A bacterial effector uncovers a metabolic pathway involved in resistance to bacterial wilt disease

Bacterial wilt caused by the soil-borne 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), activated in response to low oxygen and involved in drought stress tolerance, contributes to resistance against bacterial wilt disease. Arabidopsis and tomato 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 resistance to bacterial wilt, and, as it was reported for drought stress tolerance, acetic acid-induced resistance to bacterial wilt seems to be associated with the phytohormone jasmonic acid. This work reveals a metabolic pathway involved in resistance to biotic and abiotic stresses, and a bacterial virulence strategy to promote disease and the completion of the pathogenic life cycle.

由土传病原菌青枯劳尔氏菌（Ralstonia solanacearum）引发的细菌性青枯病是全球范围内极具破坏性的作物病害。该病原菌定植植物宿主后会大量增殖，导致植株萎蔫乃至死亡；受侵染后发生坏死的植物组织随后会成为病原菌的接种源。本研究发现，由丙酮酸脱羧酶（pyruvate decarboxylases, PDCs）介导的植物代谢通路——该通路可被低氧胁迫诱导激活，并参与干旱胁迫耐受——能够正向调控植株对细菌性青枯病的抗性。拟南芥与番茄在受到青枯劳尔氏菌侵染时，会通过提升PDC活性做出响应；而PDC活性缺陷的植株则对细菌性青枯病更为敏感。分别施加PDC通路的底物丙酮酸与产物乙酸，均可增强植株对细菌性青枯病的抗性；且如此前关于干旱胁迫耐受的研究报道所述，乙酸诱导的青枯病抗性似乎与植物激素茉莉酸（jasmonic acid）密切相关。本研究揭示了一条同时参与生物与非生物胁迫抗性的植物代谢通路，以及病原菌借以促进病害发生、完成致病生活史的毒力策略。