Traffic jam on the cellular secretory pathway generated by a replication protein from a plant RNA virus.
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 (RCNMV), 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 RCNMV interferes with the cellular secretory pathway. Here, we examined this possibility by using green fluorescent protein-fused rice SCAMP1 and Arabidopsis LRR84A as secretory pathway marker proteins and showed that p27 inhibited the trafficking of these proteins. RCNMV-mediated inhibition of the host secretion pathway and its possible impact on plant-virus interaction are discussed.
Graduate School of Agriculture; Kyoto University; Kyoto, Japan.
Kiwamu
K
Hyodo
Graduate School of Agriculture; Kyoto University; Kyoto, Japan.
Masanori
M
Kaido
Graduate School of Agriculture; Kyoto University; Kyoto, Japan.
Tetsuro
T
Okuno
D012367:RNA, Viral / Q000096:biosynthesis*; D055571:Secretory Pathway; D019183:Tombusviridae / Q000502:physiology*; D014764:Viral Proteins / Q000502:physiology*
D012367:RNA, Viral; D014764:Viral Proteins
Arf1; COPI; COPII; ER; Sar1; golgi; intracellular membrane; membrane trafficking; plant RNA virus; replication protein