Traffic jam on the cellular secretory pathway generated by a replication protein from a plant RNA virus

Abstract

Although positive-strand RNA [(+)RNA] viruses have a limited coding capacity, they can replicate efficiently in host cells because of their ability to use host-derived proteins, membranes, lipids, and metabolites, and to rewire cellular trafficking pathways. Previously, we showed that a plant RNA virus, the Red clover necrotic mosaic virus (RCNM V), hijacked Arf1 and Sar1, which are small GTPases that regulate the biogenesis of COPI and COPII vesicles, respectively, for viral RNA replication. These small GTPases are relocated from appropriate subcellular compartments to the viral RNA replication sites by p27 replication protein, which raises the possibility that RCNM V interferes with the cellular secretory pathway. Here, we examined this possibility by using green fluorescent protein-fused rice SCAM P1 and Arabidopsis LRR 84A as secretory pathway marker proteins and showed that p27 inhibited the trafficking of these proteins. RCNM Vmediated inhibition of the host secretion pathway and its possible impact on plant-virus interaction are discussed. © 2014 Landes Bioscience.