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Published on December 17, 2008; 10.1104/pp.108.126870

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Received July 23, 2008
Accepted December 10, 2008

Xanthomonas campestris Overcomes Arabidopsis Stomatal Innate Immunity Through a DSF Cell-cell signal-regulated Virulence Factor

Gustavo E. Gudesblat , Pablo S. Torres , and Adrian A. Vojnov *

Instituto de Ciencia y Tecnologia "Dr. Cesar Milstein", Fundacion Pablo Cassara. Consejo Nacional de Ciencia y Tecnologia (CONICET). Saladillo 2468. C1440FFX Buenos Aires, Argentina

* Corresponding author; email: avojnov{at}fundacioncassara.org.ar.

Pathogen-induced stomatal closure is part of the plant innate immune response. Phytopathogens using stomata as a way of entry into the leaf must avoid the stomatal response of the host. In this work we describe a factor secreted by the bacterial phytopathogen Xanthomonas campestris pv. campestris (Xcc) capable of interfering with stomatal closure induced by bacteria or by abscisic acid (ABA). We found that living Xcc, as well as ethyl acetate extracts from Xcc culture supernatants, are capable of reverting stomatal closure induced by bacteria, lypopolisaccharide or ABA. Xcc ethyl acetate extracts also complemented the infectivity of Pseudomonas syringae pv. tomato (Pst) mutants deficient in the production of the coronatine toxin, which is required to overcome stomatal defense. By contrast, the rpfF and rpfC mutant strains of Xcc, which are unable to respectively synthesize or perceive a diffusible molecule involved in bacterial cell to cell signaling, were incapable of reverting stomatal closure, indicating that suppression of stomatal response by Xcc requires an intact rpf/DSF system. In addition, we found that guard cell-specific Arabidopsis MAP kinase 3 (MPK3) antisense mutants were unresponsive to bacteria or lipopolysaccharide in promotion of stomatal closure, and also more sensitive to Pst coronatine deficient mutants, showing that MPK3 is required for stomatal immune response. Additionally, we found that unlike in wt Arabidopsis, ABA-induced stomatal closure in MPK3 antisense mutants is not affected by Xcc or by extracts from Xcc culture supernatants, suggesting that the Xcc factor might target some signaling component in the same pathway as MPK3.




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