acidic pH (5.0 to 6.5). Yops and LcrV were produced in Ca²⁺-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 Ca²⁺-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 Ca²⁺-starved yersiniae and suggest that abrupt restriction of Y. pestis requires Na⁺ and the known absence of aspartate ammonia-lyase in this species.

Editor: V. J. DiRita

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