State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing 400716, China; Key Laboratory for Sericulture Functional Genomics and Biotechnology of Agricultural Ministry, Southwest University, Chongqing 400716, China.
School of Basic Medicine, Guizhou University of Traditional Chinese Medicine, Guizhou 550002, China.
Pestic Biochem Physiol. 2019 Jun;157:143-151. doi: 10.1016/j.pestbp.2019.03.016. Epub 2019 Mar 27.
Autophagy is a cell adaptive response that involves the process of microbial infections. Our previous study has indicated that Bombyx mori nucleopolyhedrovirus (BmNPV) infection triggers the complete autophagic process in BmN-SWU1 cells, which is beneficial to the viral infection. Autophagy-related (ATG) protein ATG13, as part of the ULK complex (a serine-threonine kinase complex composed of ULK1, ULK2, ATG13, ATG101, and FIP200), is the most upstream component of the autophagy pathway, and how it affects virus infections will improve our understanding of the interaction between the virus and the host. This study has determined that the overexpression of the BmAtg13 gene promotes the expression of viral genes and increases viral production in BmN-SWU1 cells, whereas knocking down the BmAtg13 gene suppresses BmNPV replication. Moreover, the BmAtg13 overexpression transgenic line contributed to viral replication and increased mortality rate of BmNPV infection. In contrast, the BmAtg13 knockout transgenic line reduced viral replication 96 h post-infection. Furthermore, BmATG13 directly interacted with viral protein BRO-B, forming a protein complex. Taken together, the findings of this study suggest that BmATG13 may be utilized by the BRO-B protein to promote BmNPV replication and proliferation, which, in turn, provides important insights into the mechanism that autophagy influences viral infection.
自噬是一种细胞适应性反应，涉及微生物感染过程。我们之前的研究表明，家蚕核型多角体病毒（BmNPV）感染会触发 BmN-SWU1 细胞中完整的自噬过程，这有利于病毒感染。自噬相关（ATG）蛋白 ATG13 作为 ULK 复合物（由 ULK1、ULK2、ATG13、ATG101 和 FIP200 组成的丝氨酸-苏氨酸激酶复合物）的一部分，是自噬途径中最上游的成分，它如何影响病毒感染将有助于我们理解病毒与宿主之间的相互作用。本研究确定，BmAtg13 基因的过表达促进了病毒基因的表达，并增加了 BmN-SWU1 细胞中的病毒产量，而敲低 BmAtg13 基因则抑制了 BmNPV 的复制。此外，BmAtg13 过表达转基因系有助于病毒复制，并增加 BmNPV 感染的死亡率。相比之下，BmAtg13 敲除转基因系在感染后 96 小时减少了病毒复制。此外，BmATG13 可直接与病毒蛋白 BRO-B 相互作用，形成蛋白复合物。综上所述，本研究结果表明，BmATG13 可能被 BRO-B 蛋白利用来促进 BmNPV 的复制和增殖，这反过来为自噬影响病毒感染的机制提供了重要的见解。
