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.

杆状病毒的显着能力是过表达非常晚期的基因，但机制尚不清楚。在这里，我们报道了杆状病毒编码的丝氨酸/苏氨酸激酶PK1对非常晚的基因过度表达的影响。PK1基因敲除不会完全破坏很晚的基因表达，但会下调过度表达。那些在体外表现出激酶活性的截短的PK1可以挽救非常晚的高表达的下降，而其他截短的PK1和没有激酶活性的点突变体PK1（D137A）不能挽救非常晚的超表达的下降，这表明PK1调节了非常晚的超表达。通过其激酶活性。另外，那些可以挽救过度表达的PK1突变体能够与含有5'UTR的非常晚的启动子相互作用。根据以上数据，