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The Molecular Basis of Host Specialization in Bean Pathovars of Pseudomonas syringae

July 2012 , Volume 25 , Number  7
Pages  877 - 888

David A. Baltrus,1 Marc T. Nishimura,2 Kevin M. Dougherty,1 Surojit Biswas,2 M. Shahid Mukhtar,2 Joana Vicente,3 Eric B. Holub,3 and Jeffery L. Dangl2,4,5,6,7

1School of Plant Sciences, The University of Arizona, PO Box 210036, Forbes Building 303, Tucson, AZ 85721-0036, U.S.A.; 2Department of Biology, University of North Carolina (UNC), Chapel Hill, NC 27599, U.S.A.; 3University of Warwick, School of Life Sciences, Wellesbourne Campus, CV35 9EF, U.K.; 4Howard Hughes Medical Institute, 5Curriculum in Genetics and Molecular Biology, 6Carolina Center for Genome Sciences, and 7Department of Microbiology and Immunology, University of North Carolina, Chapel Hill, NC 27599, U.S.A.

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Accepted 4 March 2012.

Biotrophic phytopathogens are typically limited to their adapted host range. In recent decades, investigations have teased apart the general molecular basis of intraspecific variation for innate immunity of plants, typically involving receptor proteins that enable perception of pathogen-associated molecular patterns or avirulence elicitors from the pathogen as triggers for defense induction. However, general consensus concerning evolutionary and molecular factors that alter host range across closely related phytopathogen isolates has been more elusive. Here, through genome comparisons and genetic manipulations, we investigate the underlying mechanisms that structure host range across closely related strains of Pseudomonas syringae isolated from different legume hosts. Although type III secretion-independent virulence factors are conserved across these three strains, we find that the presence of two genes encoding type III effectors (hopC1 and hopM1) and the absence of another (avrB2) potentially contribute to host range differences between pathovars glycinea and phaseolicola. These findings reinforce the idea that a complex genetic basis underlies host range evolution in plant pathogens. This complexity is present even in host–microbe interactions featuring relatively little divergence among both hosts and their adapted pathogens.

© 2012 The American Phytopathological Society