The very late promoter-driven ptp transcription can rescue the ELA-defective phenotype of a ptp-disrupted BmNPV

Abstract

Wipfelkrankheit is a baculovirus-induced disease that causes caterpillars to migrate to the upper foliage of a plant, where they subsequently die. However, this enhanced locomotory activity (ELA) is not induced in Bombyx mori larvae infected with a mutant Bombyx mori nucleopolyhedrovirus (BmNPV) lacking a functional protein tyrosine phosphatase (ptp) gene. Previous studies have shown that BmNPV utilizes the PTP protein to establish adequate infection for ELA as a budded virus (BV)-associated structural protein rather than as an enzyme phosphatase. In this study, I investigated the importance of the stage when ptp is transcribed during virus-induced ELA. I generated a BmNPV mutant with a polyhedrin (polh) promoter-driven ptp gene in the polh locus, instead of with the endogenous ptp gene. This mutant induced typical ELA, which is similar to that observed upon infection with a control virus, indicating that the very late stage expression of the PTP protein is sufficient for ELA induction in BmNPV-infected larvae. The observation that this mutant recruited PTP protein to BVs strongly suggested PTP localization in BV to be crucial for ELA induction by BmNPV.