数字农科院2.0

Autophagy is induced by swine acute diarrhea syndrome coronavirus through the cellular IRE1-JNK-Beclin 1 signaling pathway after an interaction of viral membrane-associated papain-like protease and GRP78

文献类型： 外文期刊

作者： Da Shi;Ling Zhou;Hongyan Shi;Jiyu Zhang;Jialin Zhang;Liaoyuan Zhang;Dakai Liu;Tingshuai Feng;Miaomiao Zeng;Jianfei Chen;Xin Zhang;Mei Xue;Zhaoyang Jing;Jianbo Liu;Zhaoyang Ji;Haojie He;Longjun Guo;Yang Wu;Jingyun Ma;Li Feng

作者机构：

期刊名称： PLoS pathogens

ISSN： 1553-7374

年卷期： 2023 年 19 卷 3 期

页码：

收录情况： SCIE（2023版）

摘要： Autophagy plays an important role in the infectious processes of diverse pathogens. For instance, cellular autophagy could be harnessed by viruses to facilitate replication. However, it is still uncertain about the interplay of autophagy and swine acute diarrhea syndrome coronavirus (SADS-CoV) in cells. In this study, we reported that SADS-CoV infection could induce a complete autophagy process both in vitro and in vivo, and an inhibition of autophagy significantly decreased SADS-CoV production, thus suggesting that autophagy facilitated the replication of SADS-CoV. We found that ER stress and its downstream IRE1 pathway were indispensable in the processes of SADS-CoV-induced autophagy. We also demonstrated that IRE1-JNK-Beclin 1 signaling pathway, neither PERK-EIF2S1 nor ATF6 pathways, was essential during SADS-CoV-induced autophagy. Importantly, our work provided the first evidence that expression of SADS-CoV PLP2-TM protein induced autophagy through the IRE1-JNK-Beclin 1 signaling pathway. Furthermore, the interaction of viral PLP2-TMF451-L490 domain and substrate-binding domain of GRP78 was identified to activate the IRE1-JNK-Beclin 1 signaling pathway, and thus resulting in autophagy, and in turn, enhancing SADS-CoV replication. Collectively, these results not only showed that autophagy promoted SADS-CoV replication in cultured cells, but also revealed that the molecular mechanism underlying SADS-CoV-induced autophagy in cells.

分类号：

  • 相关文献
作者其他论文 更多>>