Gαq negatively regulates the Wnt-β-catenin pathway and dorsal embryonic Xenopus laevis development

The non‐canonical Wnt/Ca2+ signaling pathway has been implicated in the regulation of axis formation and gastrulation movements during early Xenopus laevis embryo development, by antagonizing the canonical Wnt/β‐catenin dorsalizing pathway and specifying ventral cell fate. However, the molecular mec...

Full description

Saved in:
Bibliographic Details
Published in:Journal of cellular physiology Vol. 214; no. 2; pp. 483 - 490
Main Authors: Soto, Ximena, Mayor, Roberto, Torrejón, Marcela, Montecino, Martín, Hinrichs, María Victoria, Olate, Juan
Format: Journal Article
Language:English
Published: Hoboken Wiley Subscription Services, Inc., A Wiley Company 01-02-2008
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:The non‐canonical Wnt/Ca2+ signaling pathway has been implicated in the regulation of axis formation and gastrulation movements during early Xenopus laevis embryo development, by antagonizing the canonical Wnt/β‐catenin dorsalizing pathway and specifying ventral cell fate. However, the molecular mechanisms involved in this antagonist crosstalk are not known. Since Gαq is the main regulator of Ca2+ signaling in vertebrates and from this perspective probably involved in the events elicited by the non‐canonical Wnt/Ca2+ pathway, we decided to study the effect of wild‐type Xenopus Gq (xGαq) in dorso‐ventral axis embryo patterning. Overexpression of xGαq or its endogenous activation at the dorsal animal region of Xenopus embryo both induced a strong ventralized phenotype and inhibited the expression of dorsal‐specific mesoderm markers goosecoid and chordin. Dorsal expression of an xGαq dominant‐negative mutant reverted the xGαq‐induced ventralized phenotype. Finally, we observed that the Wnt8‐induced secondary axis formation is reverted by endogenous xGαq activation, indicating that it is negatively regulating the Wnt/β‐catenin pathway. J. Cell. Physiol. 214: 483–490, 2008. © 2007 Wiley‐Liss, Inc.
Bibliography:ark:/67375/WNG-LH8KQ05H-P
CONICYT - No. PBCT ACT44
ArticleID:JCP21228
istex:C1F34F89CF8B1189C86AE8733E59E0E4E90D6498
ISSN:0021-9541
1097-4652
DOI:10.1002/jcp.21228