摘要：SummaryCell-cell communication is necessary for cellular immune response. Hemichannel closure disrupts communication between intracellular and extracellular environments during polydnavirus-induced immunosuppression in invertebrates. However, the effects of hemichannel closure on cellular immune response are unclear. Here, we examined apoptotic body formation triggered by hemichannel closure in hemocytes ofSpodoptera liturainfected with bracovirus from the parasitic wasp,Microplitis bicoloratus. We showed that Microplitis bicoloratus bracovirus (MbBV) induced apoptotic cell disassembly, accompanied by hemichannel closure. Hemocyte apoptotic body formation was caused by the dysregulation of the innexins (Inxs), Inx1, Inx2, Inx3, and Inx4, during the MbBV-mediated inhibition of pI3K/AKT signaling and activation of caspase-3, which cleaved gap junction Inx proteins. Our results showed that hemichannel opening or closure in response to various stimuli, which induces the modulation of Inx levels, could inhibit or activate apoptotic body formation, respectively. Therefore, the “hemichannel open and close” model may regulate the cellular immune response.Graphical abstractDisplay OmittedHighlights•Microplitis bicoloratus bracovirus (MbBV) induced apoptotic cell disassembly•Apoptotic body formation accompanied innexin hemichannel closure•MbBV suppressed PI3K/AKT signaling and activated caspase-3•Innexin cleavage by activated caspase-3 was involved in hemichannel closureMolecular Biology; Virology
