IRE1a knockdown rescues tunicamycin-induced developmental defects and apoptosis in Xenopus laevis

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, IRE1a plays 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 IRE1a (xIRE1a). The effects of xIRE1a during 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 xIRE1a function had no significant effect on Xenopus embryogenesis, knockdown of xIRE1a could rescue tunicamycin-induced developmental defects and apoptosis. The finding indicates that xIRE1a is not required for embryogenesis but is required for tunicamycin-induced developmental defects and apoptosis in Xenopus laevis.