We have found that PVA replication is dependent on phosphorylation of PVA CP by protein kinase CK2 and a functional HSP70/HSP40 host chaperon pathway targeting CP to proteasomal degradation [2]. We propose that a transient translational block formed by non-phosphorylated CP on viral RNA contributes to the switch of viral RNA from translation to replication.
Our results suggest that the dynamics of potyviral protein accumulation is regulated differentially from the 3’end of potato virus A RNA than from the rest of the genome [3], the significance of which would be to satisfy the needs of replication early and particle assembly late in infection. Viral protein genome-linked (VPg) specifically enhance CP accumulation. We want to solve the specific mechanism by which VPg-mediated up-regulation occurs. We have initiated ribos seq experiments in collaboration with Dr. Johannes Hanson (Umeå Plant Sciences Center, Sweden) to answer this question.