Published September 1, 2001 | Version Published
Journal Article Open

A Program of Yersinia enterocolitica Type III Secretion Reactions Is Activated by Specific Signals

Abstract

Successful establishment of Yersinia infections requires the type III machinery, a protein transporter that injects virulence factors (Yops) into macrophages. It is reported here that the Yersinia type III pathway responds to environmental signals by transporting proteins to distinct locations. Yersinia enterocolitica cells sense an increase in extracellular amino acids (glutamate, glutamine, aspartate, and asparagine) that results in the activation of the type III pathway. Another signal, provided by serum proteins such as albumin, triggers the secretion of YopD into the extracellular medium. The third signal, a decrease in calcium concentration, appears to be provided by host cells and causes Y. enterocolitica to transport YopE and presumably other virulence factors across the eukaryotic plasma membrane. Mutations in several genes encoding regulatory molecules (lcrG, lcrH, tyeA, yopD, yopN, yscM1, and yscM2) bypass the signal requirement of the type III pathway. Together these results suggest that yersiniae may have evolved distinct secretion reactions in response to environmental signals.

Additional Information

© 2001, American Society for Microbiology. Received 5 February 2001/Accepted 7 June 2001 V.T.L. acknowledges support by a fellowship from the National Science Foundation and the Warsaw Family Fellowship. S.K.M. acknowledges support by the Predoctoral Training Program in Genetic Mechanisms at the University of California-Los Angeles (GM07104). This work was supported by U.S. Public Health Service grant AI42797 from the National Institutes of Health-National Institute of Allergy and Infectious Diseases, Infectious Diseases Branch.

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Additional details

Identifiers

PMCID
PMC95371
Eprint ID
6397
Resolver ID
CaltechAUTHORS:LEEjbact01

Funding

NSF Graduate Research Fellowship
Warsaw Family Fellowship
NIH Predoctoral Fellowship
GM07104
NIH
AI42797

Dates

Created
2006-12-07
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Updated
2021-11-08
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