Abstract：
Bacterial pathogens inject effector proteins inside plant cells to manipulate cellular functions and achieve a successful infection. The soil-borne pathogen Ralstonia solanacearum (Smith), the causal agent of bacterial wilt disease, secretes > 70 different effectors inside plant cells, although only a handful of them have been thoroughly characterized. One of these effectors, named RipI, is required for full R. solanacearum pathogenicity. RipI associates with plant glutamate decarboxylases (GADs) to promote the accumulation of gamma-aminobutyric acid (GABA), which serves as bacterial nutrient. In this work, we found that RipI can also suppress plant immune responses to bacterial elicitors, which seems to be unrelated to the ability of RipI to induce GABA accumulation and plant cell death. A detailed characterization of the RipI features that contribute to its virulence activities identified two residues at the C-terminal domain that mediate RipI interaction with plant GADs and the subsequent promotion of GABA accumulation. These residues are also required for the appropriate homeostasis of RipI in plant cells and the induction of cell death, although they are partially dispensable for the suppression of plant immune responses. Altogether, we decipher and uncouple the virulence activities of an important bacterial effector at the biochemical level.
摘要：
细菌病原体在植物细胞内注射效应蛋白以操纵细胞功能并实现成功感染。土壤传播的病原体青枯菌(史密斯)，青枯病的病原体，植物细胞内分泌>70种不同的效应子，尽管其中只有少数被彻底定性。其中一个效应物，名叫Ripi,是完整的青枯菌致病性所必需的。RipI与植物谷氨酸脱羧酶（GADs）结合以促进γ-氨基丁酸（GABA）的积累，作为细菌营养素。在这项工作中,我们发现RipI还可以抑制植物对细菌诱导子的免疫反应，这似乎与RipI诱导GABA积累和植物细胞死亡的能力无关。对RipI特征的详细表征有助于其毒力活性，鉴定了C末端结构域的两个残基，它们介导RipI与植物GAD的相互作用以及随后促进GABA积累。这些残基对于植物细胞中RipI的适当稳态和诱导细胞死亡也是必需的，尽管它们对于抑制植物免疫反应是部分可有可无的。总之,我们在生化水平上破译和解开重要细菌效应物的毒力活动。
