Key Laboratory of South China Sea Fishery Resources Exploitation and Utilization, Ministry of Agriculture and Rural Affairs, South China Sea Fisheries Research Institute, Chinese Academy of Fishery Sciences, Guangzhou, China.
Sanya Tropical Fisheries Research Institute, Sanya, China.
Front Immunol. 2021 May 11;12:682562. doi: 10.3389/fimmu.2021.682562. eCollection 2021.
Most tripartite motif (TRIM) family proteins are critical components of the autophagy machinery and play important roles in host defense against viral pathogens in mammals. However, the roles of TRIM proteins in autophagy and viral infection have not been studied in lower invertebrates, especially crustaceans. In this study, we first identified a gene from (designated ), which, after a white spot syndrome virus (WSSV) challenge, was significantly upregulated at the mRNA and protein levels in the intestine and hemocytes. Knockdown of led to an increase in the WSSV quantity in shrimp, while its overexpression led to a decrease compared with the controls. Autophagy can be induced by WSSV or rapamycin challenge and has been shown to play a positive role in restricting WSSV replication in . The mRNA and protein expression levels of PmTRIM50-like significantly increased with the enhancement of rapamycin-induced autophagy. The autophagy activity induced by WSSV or rapamycin challenge could be inhibited by silencing in shrimp. Further studies showed that rapamycin failed to induce autophagy or inhibit WSSV replication after knockdown of . Moreover, pull-down and ubiquitination assays demonstrated that PmTRIM50-like could interact with WSSV envelope proteins and target them for ubiquitination . Collectively, this study demonstrated that PmTRIM50-like is required for autophagy and is involved in restricting the proliferation of WSSV through its ubiquitination. This is the first study to report the role of a TRIM family protein in virus infection and host autophagy in crustaceans.
大多数三联基序（TRIM）家族蛋白是自噬机制的关键组成部分，在哺乳动物宿主防御病毒病原体方面发挥着重要作用。然而，TRIM 蛋白在自噬和病毒感染中的作用在较低等的无脊椎动物，特别是甲壳类动物中尚未得到研究。在这项研究中，我们首先从 （命名为 ）中鉴定出一个基因，该基因在受到白斑综合征病毒（WSSV）挑战后，在肠道和血细胞中的 mRNA 和蛋白质水平均显著上调。 基因的敲低导致虾体内的 WSSV 数量增加，而过表达则与对照组相比减少。自噬可以被 WSSV 或雷帕霉素诱导，并且已经表明在 中对限制 WSSV 复制具有积极作用。PmTRIM50-like 的 mRNA 和蛋白质表达水平随着雷帕霉素诱导的自噬增强而显著增加。WSSV 或雷帕霉素挑战诱导的自噬可以通过在虾中沉默 来抑制。进一步的研究表明，在 基因敲低后，雷帕霉素无法诱导自噬或抑制 WSSV 复制。此外，下拉和泛素化测定表明，PmTRIM50-like 可以与 WSSV 包膜蛋白相互作用，并将其靶向泛素化。总的来说，这项研究表明 PmTRIM50-like 是自噬所必需的，并且通过其泛素化参与限制 WSSV 的增殖。这是首次报道 TRIM 家族蛋白在甲壳类动物病毒感染和宿主自噬中的作用。
