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

書誌事項

公開日
2014-04-08
資源種別
journal article
権利情報
  • © 2014 Landes Bioscience
  • This is not the published version. Please cite only the published version.
  • この論文は出版社版でありません。引用の際には出版社版をご確認ご利用ください。
DOI
  • 10.4161/psb.28644
公開者
Landes Bioscience

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説明

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, 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.

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