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XB-ART-36462
Dev Dyn October 1, 2007; 236 (10): 2844-51.

Endoplasmic reticulum stress induced by tunicamycin disables germ layer formation in Xenopus laevis embryos.

Yuan L , Cao Y , Knöchel W .


Abstract
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.

PubMed ID: 17849439
Article link: Dev Dyn


Species referenced: Xenopus laevis
Genes referenced: ddit3 hspa5 inhba nodal5.2 nodal5.4 odc1 osbpl8 xbp1


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