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...
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Published in: | Journal of cellular physiology Vol. 214; no. 2; pp. 483 - 490 |
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Main Authors: | , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Hoboken
Wiley Subscription Services, Inc., A Wiley Company
01-02-2008
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Online Access: | Get full text |
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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. |
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Bibliography: | ark:/67375/WNG-LH8KQ05H-P CONICYT - No. PBCT ACT44 ArticleID:JCP21228 istex:C1F34F89CF8B1189C86AE8733E59E0E4E90D6498 |
ISSN: | 0021-9541 1097-4652 |
DOI: | 10.1002/jcp.21228 |