Potato virus Y viral protein 6K1 inhibits the interaction between defense proteins during virus infection.

14-3-3 proteins play vital roles in plant defense against various pathogen invasions. To date, how 14-3-3 affects virus infections in plants remains largely unclear. In this study, we found that Nicotiana benthamiana 14-3-3 h interacts with TRANSLATIONALLY CONTROLLED TUMOR PROTEIN (TCTP), a susceptibility factor of potato virus Y (PVY). Silencing of Nb14-3-3 h facilitates PVY accumulation, whereas over-expression of Nb14-3-3 h inhibits PVY replication. The antiviral activities of three Nb14-3-3 h dimerization defective mutants are significantly decreased, indicating that dimerization of Nb14-3-3 h is indispensable for restricting PVY infection. Our results also showed that the mutant Nb14-3-3hE16A, which is capable of dimerizing but not interacting with NbTCTP, has reduced anti-PVY activity; the mutant NbTCTPI65A, which is unable to interact with Nb14-3-3 h, facilitates PVY replication compared to the wild-type NbTCTP, indicating that dimeric Nb14-3-3 h restricts PVY infection by interacting with NbTCTP and preventing its pro-viral function. As a counter-defense, PVY 6K1 interferes with the interaction between Nb14-3-3 h and NbTCTP by competitively binding to Nb14-3-3 h and rescues NbTCTP to promote PVY infection. Our results provide insights into the arms race between plants and potyviruses.