Many bacterial plant pathogens employ a type III secretion system to inject effector proteins within plant cells to suppress plant immunity. Whether and how effector proteins also co-opt plant metabolism to support extensive bacterial replication remains an open question. Here, we show that Ralstonia solanacearum, the causal agent of bacterial wilt disease, secretes the effector protein RipI, which interacts with plant glutamate decarboxylases (GADs) to alter plant metabolism and support bacterial growth. GADs are activated by calmodulin and catalyze the biosynthesis of gamma-aminobutyric acid (GABA), an important signaling molecule in plants and animals. RipI promotes the interaction of GADs with calmodulin, enhancing the production of GABA. R. solanacearum is able to replicate efficiently using GABA as a nutrient, and both RipI and plant GABA contribute to a successful infection. This work reveals a pathogenic strategy to hijack plant metabolism for the biosynthesis of nutrients that support microbial growth during plant colonization.

许多细菌性植物病原体采用III型分泌系统将效应蛋白注入植物细胞内，从而抑制植物免疫力。效应蛋白是否以及如何共同吸收植物代谢以支持广泛的细菌复制仍是一个悬而未决的问题。在这里，我们显示了青枯菌（Ralstonia solanacearum）是细菌性枯萎病的病因，它分泌效应蛋白RipI，该蛋白与植物谷氨酸脱羧酶（GADs）相互作用以改变植物的代谢并支持细菌的生长。GAD被钙调蛋白激活，并催化γ-氨基丁酸（GABA）的生物合成，γ-氨基丁酸是动植物中的重要信号分子。RipI促进GAD与钙调蛋白的相互作用，从而提高GABA的产生。青枯菌能够使用GABA作为营养素有效复制，RipI和植物GABA均可成功感染。这项工作揭示了一种劫持植物新陈代谢的致病策略，以支持植物定居过程中支持微生物生长的营养素的生物合成。