Bracovirus-mediated innexin hemichannel closure in cell disassembly
Chang-Xu Chen,
Hao-Juan He,
Qiu-Chen Cai,
Wei Zhang,
Tian-Chao Kou,
Xue-Wen Zhang,
Shan You,
Ya-Bin Chen,
Tian Liu,
Wei Xiao,
Qi-Shun Zhu,
Kai-Jun Luo
Affiliations
Chang-Xu Chen
School of Life Sciences, Yunnan University, Kunming 650500, P.R. China; Key Laboratory of the University in Yunnan Province for International Cooperation in Intercellular Communications and Regulations, Yunnan University, Kunming 650500, P.R. China; Biocontrol Engineering Research Centre of Crop Disease & Pest in Yunnan Province, Kunming 650500, P. R. China
Hao-Juan He
School of Life Sciences, Yunnan University, Kunming 650500, P.R. China; Key Laboratory of the University in Yunnan Province for International Cooperation in Intercellular Communications and Regulations, Yunnan University, Kunming 650500, P.R. China; Biocontrol Engineering Research Centre of Crop Disease & Pest in Yunnan Province, Kunming 650500, P. R. China
Qiu-Chen Cai
School of Life Sciences, Yunnan University, Kunming 650500, P.R. China; Key Laboratory of the University in Yunnan Province for International Cooperation in Intercellular Communications and Regulations, Yunnan University, Kunming 650500, P.R. China; Biocontrol Engineering Research Centre of Crop Disease & Pest in Yunnan Province, Kunming 650500, P. R. China
Wei Zhang
School of Life Sciences, Yunnan University, Kunming 650500, P.R. China; Key Laboratory of the University in Yunnan Province for International Cooperation in Intercellular Communications and Regulations, Yunnan University, Kunming 650500, P.R. China; Biocontrol Engineering Research Centre of Crop Disease & Pest in Yunnan Province, Kunming 650500, P. R. China
Tian-Chao Kou
School of Life Sciences, Yunnan University, Kunming 650500, P.R. China
Xue-Wen Zhang
School of Life Sciences, Yunnan University, Kunming 650500, P.R. China
Shan You
School of Life Sciences, Yunnan University, Kunming 650500, P.R. China
Ya-Bin Chen
School of Life Sciences, Yunnan University, Kunming 650500, P.R. China
Tian Liu
School of Life Sciences, Yunnan University, Kunming 650500, P.R. China; Key Laboratory of the University in Yunnan Province for International Cooperation in Intercellular Communications and Regulations, Yunnan University, Kunming 650500, P.R. China; Biocontrol Engineering Research Centre of Crop Disease & Pest in Yunnan Province, Kunming 650500, P. R. China
Wei Xiao
School of Life Sciences, Yunnan University, Kunming 650500, P.R. China; Key Laboratory of the University in Yunnan Province for International Cooperation in Intercellular Communications and Regulations, Yunnan University, Kunming 650500, P.R. China
Qi-Shun Zhu
School of Life Sciences, Yunnan University, Kunming 650500, P.R. China; Key Laboratory of the University in Yunnan Province for International Cooperation in Intercellular Communications and Regulations, Yunnan University, Kunming 650500, P.R. China
Kai-Jun Luo
School of Life Sciences, Yunnan University, Kunming 650500, P.R. China; Key Laboratory of the University in Yunnan Province for International Cooperation in Intercellular Communications and Regulations, Yunnan University, Kunming 650500, P.R. China; Biocontrol Engineering Research Centre of Crop Disease & Pest in Yunnan Province, Kunming 650500, P. R. China; Corresponding author
Summary: Cell-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 of Spodoptera litura infected 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.
