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Comparative Large-Scale Analysis of Interactions between Several Crop Species and the Effector Repertoires from Multiple Pathovars of Pseudomonas and Ralstonia^1,[W],[OA]

Genome Center and Department of Plant Sciences, University of California, Davis, California 95616 (T.W., K.S.C., U.P., K.A.C., H.X., A.K., O.O., L.K.M., K.L., R.W.M.); Department of Molecular and Cell Biology, University of Chicago, Chicago, Illinois 60637 (J.J., J.A.C., D.B., B.A.V., J.T.G.); and Department of Plant Pathology, Physiology, and Weed Science, Virginia Tech, Blacksburg, Virginia 24061 (B.A.V.)

Bacterial plant pathogens manipulate their hosts by injection of numerous effector proteins into host cells via type III secretion systems. Recognition of these effectors by the host plant leads to the induction of a defense reaction that often culminates in a hypersensitive response manifested as cell death. Genes encoding effector proteins can be exchanged between different strains of bacteria via horizontal transfer, and often individual strains are capable of infecting multiple hosts. Host plant species express diverse repertoires of resistance proteins that mediate direct or indirect recognition of bacterial effectors. As a result, plants and their bacterial pathogens should be considered as two extensive coevolving groups rather than as individual host species coevolving with single pathovars. To dissect the complexity of this coevolution, we cloned 171 effector-encoding genes from several pathovars of Pseudomonas and Ralstonia. We used Agrobacterium tumefaciens-mediated transient assays to test the ability of each effector to induce a necrotic phenotype on 59 plant genotypes belonging to four plant families, including numerous diverse accessions of lettuce (Lactuca sativa) and tomato (Solanum lycopersicum). Known defense-inducing effectors (avirulence factors) and their homologs commonly induced extensive necrosis in many different plant species. Nonhost species reacted to multiple effector proteins from an individual pathovar more frequently and more intensely than host species. Both homologous and sequence-unrelated effectors could elicit necrosis in a similar spectrum of plants, suggesting common effector targets or targeting of the same pathways in the plant cell.

² Present address: Plant Molecular Genetics Laboratory, Université de Genève, CH–1211 Geneva, Switzerland.

³ Present address: Proinpa Foundation, Casilla 4285, Cochabamba, Bolivia.

The author responsible for distribution of materials integral to the findings presented in this article in accordance with the policy described in the Instructions for Authors (www.plantphysiol.org) is: Richard W. Michelmore (rwmichelmore{at}ucdavis.edu).

^[W] The online version of this article contains Web-only data.

^[OA] Open Access articles can be viewed online without a subscription.

www.plantphysiol.org/cgi/doi/10.1104/pp.109.140251

^* Corresponding author; e-mail rwmichelmore{at}ucdavis.edu.

Received April 21, 2009; accepted June 23, 2009; published July 1, 2009.

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