Paul R. J.
Michael J. D.
1Department of Biological Sciences and Center for Biotechnology and Genomics, Texas Tech University, Lubbock 79409, U.S.A.; 2Department of Biological Sciences, University of California—San Diego, San Diego, U.S.A.; 3United States Department of Agriculture—Agricultural Research Service Cropping Systems Research Laboratory, Lubbock, TX 79415, U.S.A.; 4Unité de Microbiologie et Genetique, UMR CNRS-INSA-UCB 5122, 69622 Villeurbanne, France; 5School of Allied Health, Texas Tech University Health Sciences Center, Lubbock 79410, U.S.A.; 6Scottish Crop Research Institute, Dundee, Scotland
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Accepted 20 September 2006.
Salicylic acid (SA) is an important signaling molecule in local and systemic plant resistance. Following infection by microbial pathogens and the initial oxidative burst in plants, SA accumulation functions in the amplification of defense gene expression. Production of pathogenesis-related proteins and toxic antimicrobial chemicals serves to protect the plant from infection. Successful microbial pathogens utilize a variety of mechanisms to rid themselves of toxic antimicrobial compounds. Important among these mechanisms are multidrug-resistance pumps that bring about the active efflux of toxic compounds from microbial cells. Here, we show that a combination SA and its precursors, t-cinnamic acid and benzoic acid, can activate expression of specific multidrug efflux pump-encoding genes in the plant pathogen Erwinia chrysanthemi and enhance survival of the bacterium in the presence of model as well as plant-derived antimicrobial chemicals. This ability of plant-pathogenic bacteria to co-opt plant defense-signaling molecules to activate multidrug efflux pumps may have evolved to ensure bacterial survival in susceptible host plants.
© 2007 The American Phytopathological Society