Abstract
Autophagy, as a conserved protein degradation pathway in plants, has also been reported to be intricately associated with antiviral defense mechanisms. However, the relationship between chilli veinal mottle virus (ChiVMV) and autophagy has not been investigated in the existing research. Here, we reveal that ChiVMV infection caused the accumulation of autophagosomes in infected Nicotiana benthamiana leaves and the upregulation of autophagy-related genes (ATGs). Moreover, the changes in gene expression were correlated with the development of symptoms. Treatment with autophagy inhibitors (3-MA or E-64D) could increase the infection sites and facilitate virus infection, whereas treatment with the autophagy activator (Rapamycin) limited virus infection. Then, ATG8f was identified to interact with ChiVMV 6K2 protein directly in vitro and in vivo. The silencing of ATG8f promoted virus infection, whereas the overexpression of ATG8f inhibited virus infection. Furthermore, the expression of 6K2-GFP in ATG8f- or ATG7-silenced plants was significantly higher than that in control plants. Rapamycin treatment reduced the accumulation of 6K2-GFP in plant cells, whereas treatment with the inhibitor of the ubiquitin pathway (MG132), 3-MA, or E-64D displayed little impact on the accumulation of 6K2-GFP. Thus, our results demonstrated that ATG8f interacts with the ChiVMV 6K2 protein, promoting the degradation of 6K2 through the autophagy pathway.