1 State Key Laboratory of Rice Biology, Institute of Biotechnology, Zhejiang University , Hangzhou, Zhejiang 310058 , People's Republic of China.
2 Institute of Plant Protection, Jiangsu Academy of Agricultural Sciences , Nanjing 210014 , People's Republic of China.
Philos Trans R Soc Lond B Biol Sci. 2019 Mar 4;374(1767):20180315. doi: 10.1098/rstb.2018.0315.
Rice black-streaked dwarf virus (RBSDV) was known to be transmitted by the small brown planthopper (SBPH) in a persistent, circulative and propagative manner in nature. Here, we show that RBSDV major outer capsid protein (also known as P10) suppresses the protein kinase C (PKC) activity of SBPH through interacting with the receptor for activated protein kinase C 1 (LsRACK1). The N terminal of P10 (amino acids (aa) 1-270) and C terminal of LsRACK1 (aa 268-315) were mapped as crucial for the interaction. Confocal microscopy and subcellular fractionation showed that RBSDV P10 fused to enhanced green fluorescent protein formed vesicular structures associated with endoplasmic reticulum (ER) membranes in Spodoptera frugiperda nine cells. Our results also indicated that RBSDV P10 retargeted the initial subcellular localization of LsRACK1 from cytoplasm and cell membrane to ER and affected the function of LsRACKs to activate PKC. Inhibition of RACK1 by double stranded RNA-induced gene silencing significantly promoted the replication of RBSDV in SBPH. In addition, the PKC pathway participates in the antivirus innate immune response of SBPH. This study highlights that RACK1 negatively regulates the accumulation of RBSDV in SBPH through activating the PKC signalling pathway, and RBSDV P10 changes the subcellular localization of LsRACK1 and affects its function to activate PKC. This article is part of the theme issue 'Biotic signalling sheds light on smart pest management'.
水稻黑条矮缩病毒（RBSDV）被认为是通过持续、循环和增殖的方式在自然中由小褐飞虱（SBPH）传播的。在这里，我们表明 RBSDV 主要外壳蛋白（也称为 P10）通过与蛋白激酶 C（PKC）激活蛋白受体 1（LsRACK1）相互作用来抑制 SBPH 的 PKC 活性。P10 的 N 端（氨基酸（aa）1-270）和 LsRACK1 的 C 端（aa 268-315）被定位为相互作用的关键。共聚焦显微镜和亚细胞分级显示，与增强型绿色荧光蛋白融合的 RBSDV P10 形成与内质网（ER）膜相关的囊泡结构在 Spodoptera frugiperda 9 细胞中。我们的结果还表明，RBSDV P10 将 LsRACK1 的初始亚细胞定位从细胞质和细胞膜重新靶向到 ER，并影响 LsRACKs 激活 PKC 的功能。双链 RNA 诱导的基因沉默抑制 RACK1 显著促进了 SBPH 中 RBSDV 的复制。此外，PKC 途径参与了 SBPH 的抗病毒先天免疫反应。这项研究强调，RACK1 通过激活 PKC 信号通路负调控 SBPH 中 RBSDV 的积累，而 RBSDV P10 改变了 LsRACK1 的亚细胞定位并影响其激活 PKC 的功能。本文是“生物信号揭示智能害虫管理”主题特刊的一部分。
