The roles of mucD and alginate in the virulence of Pseudomonas aeruginosa in plants, nematodes and mice

Authors

  • Peter Yorgey,

    1. Department of Genetics, Harvard Medical School, and Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114, USA.
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    • Microbia, Inc., One Kendall Square, Building 1400W, Cambridge, MA 02139, USA.

  • Laurence G. Rahme,

    1. Department of Surgery, Harvard Medical School, and Department of Surgery, Massachusetts General Hospital and Shriner's Burn Institute, Boston, MA 02114, USA.
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  • Man-Wah Tan,

    1. Department of Genetics, Harvard Medical School, and Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114, USA.
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    • Departments of Genetics, and Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.

  • Frederick M. Ausubel

    Corresponding author
    1. Department of Genetics, Harvard Medical School, and Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114, USA.
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Abstract

We are exploiting the broad host range of the human opportunistic pathogen Pseudomonas aeruginosa strain PA14 to elucidate the molecular basis of bacterial virulence in plants, nematodes, insects and mice. In this report, we characterize the role that two PA14 gene products, MucD and AlgD, play in virulence. MucD is orthologous to the Escherichia coli periplasmic protease and chaperone DegP. DegP homologues are known virulence factors that play a protective role in stress responses in various species. AlgD is an enzyme involved in the biosynthesis of the exopolysaccharide alginate, which is hyperinduced in mucD mutants. A PA14 mucD mutant was significantly impaired in its ability to cause disease in Arabidopsis thaliana and mice and to kill the nematode Caenorhabditis elegans. Moreover, MucD was found to be required for the production of an extracellular toxin involved in C. elegans killing. In contrast, a PA14 algD mutant was not impaired in virulence in plants, nematodes or mice. A mucDalgD double mutant had the same phenotype as the mucD single mutant in the plant and nematode pathogenesis models. However, the mucDalgD double mutant was synergistically reduced in virulence in mice, suggesting that alginate can partially compensate for the loss of MucD function in mouse pathogenesis.

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