Abstract
Viral diseases of silkworm are mainly caused by Bombyx mori nucleopolyhedrovirus (BmNPV), B. mori cytoplasmic polyhedrosis virus (BmCPV) and B. mori bidensovirus (BmBDV). The virus alters host cellular pathways to facilitate its proliferation. It is still unclear whether the three silkworm viruses regulate a certain host pathway. Spry is a negative regulator upstream of ERK. In this study, we found that BmSpry was decreased and p-ERK was increased in silkworm after infection with each virus. A transgenic RNAi vector of BmSpry was constructed and used for embryo microinjection to generate the transgenic line Spry-I. The expression of BmSpry was significantly reduced in Spry-I compared to that in non-transgenic silkworm. The viral content and mortality in Spry-I were significantly higher than those in non-transgenic larvae after infection with the three viruses. p-ERK was increased in Spry-I compared to that in non-transgenic control after virus infection. These results suggest that BmSpry is downregulated by multiple different classes of viruses to elevate p-ERK and ensure viral reproduction in the silkworm.
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