Premium
Endoplasmic reticulum stress induced by tunicamycin disables germ layer formation in Xenopus laevis embryos
Author(s) -
Yuan Li,
Cao Ying,
Knöchel Walter
Publication year - 2007
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.21299
Subject(s) - biology , tunicamycin , endoplasmic reticulum , microbiology and biotechnology , unfolded protein response , activin type 2 receptors , mesoderm , xenopus , medicine , endocrinology , embryonic stem cell , tgf beta signaling pathway , genetics , transforming growth factor , gene
Maintenance of endoplasmic reticulum (ER) homeostasis is essential for correct protein targeting and secretion. ER stress caused by accumulation of unfolded or misfolded proteins leads to disruption of cellular functions. We have investigated the effect of ER stress on Xenopus embryogenesis. ER stress induced by tunicamycin (TM) treatment of embryos resulted in defects affecting germ layer formation. We observed up‐regulation of ER stress response genes, enhanced cytoplasmic splicing of xXBP1 RNA, and increased rate of apoptosis. In animal cap assays, TM treatment inhibited mesoderm formation induced by overexpression of activin/nodal RNA but did not affect mesoderm formation induced by functional activin protein, suggesting that dysfunction of ER caused a failure in activin/nodal processing and/or secretion. The observation that activin protein renders mesoderm formation under ER stress strengthens the role of activin/nodal for mesoderm induction. The results underline the functional significance of ER homeostasis in germ layer formation during Xenopus embryogenesis. Developmental Dynamics 236:2844–2851, 2007 © 2007 Wiley‐Liss, Inc.