State Key Laboratory of Plant Environmental Resilience, College of Biological Sciences, China Agricultural University, 100193, Beijing, China.
College of Plant Protection, China Agricultural University, 100193, Beijing, China.
Nat Commun. 2023 Jun 29;14(1):3852. doi: 10.1038/s41467-023-39426-0.
Selective autophagy is a double-edged sword in antiviral immunity and regulated by various autophagy receptors. However, it remains unclear how to balance the opposite roles by one autophagy receptor. We previously identified a virus-induced small peptide called VISP1 as a selective autophagy receptor that facilitates virus infections by targeting components of antiviral RNA silencing. However, we show here that VISP1 can also inhibit virus infections by mediating autophagic degradation of viral suppressors of RNA silencing (VSRs). VISP1 targets the cucumber mosaic virus (CMV) 2b protein for degradation and attenuates its suppression activity on RNA silencing. Knockout and overexpression of VISP1 exhibit compromised and enhanced resistance against late infection of CMV, respectively. Consequently, VISP1 induces symptom recovery from CMV infection by triggering 2b turnover. VISP1 also targets the C2/AC2 VSRs of two geminiviruses and enhances antiviral immunity. Together, VISP1 induces symptom recovery from severe infections of plant viruses through controlling VSR accumulation.
选择性自噬是抗病毒免疫的双刃剑，由各种自噬受体调节。然而，目前尚不清楚如何通过一个自噬受体来平衡其相反的作用。我们之前发现一种叫做 VISP1 的病毒诱导小肽，它是一种选择性自噬受体，可以通过靶向抗病毒 RNA 沉默的成分来促进病毒感染。然而，我们在这里表明，VISP1 也可以通过介导抗病毒 RNA 沉默（VSR）的自噬降解来抑制病毒感染。VISP1 将黄瓜花叶病毒（CMV）2b 蛋白作为靶标进行降解，并削弱其对 RNA 沉默的抑制活性。VISP1 的敲除和过表达分别表现出对 CMV 晚期感染的易感性和增强的抗性。因此，VISP1 通过触发 2b 周转，诱导 CMV 感染后的症状恢复。VISP1 还靶向两种花椰菜花叶病毒的 C2/AC2 VSR，并增强抗病毒免疫。总之，VISP1 通过控制 VSR 积累，从植物病毒的严重感染中诱导症状恢复。
