A bacterial effector protein uncovers a plant metabolic pathway involved in tolerance to bacterial wilt disease

Abstract

Bacterial wilt caused by the soil-borne plant pathogen Ralstonia solanacearum is a devastating disease worldwide. Upon plant colonization, R. solanacearum replicates massively, causing plant wilting and death; collapsed infected tissues then serve as a source of inoculum. In this work, we show that the plant metabolic pathway mediated by pyruvate decarboxylases (PDCs) contributes to plant tolerance to bacterial wilt disease. Arabidopsis and tomato plants respond to R. solanacearum infection by increasing PDC activity, and plants with deficient PDC activity are more susceptible to bacterial wilt. Treatment with either pyruvic acid or acetic acid (substrate and product of the PDC pathway, respectively) enhances plant tolerance to bacterial wilt disease. An effector protein secreted by R. solanacearum, RipAK, interacts with PDCs and inhibits their oligomerization and enzymatic activity. Collectively, our work reveals a metabolic pathway involved in plant resistance to biotic and abiotic stresses, and a bacterial virulence strategy to promote disease and the completion of the pathogenic life cycle.

Keywords: Ralstonia solanacearum; acetic acid; bacterial wilt; pyruvate decarboxylase; pyruvic acid; type-III effector.