Galphaq negatively regulates the Wnt-beta-catenin pathway and dorsal embryonic Xenopus laevis development
Graduate School of Biomedical Sciences; Department of Cell Biology
Medical Subject Headings
Animals; *Body Patterning; Embryo, Nonmammalian; Embryonic Development; GTP-Binding Protein alpha Subunits, Gq-G11; Gastrulation; *Gene Expression Regulation, Developmental; Wnt Proteins; Xenopus laevis; beta Catenin
Life Sciences | Medicine and Health Sciences
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/beta-catenin dorsalizing pathway and specifying ventral cell fate. However, the molecular mechanisms involved in this antagonist crosstalk are not known. Since Galphaq 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 (xGalphaq) in dorso-ventral axis embryo patterning. Overexpression of xGalphaq 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 xGalphaq dominant-negative mutant reverted the xGalphaq-induced ventralized phenotype. Finally, we observed that the Wnt8-induced secondary axis formation is reverted by endogenous xGalphaq activation, indicating that it is negatively regulating the Wnt/beta-catenin pathway.
Rights and Permissions
Citation: J Cell Physiol. 2008 Feb;214(2):483-90. Link to article on publisher's site
DOI of Published Version
Journal of cellular physiology
Soto, Ximena; Mayor, Roberto; Torrejon, Marcela; Montecino, Martin A.; Hinrichs, Maria Victoria; and Olate, Juan, "Galphaq negatively regulates the Wnt-beta-catenin pathway and dorsal embryonic Xenopus laevis development" (2007). GSBS Student Publications. 1400.