The role of the phytotoxin coronatine in symptom development and growth in Nicotiana benthamiana
S. CHAKRAVARTHY (1), J. Worley (1), P. Parrish (2), A. Collmer (1) (1) Cornell University, U.S.A.; (2) Davidson College, U.S.A.

Pseudomonas syringae pv. tomato DC3000 causes bacterial speck disease in Nicotiana benthamiana when it carries a deletion of the avirulence gene hopQ1-1. Disease is caused by the action of type III secretion system effectors (T3Es) and the phytotoxin coronatine (COR). COR is formed by linkage of coronafacic acid (CFA) and coronamic acid (CMA). We recently identified the DC3000 cmaL gene as being required for the biosynthesis of CMA. We reported previously the construction of DC3000D28E, a “nearly effectorless” mutant of DC3000. D28E has a deletion of cmaL but a functional cfa operon, which enables this strain to support study of the action of COR in pathogenesis with minimal T3E interference. We restored cmaL to D28E derivatives carrying minimal T3E sets and studied their ability to cause disease symptoms and growth in N. benthamiana. COR caused chlorosis even in the absence of T3Es, but the intensity of symptoms increased with the number of T3Es present in the background. Importantly, COR can act as a marker for the presence of DC3000 colonies in leaf tissues. COR did not contribute to growth in backgrounds containing T3Es. We also used plants with knocked-down expression of genes involved in salicylic acid biosynthesis or vesicle trafficking, which are known to be targeted by COR and/or T3Es. The responses of these immune-compromised plants provided further evidence that the primary impact of COR in DC3000 interactions with N. benthamiana is in symptom development.

Abstract Number: P9-245
Session Type: Poster