Key Laboratory of Microbial Resources Collection and Preservation, Ministry of Agriculture and Rural Affairs, Institute of Agricultural Resources and Regional Planning, Chinese Academy of Agricultural Sciences, Beijing 100081, China.
Key Laboratory of Microbial Resources Collection and Preservation, Ministry of Agriculture and Rural Affairs, Institute of Agricultural Resources and Regional Planning, Chinese Academy of Agricultural Sciences, Beijing 100081, China.
J Genet Genomics. 2023 May;50(5):341-352. doi: 10.1016/j.jgg.2022.04.018. Epub 2022 May 18.
Ralstonia solanacearum is a widespread plant bacterial pathogen that can launch a range of type III effectors (T3Es) to cause disease. In this study, we isolate a pathogenic R. solanacearum strain named P380 from tomato rhizosphere. Five out of 12 core T3Es of strain P380 are introduced into Pseudomonas syringae DC3000D36E separately to determine their functions in interacting with plants. DC3000D36E that harbors each effector suppresses FliC-triggered Pti5 and ACRE31 expression, ROS burst, and callose deposition. RipAE, RipU, and RipW elicit cell death as well as upregulate the MAPK cascades in Nicotiana benthamiana. The derivatives RipC1 and RipW but not RipAE fail to suppress ROS burst. Moreover, RipAE and RipW retain the cell death elicitation ability. RipAE and RipW are associated with salicylic acid and jasmonic acid pathways, respectively. RipAE and RipAQ significantly promote the propagation of DC3000D36E in plants. The five core T3Es localize in diverse subcellular organelles of nucleus, plasma membrane, endoplasmic reticulum, and Golgi network. The suppressor of G2 allele of Skp1 is required for RipAE but not RipU-triggered cell death in N. benthamiana. These results indicate that the core T3Es in R. solanacearum play diverse roles in plant-pathogen interactions.
青枯雷尔氏菌是一种广泛分布的植物细菌性病原体,能够产生一系列 III 型效应蛋白(T3E)引起疾病。在本研究中,我们从番茄根际中分离到一株致病青枯雷尔氏菌 P380 菌株。将 P380 菌株的 12 个核心 T3E 中的 5 个分别导入丁香假单胞菌 DC3000D36E 中,以确定它们在与植物相互作用中的功能。携带每个效应物的 DC3000D36E 抑制 FliC 触发的 Pti5 和 ACRE31 表达、ROS 爆发和几丁质沉积。RipAE、RipU 和 RipW 在本氏烟中引发细胞死亡并上调 MAPK 级联反应。RipC1 和 RipW 但不是 RipAE 衍生物不能抑制 ROS 爆发。此外,RipAE 和 RipW 保留了细胞死亡诱导能力。RipAE 和 RipW 分别与水杨酸和茉莉酸途径相关。RipAE 和 RipAQ 显著促进了 DC3000D36E 在植物中的繁殖。这 5 个核心 T3E 定位于细胞核、质膜、内质网和高尔基体等不同的亚细胞细胞器中。Skp1 的 G2 等位基因的抑制物是 RipAE 但不是 RipU 触发本氏烟细胞死亡所必需的。这些结果表明,青枯雷尔氏菌的核心 T3E 在植物-病原体相互作用中发挥着不同的作用。