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水稻黑条矮缩病毒编码的 P5-1 调节 SCF E3 连接酶的泛素化活性,抑制茉莉酸信号通路,从而有利于其在水稻中的感染。

Rice black-streaked dwarf virus-encoded P5-1 regulates the ubiquitination activity of SCF E3 ligases and inhibits jasmonate signaling to benefit its infection in rice.

机构信息

State Key Laboratory for Quality and Safety of Agro-products, Institute of Plant Virology, Ningbo University, Ningbo, 315000, China.

State Key Laboratory Breeding Base for Zhejiang Sustainable Pest and Disease Control, Zhejiang Provincial Key Laboratory of Plant Virology, Institute of Virology and Biotechnology, Zhejiang Academy of Agricultural Sciences, Hangzhou, 310021, China.

出版信息

New Phytol. 2020 Jan;225(2):896-912. doi: 10.1111/nph.16066. Epub 2019 Aug 9.

Abstract

SCF (Skp1/Cullin1/F-box) complexes are key regulators of many cellular processes. Viruses encode specific factors to interfere with or hijack these complexes and ensure their infection in plants. The molecular mechanisms controlling this interference/hijack are currently largely unknown. Here, we present evidence of a novel strategy used by Rice black-streaked dwarf virus (RBSDV) to regulate ubiquitination in rice (Oryza sativa) by interfering in the activity of OsCSN5A. We also show that RBSDV P5-1 specifically affects CSN-mediated deRUBylation of OsCUL1, compromising the integrity of the SCF complex. We demonstrate that the expressions of jasmonate (JA) biosynthesis-associated genes are not inhibited, whereas the expressions of JA-responsive genes are down-regulated in transgenic P5-1 plants. More importantly, application of JA to P5-1 transgenic plants did not reduce their susceptibility to RBSDV infection. Our results suggest that P5-1 inhibits the ubiquitination activity of SCF E3 ligases through an interaction with OsCSN5A, and hinders the RUBylation/deRUBylation of CUL1, leading to an inhibition of the JA response pathway and an enhancement of RBSDV infection in rice.

摘要

SCF(Skp1/Cullin1/F-box)复合物是许多细胞过程的关键调节剂。病毒编码特定的因子来干扰或劫持这些复合物,以确保它们在植物中的感染。目前,控制这种干扰/劫持的分子机制在很大程度上尚不清楚。在这里,我们提出了一种新的策略的证据,该策略由水稻黑条矮缩病毒(RBSDV)用于通过干扰 OsCSN5A 的活性来调节水稻(Oryza sativa)中的泛素化。我们还表明,RBSDV P5-1 特异性地影响 CSN 介导的 OsCUL1 的去 RUB 化,从而破坏 SCF 复合物的完整性。我们证明,茉莉酸(JA)生物合成相关基因的表达没有受到抑制,而 JA 反应基因的表达在 P5-1 转基因植物中被下调。更重要的是,JA 处理 P5-1 转基因植物并没有降低它们对 RBSDV 感染的敏感性。我们的结果表明,P5-1 通过与 OsCSN5A 的相互作用抑制 SCF E3 连接酶的泛素化活性,并阻碍 CUL1 的 RUB 化/去 RUB 化,从而抑制 JA 反应途径,并增强水稻中 RBSDV 的感染。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f060/6972624/8e104e4b907f/NPH-225-896-g001.jpg

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