Autographa californica multiple nucleopolyhedrovirus PK1 is a factor that regulates high-level expression of very late genes in viral infection

- PK1 knockout does not completely disrupt very late gene expression.
- PK1 knockout down regulates very late gene hyperexpression.
- The catalytic domain of PK1 is essential to very late gene hyperexpression.
- PK1 interacts with very late promoter with 5′ UTR containing burst sequence.
- Kinase activity of PK1 is involved in very late hyperexpression and infectivity.

The remarkable ability of baculovirus is to hyperexpress very late genes, but the mechanisms remain unclear. Here we report the effect of PK1, a baculovirus-encoded serine/threonine kinase, on very late gene hyperexpression. PK1 knockout does not completely disrupt very late gene expression, but down regulates the hyperexpression. Those truncated PK1s that exhibit kinase activity in vitro rescue the decline of very late hyperexpression, while other truncated PK1s and a point mutant PK1 (D137A) without kinase activity fail to rescue the decline of very late hyperexpression, suggesting that PK1 regulates very late gene expression by its kinase activity. In addition, those PK1 mutants that can rescue the hyperexpression are able to interact with very late promoter containing 5′ UTR. Based on the above data, we hypothesize that PK1 binds to very late promoter containing 5′ UTR to regulate the hyperexpression of very late genes by its kinase activity.