Laodelphax striatellus Atg8 facilitates Rice stripe virus infection in an autophagy-independent manner

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 striatellus is the major insect vector for RSV. In this study, we explored the interactions between RSV infection and L. striatellus autophagy, a potential intrinsic antiviral mechanism in insects. We found that the L. striatellus autophagic activity did not affect RSV infection; however, the autophagy-related-8 (Atg8) gene significantly enhanced virus infection. During RSV initial infection within the L. striatellus midgut, silencing of Atg8 expression significantly decreased the phosphorylation of c-Jun N-terminal kinase (p-JNK); however, when RSV infection is absent, silencing of Atg8 did not alter p-JNK level. These results indicated that Atg8 might activate the JNK machinery by allowing more virus infected into cells. We further revealed that Atg8-deficiency significantly decreased RSV accumulation on the surface of the insect midgut epithelial cells, suggesting a receptor trafficking function of the GABARAP family proteins. Using the RSV ovary entry as a model, in which vitellogenin receptor (VgR) mediates RSV cell entry, we clarified that Atg8-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 of L. striatellus Atg8 that enhances RSV initial infection by increasing virus attachment on the infection sites. This article is protected by copyright. All rights reserved.,This article is protected by copyright. All rights reserved.