Laodelphax striatellusAtg8 facilitates Rice stripe virus infection in an autophagy-independent manner
Laodelphax striatellusAtg8 facilitates Rice stripe virus infection in an autophagy-independent manner
复制标题
灰飞虱Atg8以不依赖自噬的方式促进水稻条纹病毒感染
DOI：
10.1111/1744-7917.12771
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发表时间：
2020-07-24
期刊：
影响因子：
4
通讯作者：
Zhang，Li-Li
中科院分区：
文献类型：
--
作者：
Yu，Yuan-Ling;Zhang，Meng-Ting;Zhang，Li-Li
水稻条纹病毒（RSV）是水稻条纹病的病原体，其在植物间传播完全依赖于昆虫载体。纹状老年虫是RSV的主要媒介昆虫。在本研究中，我们探讨了RSV感染与l的相互作用。纹状体自噬：昆虫潜在的内在抗病毒机制。我们发现l。纹状体自噬活性对RSV感染无影响；然而，自噬相关- 8 （Atg8）基因显著增强病毒感染。在呼吸道合胞病毒初次感染期间。纹状体中肠，沉默atg8表达可显著降低c - Jun N -末端激酶（p - JNK）的磷酸化；然而，当没有RSV感染时，沉默at8并不会改变‐JNK水平。这些结果表明，at8可能通过允许更多的病毒感染进入细胞来激活JNK机制。我们进一步发现，at8‐缺乏显著减少了RSV在昆虫中肠上皮细胞表面的积累，这表明γ -氨基丁酸受体相关蛋白家族具有受体运输功能。我们以卵黄原蛋白受体（VgR）介导RSV进入卵巢为模型，阐明了at8‐缺乏降低了定位在细胞膜上的VgR的丰度，并干扰了RSV在胚乳区的附着。总的来说，这些结果揭示了l的自噬无关功能。striatellusat8通过增加病毒在感染部位的附着来增强RSV的初始感染。
Rice stripe virus (RSV) is the causative agent of rice stripe disease and is completely dependent on insect vectors for its plant‐to‐plant transmission.Laodelphax striatellusis the major insect vector for RSV. In this study, we explored the interactions between RSV infection andL. striatellusautophagy, a potential intrinsic antiviral mechanism in insects. We found thatL. striatellusautophagic activity did not affect RSV infection; however, the autophagy‐related‐8 (Atg8) gene significantly enhanced virus infection. During RSV initial infection within theL. striatellusmidgut, silencing ofAtg8expression significantly decreased the phosphorylation of c‐Jun N‐terminal kinase (p‐JNK); however, when RSV infection is absent, silencing of Atg8 did not alterp‐JNK levels. These results indicated that Atg8 might activate the JNK machinery by allowing more virus infection into cells. We further revealed thatAtg8‐deficiency significantly decreased RSV accumulation on the surface of the insect midgut epithelial cells, suggesting a receptor trafficking function of the γ‐aminobutyric acid receptor‐associated protein family. Using the RSV ovary entry as a model, in which vitellogenin receptor (VgR) mediates RSV cell entry, we clarified thatAtg8‐deficiency decreased the abundance of VgR localizing on the cytomembrane and disturbed the attachment of RSV in the germarium zones. Collectively, these results revealed an autophagy‐independent function ofL. striatellusAtg8 that enhances RSV initial infection by increasing virus attachment on the infection sites.