A plant virus hijacks phosphatidylinositol-3,5-bisphosphate to escape autophagic degradation in its insect vector
A plant virus hijacks phosphatidylinositol-3,5-bisphosphate to escape autophagic degradation in its insect vector
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植物病毒劫持磷脂酰肌醇-3,5-二磷酸以逃避其昆虫载体的自噬降解
DOI：
10.1080/15548627.2022.2116676
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发表时间：
2022-09-11
期刊：
影响因子：
13.3
通讯作者：
Xu, Qiufang
中科院分区：
文献类型：
--
作者：
Wang, Haitao;Zhang, Jianhua;Xu, Qiufang
摘要自噬作为一种抗病毒防御反应，能够启动巨自噬/自噬，而病毒则通过多种途径逃避宿主的自噬降解。然而，很少有人知道病毒是否可以靶向脂质破坏自噬降解。在这里，我们表明，低丰度的信号脂质，磷脂酰肌醇3，5-二磷酸（PtdIns（3，5）P2），是水稻黑条矮缩病毒（RBSDV）所需的逃避自噬降解的昆虫载体灰飞虱。RBSDV与PtdIns（3，5）P2结合并通过其主要衣壳蛋白P10提高其水平，导致抑制自噬并促进病毒繁殖。此外，我们表明PtdIns（3，5）P2通过激活PtdIns（3，5）P2的效应物Trpml（瞬时受体电位阳离子通道，粘磷脂）阻止自噬体和溶酶体的融合来抑制自噬途径。这些发现揭示了植物病毒通过其病毒衣壳蛋白劫持PtdIns（3，5）P2以逃避自噬降解并促进其在昆虫中存活的策略。
ABSTRACT 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)P2), 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)P2 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)P2 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)P2. These findings uncover a strategy whereby a plant virus hijacks PtdIns(3,5)P2 via its viral capsid protein to evade autophagic degradation and promote its survival in insects.