Hiles Rachel, Rogers Abigail, Jaiswal Namrata, Zhang Weiwei, Butchacas Jules, Merfa Marcus V, Klass Taylor, Barua Pragya, Thirumalaikumar Venkatesh P, Jacobs Jonathan M, Staiger Christopher J, Helm Matthew, Iyer-Pascuzzi Anjali S
Department of Botany and Plant Pathology, and Center for Plant Biology, Purdue University, West Lafayette, Indiana, United States of America.
EMBRIO Institute, Purdue University, West Lafayette, Indiana, United States of America.
PLoS Pathog. 2024 Dec 26;20(12):e1012814. doi: 10.1371/journal.ppat.1012814. eCollection 2024 Dec.
Cellular responses to biotic stress frequently involve signaling pathways that are conserved across eukaryotes. These pathways include the cytoskeleton, a proteinaceous network that senses external cues at the cell surface and signals to interior cellular components. During biotic stress, dynamic cytoskeletal rearrangements serve as a platform from which early immune-associated processes are organized and activated. Bacterial pathogens of plants and animals use proteins called type III effectors (T3Es) to interfere with host immune signaling, thereby promoting virulence. We previously found that RipU, a T3E from the soilborne phytobacterial pathogen Ralstonia solanacearum, co-localizes with the plant cytoskeleton. Here, we show that RipU from R. solanacearum K60 (RipUK60) associated with and altered the organization of both the actin and microtubule cytoskeleton. We found that pharmacological disruption of the tomato (Solanum lycopersicum) cytoskeleton promoted R. solanacearum K60 colonization. Importantly, tomato plants inoculated with R. solanacearum K60 lacking RipUK60 (ΔripUK60) had reduced wilting symptoms and significantly reduced root colonization when compared to plants inoculated with wild-type R. solanacearum K60. Collectively, our data suggest that R. solanacearum K60 uses the type III effector RipUK60 to remodel cytoskeletal organization, thereby promoting pathogen virulence.
细胞对生物胁迫的反应通常涉及真核生物中保守的信号通路。这些通路包括细胞骨架，它是一个蛋白质网络，能在细胞表面感知外部线索并向细胞内部成分发出信号。在生物胁迫期间，动态的细胞骨架重排充当了一个平台，早期免疫相关过程在此平台上得以组织和激活。动植物的细菌病原体利用一种称为III型效应子（T3E）的蛋白质来干扰宿主免疫信号传导，从而增强毒力。我们之前发现，来自土壤传播的植物病原菌青枯雷尔氏菌的T3E RipU与植物细胞骨架共定位。在此，我们表明青枯雷尔氏菌K60（RipUK60）的RipU与肌动蛋白和微管细胞骨架的组织相关并改变了其组织。我们发现，番茄（Solanum lycopersicum）细胞骨架的药理学破坏促进了青枯雷尔氏菌K60的定殖。重要的是，与接种野生型青枯雷尔氏菌K60的植物相比，接种缺乏RipUK60（ΔripUK60）的青枯雷尔氏菌K60的番茄植株枯萎症状减轻，根部定殖显著减少。总体而言，我们的数据表明，青枯雷尔氏菌K60利用III型效应子RipUK60重塑细胞骨架组织，从而增强病原体的毒力。
