Li Huiling, Zhang Yulan, Rao Guibo, Zhang Chongtao, Guan Zhenqiong, Huang Ziyan, Li Shufen, Lozach Pierre-Yves, Cao Sheng, Peng Ke
State Key Laboratory of Virology, Wuhan Institute of Virology, Center for Antiviral Research, Chinese Academy of Sciences, Wuhan 430071, People's Republic of China; University of Chinese Academy of Sciences, Beijing 100049, People's Republic of China.
State Key Laboratory of Virology, Wuhan Institute of Virology, Center for Antiviral Research, Chinese Academy of Sciences, Wuhan 430071, People's Republic of China.
Cell. 2024 Nov 27;187(24):6896-6913.e15. doi: 10.1016/j.cell.2024.09.008. Epub 2024 Oct 3.
Viruses encode strategies to degrade cellular proteins to promote infection and pathogenesis. Here, we revealed that the non-structural protein NSs of Rift Valley fever virus forms a filamentous E3 ligase to trigger efficient degradation of targeted proteins. Reconstitution in vitro and cryoelectron microscopy analysis with the 2.9-Å resolution revealed that NSs forms right-handed helical fibrils. The NSs filamentous oligomers associate with the cellular FBXO3 to form a remodeled E3 ligase. The NSs-FBXO3 E3 ligase targets the cellular TFIIH complex through the NSs-P62 interaction, leading to ubiquitination and proteasome-dependent degradation of the TFIIH complex. NSs-FBXO3-triggered TFIIH complex degradation resulted in robust inhibition of antiviral immunity and promoted viral pathogenesis in vivo. Furthermore, it is demonstrated that NSs can be programmed to target additional proteins for proteasome-dependent degradation, serving as a versatile targeted protein degrader. These results showed that a virulence factor forms a filamentous and programmable degradation machinery to induce organized degradation of cellular proteins to promote viral infection.
病毒编码降解细胞蛋白的策略以促进感染和发病机制。在此,我们揭示了裂谷热病毒的非结构蛋白NSs形成一种丝状E3连接酶,以触发靶向蛋白的有效降解。体外重组以及分辨率为2.9埃的冷冻电子显微镜分析表明,NSs形成右手螺旋纤维。NSs丝状寡聚体与细胞中的FBXO3结合,形成一种重塑的E3连接酶。NSs - FBXO3 E3连接酶通过NSs与P62的相互作用靶向细胞TFIIH复合物,导致TFIIH复合物的泛素化和蛋白酶体依赖性降解。NSs - FBXO3触发的TFIIH复合物降解导致体内抗病毒免疫受到强烈抑制,并促进病毒发病机制。此外,研究表明NSs可被设计用于靶向其他蛋白进行蛋白酶体依赖性降解,作为一种通用的靶向蛋白降解剂。这些结果表明,一种毒力因子形成一种丝状且可编程的降解机制,以诱导细胞蛋白的有序降解,从而促进病毒感染。