Abstract

Bacterial diseases are a threat to food security. Most bacterial pathogens inject effector proteins inside plant cells, using a type-III secretion system, to suppress plant immunity. However, whether and how effector proteins co-opt plant metabolism to produce nutrients that support extensive bacterial replication is not understood. In this work, we found that Ralstonia solanacearum, the causal agent of bacterial wilt disease, secretes an effector protein, named RipI, which interacts with host glutamate decarboxylases (GADs) inside plant cells. GADs catalyse the biosynthesis of GABA, and are activated by calmodulin. RipI promotes the interaction of GADs with calmodulin, enhancing the production of GABA. Unlike other pathogens, Ralstonia is able to replicate efficiently using GABA as a nutrient, and requires both RipI and plant GABA to achieve a successful infection. This reveals a pathogenic strategy to hijack plant metabolism for the biosynthesis of nutrients to support microbial growth during plant colonization.

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