To establish a systemic infection, plant viruses invade neighboring cells via cell to cell movement trough plasmodesmata channels until they reach the vascular system. This cell to cell movement is an active process involving one or more movement proteins encoded by the virus, which interact with other virus and host factors. Exactly how these movement proteins function is still a mystery in most cases. A new paper in PLoS ONE reveals new details on how this process works for Prunus necrotic ringspot virus (PNRSV), a serious pathogen of cultivated stone fruit trees.
A Plant Virus Movement Protein Regulates the Gcn2p Kinase in Budding Yeast. (2011) PLoS ONE 6(11): e27409. doi:10.1371/journal.pone.0027409
Virus life cycle heavily depends on their ability to command the host machinery in order to translate their genomes. Animal viruses have been shown to interfere with host translation machinery by expressing viral proteins that either maintain or inhibit eIF2α function by phosphorylation. However, this interference mechanism has not been described for any plant virus yet. Prunnus necrotic ringspot virus (PNRSV) is a serious pathogen of cultivated stone fruit trees. The movement protein (MP) of PNRSV is necessary for the cell-to-cell movement of the virus. By using a yeast-based approach we have found that over-expression of the PNRSV MP caused a severe growth defect in yeast cells. cDNA microarrays analysis carried out to characterise at the molecular level the growth interference phenotype reported the induction of genes related to amino acid deprivation suggesting that expression of MP activates the GCN pathway in yeast cells. Accordingly, PNRSV MP triggered activation of the Gcn2p kinase, as judged by increased eIF2α phosphorylation. Activation of Gcn2p by MP expression required a functional Tor1p kinase, since rapamycin treatment alleviated the yeast cell growth defect and blocked eIF2α phosphorylation triggered by MP expression. Overall, these findings uncover a previously uncharacterised function for PNRSV MP viral protein, and point out at Tor1p and Gcn2p kinases as candidate susceptibility factors for plant viral infections.