It is established that the medically significant yersiniae require the presence of physiological levels of Ca2+ (ca. 2.5 mM) for sustained growth at 37°C and that this nutritional requirement is mediated by a shared ca. 70-kb Lcr plasmid. The latter also encodes virulence factors (Yersinia outer membrane proteins lYops] and V antigen) known to be selectively synthesized in vitro at 37°C in Ca2"-deficient medium. In this study, cells of Yersinia pestis KIM were first starved for Ca2+ at 37°C to prevent synthesis of bulk vegetative protein and then, after cell division had ceased, pulsed with [35S]methionine. After sufficient chase to ensure plasminogen activator-mediated degradation of Yops, the remaining major radioactive peptides were separated by conventional chromatographic methods and identified as Lcr plasmid-encoded V antigen and LcrH (and possibl LcrG), ca. 10-kb Pst plasmid-encoded pesticin and plasminogen activator, ca. 100-kb Tox plasmidencoded fraction 1 (capsular) antigen and murine exotoxin, and chromosomally encoded antigen 4 (pH 6 antigen) and antigen 5 (a novel hemin-rich peptide possessing modest catalase activity but not superoxide dismutase activity). Also produced at high concentration was a chromosome-encoded GroEL-like chaperone protein. Accordingly, the transcriptional block preventing synthesis of bulk vegetative protein at 37°C in Ca2+-deficient medium may not apply to genes encoding virulence factors or to highly conserved GroEL (known in other species to utilize a secondary stress-induced sigma factor).The medically significant yersiniae consist of Yersinia pestis, the causative agent of bubonic plague, and the closely related enteropathogenic species Yersinia pseudotuberculosis and Yersinia enterocolitica. Wild-type cells of these three species share an approximately 70-kb Lcr (low-calcium response) plasmid encoding a set of regulatory genes that mediate shutoff of cell division at 37°C in Ca2"-deficient media (Lcr+ phenotype) (4,8,14,46,59). Little is known about the mechanism responsible for this unique form of restriction other than that Ca2+-starved yersiniae remain viable while undergoing an ordered metabolic stepdown resulting in concomitant reduction of adenylate energy charge and shutoff of stable RNA synthesis (12, 66). As an indirect consequence of these events, the organisms become progressively blocked in synthesis of the bulk cellular protein needed for vegetative growth (12,34). It is therefore significant that this same Ca2+-deficient environment promotes selective expression of most Lcr plasmid-encoded virulence factors (4,8,14,46,59).These virulence factors consist of a series of released proteins termed Yersinia outer membrane proteins (Yops) (6) and a secreted ca. 38-kDa peptide designated LcrV (43) or V antigen (11). This peptide possesses the potential to express an internal secretion sequence (47) that may account for its observed exit from all three species of yersiniae without significant detectable accumulation at the cell surface (52, 59, 60). Evidence derived...
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