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7月，中国科学院分子植物科学卓越创新中心上海植物逆境生物学研究中心Alberto Macho研究组在Cell Host & Microbe发表了一篇题为A Bacterial Effector Protein Hijacks Plant Metabolism to Support Pathogen Nutrition的文章，揭示了青枯病菌的效应蛋白挟持植物代谢以合成GABA，促进细菌生长和定殖的机制。
摘 要
细菌分泌效应蛋白抑制植物免疫反应。效应蛋白能否利用植物的代谢产物以支持细菌营养尚不清楚。该研究发现青枯病菌的效应蛋白Ripl与植物的谷氨酸脱羧酶（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-氨基丁酸是植物和动物中的重要信号分子。Pipl促进GAD与钙调蛋白的互作，从而增强GABA的产生。青枯病菌利用GABA作为自身繁殖的营养来源，Ripl和植物GABA共同促进细菌的侵染。该研究揭示了病原菌劫持植物新陈代谢以支持细菌营养的致病策略。
Abstract
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 thatRalstonia 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.solanacearumis 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.
论文链接：
/10.1016/j.chom..07.003
