Involvement of coronatine-inducible reactive oxygen species in bacterial speck disease of tomato

Abstract

Pseudomonas syringae pv. tomato DC3000 (Pst DC3000) produces a chlorosis-inducing phytotoxin coronatine (COR), which has multiple virulence functions in planta. One of the hallmarks of bacterial speck disease on tomato leaves is the formation of necrotic lesions surrounded by chlorosis. The physiological significance of COR-induced chlorosis in disease development is still unknown. In our recent publication in New Phytologist, we demonstrated that COR-induced effects on photosynthetic machinery resulted in the accumulation of reactive oxygen species (ROS). Tomato seedlings inoculated with Pst DC3000 and incubated in light showed more disease-associated necrotic cell death than inoculated seedlings incubated in either dark or low light conditions. Furthermore, COR suppressed the expression of thylakoid-localized Cu/Zn superoxide dismutase (Cu/Zn SOD), but not the cytosolic-localized Cu/Zn SOD. In this addendum, we propose a model for the function of COR as a regulator of plant ROS production in different cellular sites leading to disease-associated necrotic cell death during bacterial speck of tomato.

This article refers to:

Acknowledgements

C. Bender acknowledges support from National Science Foundation grant IBN-0620469 and the Oklahoma Agricultural Experiment Station. Y. Ishiga was supported by a postdoctoral fellowship from the Japan Society for the Promotion of Science (JSPS). The OSU Microarray Core Facility was supported by grants from NSF (EOS-0132534) and NIH (1P20RR16478-02 and 5P20RR15564-03).

Figures and Tables

Figure 1 Bacterial growth of P. syringae pv. tomato DC3000 (Pst DC3000) and the COR defective-mutant DB29 in tomato seedlings leaves pretreated with diphenylene inodonium (DPI), which inhibits the activity of membrane-bound NADPH oxidase. Seedlings were inoculated with Pst DC3000 or DB29 following pretreatment with water (control) or DPI (20 mM) for 24 h. The population of Pst DC3000 were measured at 0 days post-inoculation (dpi) and 4 dpi. Vertical bars indicate the standard error for three independent experiments.

Figure 2 A model for the virulence function of COR in the pathogenicity of P. syringae pv. tomato DC3000 (Pst DC3000). COR from Pst DC3000 regulates both cytosolic and chloroplast ROS homeostasis, and COR-inducible ROS might function with T3SS effector proteins to induce disease-associated cell death.

Addendum to: