Inositol requiring enzyme-1(IRE1)is highly conserved from yeasts to humans.Upon endoplasmic reticulum(ER)stress,IRE1 activates X-box-binding protein 1(XBP1)by unconventional splicing of XBP1 mRNA,which activates unfolded protein response(UPR)to restore ER homeostasis.In mice,IRElαplays an essential role in extraembryonic tissues.However,its precise action during the early stage of development is unknown.In this study,the gain and loss-of-function analyses were used to investigate the function of Xenopus IRElα(xIRElα).The effects of xIRElαduring embryo development were detected with RT-PCR and whole mount in situ hybridization.ER stress was induced by tunicamycin.The apoptotic cells were measured by TUNNEL assays.Although both gain and loss of xIRElαfunction had no significant effect on Xenopus embryogenesis,knockdown of xIRElαcould rescue tunicamycin-induced developmental defects and apoptosis.The finding indicates that xIRElαis not required for embryogenesis but is required for tunicamycin-induced developmental defects and apoptosis in Xenopus laevis. IRE1 activates X-box-binding protein 1 (XBP1) by unconventional splicing of XBP1 mRNA, which activates unfolded protein response (UPR ) to restore ER homeostasis. In mice, IRElαplays an essential role in extraembryonic tissues. However, its precise action during the early stage of development is unknown. In this study, the gain and loss-of-function analyzes were used to investigate the function of Xenopus IRElα (xIRElα). The effects of xIRElαduring embryo development were detected with RT-PCR and whole mount in situ hybridization. ER stress was induced by tunicamycin. apoptotic cells were measured by TUNNEL assays. Although both gain and loss of xIRElαfunction had no significant effect on Xenopus embryogenesis, knockdown of xIRElαcould rescue tunicamycin-induced developmental defects and apoptosis. The finding indicates that xIRElαis not required for embryogenesis but is required for tunicamycin-induced developmental defects and apoptosis in Xenopus laevis.