The Bombyx mori G protein β subunit 1 (BmGNβ1) gene inhibits BmNPV infection

[Display omitted] •BmGNβ1 gene was cloned and analyzed.•BmGNβ1 was localized to the cytoplasm, downregulated in hemolymph and midgut after BmNPV infection.•BmGNβ1 causing apoptosis and inhibiting the proliferative replication of BmNPV. G protein β subunit 1 (GNβ1) has several functions, including cell growth regulation, the control of second messenger levels, and ion channel switching. Previous transcriptome analyses in our laboratory have shown that BmGNβ1 transcription is reduced following infection with Bombyx mori nucleopolyhedrovirus (BmNPV), but it is unknown what role this gene may have in the host response to BmNPV infection. In this study, the BmGNβ1 gene was cloned using the RACE method. After BmNPV infection, BmGNβ1 was downregulated in Baiyu strains in tissues such as the hemolymph and midgut. Indirect immunofluorescence showed that BmGNβ1 was localized to the cytoplasm. We further constructed a BmGNβ1-pIZ/V5-His-mCherry overexpression plasmid and designed siRNA to evaluate the role of BmGNβ1 in host response to infection. The results showed that BmGNβ1 overexpression inhibited BmNPV proliferation, while knockdown of BmGNβ1 was correlated with increased BmNPV proliferation. The siRNA-mediated reduction of BmGNβ1 was correlated with an increase in BmNPV infection of BmN cells, increased BmNPV vp39 transcription, and reduced survival time of BmNPV-infected B. mori. Overexpression of BmGNβ1 in BmN cells was also correlated with apoptosis and a modification in transcript levels of genes involved in host response to BmNPV infection (PI3K, AKT, Bmp53, BmFOXO, Caspase-1, Bmp21, BmPKN and BmCREB), suggesting that BmGNβ1 may influence the apoptotic host response of infected B. mori through the PI3K-AKT pathway. This study provides potential targets and theoretical support for breeding BmNPV-resistant silkworm varieties.