A Surface Protease and the Invasive Character of Plague

A 9.5-kilobase plasmid of Yersinia pestis, the causative agent of plague, is required for high virulence when mice are inoculated with the bacterium by subcutaneous injection. Inactivation of the plasmid gene pla, which encodes a surface protease, increased the median lethal dose of the bacteria for...

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Bibliographic Details
Published in:Science (American Association for the Advancement of Science) 1992-11, Vol.258 (5084), p.1004-1007
Main Authors: Sodeinde, Ola A., Y. V. B. K. Subrahmanyam, Stark, Kimberly, Quan, Thomas, Bao, Youdi, Goguen, Jon D.
Format: Article
Language:English
Subjects:
activators
Amino Acid Sequence
Animals
Bacteria
Bacterial Proteins
Bacteriology
Biological and medical sciences
Colony Count, Microbial
Death
Dosage
enzymatic activity
Escherichia coli - enzymology
Fibrinolysin - chemistry
Fibrinolysin - metabolism
Fundamental and applied biological sciences. Psychology
Genetics
Infections
Injections, Intravenous
Kinetics
Lesions
Lethal dose 50
Liver
Liver - microbiology
Mice
Microbiology
Molecular Sequence Data
Multidisciplinary Sciences
Mutation
Numbers
Pathogenicity, virulence, toxins, bacteriocins, pyrogens, host-bacteria relations, miscellaneous strains
Personality
Physiological aspects
Plague
Plague - microbiology
Plasmids
plasminogen
Plasminogen Activators - genetics
Plasminogen Activators - physiology
proteinase Pla
Recombinant Proteins - metabolism
Rodents
Science & Technology
Science & Technology - Other Topics
Spleen
Spleen - microbiology
Tissue Plasminogen Activator - metabolism
Urokinase-Type Plasminogen Activator - metabolism
Virulence
Virulence (Microbiology)
Yersinia pestis
Yersinia pestis - enzymology
Yersinia pestis - isolation & purification
Yersinia pestis - pathogenicity
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Description
Summary:A 9.5-kilobase plasmid of Yersinia pestis, the causative agent of plague, is required for high virulence when mice are inoculated with the bacterium by subcutaneous injection. Inactivation of the plasmid gene pla, which encodes a surface protease, increased the median lethal dose of the bacteria for mice by a millionfold. Moreover, cloned pla was sufficient to restore segregants lacking the entire pla-bearing plasmid to full virulence. Both pla$^+$ strains injected subcutaneously and pla$^-$ mutants injected intravenously reached high titers in liver and spleen of infected mice, whereas pla$^-$ mutants injected subcutaneously failed to do so even though they establish a sustained local infection at the injection site. More inflammatory cells accumulated in lesions caused by the pla$^-$ mutants than in lesions produced by the pla$^+$ parent. The Pla protease was shown to be a plasminogen activator with unusual kinetic properties. It can also cleave complement C3 at a specific site.
ISSN:0036-8075
1095-9203
DOI:10.1126/science.1439793