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Variations in type III effector repertoires do not correlate with differences in pathological phenotypes and host range observed for Xanthomonas citri pv. citri pathotypes

Escalon A., Javegny S., Vital K., Vernière C., Noel L.D., Pruvost O., Arlat M., Gagnevin L.. 2012. In : IS-MPMI 2012 XV International Congress, program and abstracts, July 29 (Sun.) - August 2 (Thu), 2012. Kyoto, Japan. Saint-Paul : IS-MPMI, p. 278-279. International Congress on Molecular Plant-Microbe Interactions. 15, 2012-07-29/2012-08-02, Kyoto (Japon).

Xanthomonas citri pv. citri (Xac) is a quarantine bacterium causing Asiatic citrus canker. Strains of Xac are classified as pathogenic variants i.e. pathotypes, according to their host range: strains of pathotype A infect a wide range of rutaceous species, whereas strains of pathotype A*/Aw infect a restricted host range consisting of Mexican lime (C. aurantifolia) and alemow (C. macrophylla). Based on a collection of 55 strains we investigated the role of type III effectors (T3E) in host specialization. By PCR we screened 56 Xanthomonas T3Es and showed that Xac possesses a repertoire of 28 effectors, 24 of which are shared by all strains, while 4 (xopAI, xopAD, xopAG and xopC1) are present only in some A*/ Aw strains. However, their distribution could not account for host specialization. XopAG is present in all Aw strains, but also in three A* strains genetically distant from Aw , and all xopAG-containing strains induced HR-like reactions on grapefruit and sweet orange. A strains are genetically less diverse, induce identical phenotypic responses, and share exactly the same T3Es. Conversely, A*/ Aw strains exhibited a wider genetic diversity in which clades correlated to geographical origin and T3Es repertoire but not to pathogenicity. A*/Aw strains showed a broad range of reactions on several Citrus, but genetically related strains did not share phenotypic responses. Our results showed that A*/Aw strains are more variable (genetically and pathogenetically) than initially expected and that this variability should not be ignored when trying to describe mechanisms involved in the pathogen evolution and host specialization. (Texte intégral)

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