Syncytia generated by hemagglutinin-neuraminidase and fusion proteins of virulent Newcastle disease virus induce complete autophagy by activating AMPK-mTORC1-ULK1 signaling >

文献类型： 外文期刊

第一作者： Ren, Shanhui

作者： Ren, Shanhui;Rehman, Zaib Ur;Shi, Mengyu;Qu, Yurong;Yang, Xiao Feng;Shao, Qi;Meng, Chunchun;Sun, Yingjie;Ding, Chan;Yang, Bin;Yang, Zengqi;Gao, Xiaolong;Ding, Chan

作者机构：

关键词： Fusion protein; Hemagglutinin-neuraminidase protein; Autophagy; Newcastle disease virus

期刊名称：VETERINARY MICROBIOLOGY （ 影响因子：3.293； 五年影响因子：3.599 ）

ISSN： 0378-1135

年卷期： 2019 年 230 卷

页码：

收录情况： SCI

摘要： Autophagy triggered by glycoprotein-mediated membrane fusion has been reported for several paramyxoviruses. However, the function of HN and F glycoproteins of NDV and their role in autophagy induction have not been studied. Here, we found that co-transfection of HN and F of virulent NDV rapidly induced syncytium formation and triggered a steady state autophagy flux in adenocarcinomic human alveolar basal epithelial (A549) cells and chicken embryo fibroblast (DF-1) cells. Furthermore, we clearly identified that F and HN synergistically induced autophagosome fusion with lysosomes for subsequent degradation. The seven cleavage site mutations of F significantly decreased the autophagy induction, compared with those of wildtype virulent F. RNAi and pharmacological experiments suggested that autophagy benefitted membrane fusion and syncytium formation induced by F and HN of NDV. Activated F-1 co-operated with HN to stimulate AMPK kinase and downstream ULK1 activation to suppress mTORC1 signaling. Our data described the synergistic role of HN and F in the induction of completed autophagic flux through the activation of AMPK- mTORC1- ULK1 pathway.

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