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A plant virus hijacks phosphatidylinositol-3,5-bisphosphate to escape autophagic degradation in its insect vector

文献类型： 外文期刊

作者： Wang, Haitao 1 ; Zhang, Jianhua 1 ; Liu, Haoqiu 1 ; Wang, Man 1 ; Dong, Yan 1 ; Zhou, Yijun 1 ; Wong, Sek-Man 2 ; Xu, Kai 4 ; Xu, Qiufang 1 ;

作者机构： 1.Jiangsu Acad Agr Sci, Inst Plant Protect, Key Lab Food Qual & Safety Jiangsu Prov, State Key Lab Breeding Base, Nanjing, Peoples R China

2.Natl Univ Singapore, Dept Biol Sci, Singapore, Singapore

3.Natl Univ Singapore, Res Inst, Suzhou, Peoples R China

4.Nanjing Normal Univ, Coll Life Sci, Jiangsu Key Lab Microbes & Funct Genom, Nanjing, Peoples R China

5.Anhui Normal Univ, Coll Life Sci, Wuhu, Peoples R China

6.Shandong Acad Agr Sci, Inst Ind Crops, Jinan, Peoples R China

关键词： Autophagy; lysosome-autophagosome fusion; PtdIns(3; 5)P-2; RBSDV; trpml

期刊名称：AUTOPHAGY （ 影响因子：13.391； 五年影响因子：16.142 ）

ISSN： 1554-8627

年卷期：

页码：

收录情况： SCI

摘要： Hosts can initiate macroautophagy/autophagy as an antiviral defense response, while viruses have developed multiple ways to evade the host autophagic degradation. However, little is known as to whether viruses can target lipids to subvert autophagic degradation. Here, we show that a low abundant signaling lipid, phosphatidylinositol 3,5-bisphosphate (PtdIns(3,5)P-2), is required for rice black-streaked dwarf virus (RBSDV) to evade the autophagic degradation in the insect vector Laodelphax striatellus. RBSDV binds to PtdIns(3,5)P-2 and elevates its level through its main capsid protein P10, leading to inhibited autophagy and promoted virus propagation. Furthermore, we show that PtdIns(3,5)P-2 inhibits the autophagy pathway by preventing the fusion of autophagosomes and lysosomes through activation of Trpml (transient receptor potential cation channel, mucolipin), an effector of PtdIns(3,5)P-2. These findings uncover a strategy whereby a plant virus hijacks PtdIns(3,5)P-2 via its viral capsid protein to evade autophagic degradation and promote its survival in insects.

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