State Key Laboratory of Rice Biology, Institute of Biotechnology, Zhejiang University, Hangzhou, China.
State Key Laboratory for Biology of Plant Diseases and Insect Pests, Institute of Plant Protection, Chinese Academy of Agricultural Sciences, Beijing, China.
PLoS Pathog. 2021 Mar 4;17(3):e1009370. doi: 10.1371/journal.ppat.1009370. eCollection 2021 Mar.
The movement of plant viruses is a complex process that requires support by the virus-encoded movement protein and multiple host factors. The unfolded protein response (UPR) plays important roles in plant virus infection, while how UPR regulates viral infection remains to be elucidated. Here, we show that rice stripe virus (RSV) elicits the UPR in Nicotiana benthamiana. The RSV-induced UPR activates the host autophagy pathway by which the RSV-encoded movement protein, NSvc4, is targeted for autophagic degradation. As a counteract, we revealed that NSvc4 hijacks UPR-activated type-I J-domain proteins, NbMIP1s, to protect itself from autophagic degradation. Unexpectedly, we found NbMIP1 stabilizes NSvc4 in a non-canonical HSP70-independent manner. Silencing NbMIP1 family genes in N. benthamiana, delays RSV infection, while over-expressing NbMIP1.4b promotes viral cell-to-cell movement. Moreover, OsDjA5, the homologue of NbMIP1 family in rice, behaves in a similar manner toward facilitating RSV infection. This study exemplifies an arms race between RSV and the host plant, and reveals the dual roles of the UPR in RSV infection though fine-tuning the accumulation of viral movement protein.
植物病毒的运动是一个复杂的过程，需要病毒编码的运动蛋白和多种宿主因子的支持。未折叠蛋白反应（UPR）在植物病毒感染中发挥重要作用，而 UPR 如何调节病毒感染仍有待阐明。在这里，我们表明水稻条纹病毒（RSV）在本氏烟中引发 UPR。RSV 诱导的 UPR 通过自噬途径激活宿主，RSV 编码的运动蛋白 NSvc4 被靶向进行自噬降解。作为一种对抗，我们揭示 NSvc4 劫持 UPR 激活的 I 型 J 结构域蛋白 NbMIP1s 来保护自身免受自噬降解。出乎意料的是，我们发现 NbMIP1 以非典型 HSP70 独立的方式稳定 NSvc4。在本氏烟中沉默 NbMIP1 家族基因会延迟 RSV 感染，而过表达 NbMIP1.4b 则促进病毒的细胞间运动。此外，水稻中 NbMIP1 家族的同源物 OsDjA5 也表现出类似的方式促进 RSV 感染。本研究例证了 RSV 和宿主植物之间的一场军备竞赛，并揭示了 UPR 通过精细调节病毒运动蛋白的积累在 RSV 感染中的双重作用。
