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    Galphaq negatively regulates the Wnt-beta-catenin pathway and dorsal embryonic Xenopus laevis development

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    Authors
    Soto, Ximena
    Mayor, Roberto
    Torrejon, Marcela
    Montecino, Martin A.
    Hinrichs, Maria Victoria
    Olate, Juan
    UMass Chan Affiliations
    Department of Cell Biology
    Graduate School of Biomedical Sciences
    Document Type
    Journal Article
    Publication Date
    2007-07-27
    Keywords
    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
    
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    Link to Full Text
    http://dx.doi.org/10.1002/jcp.21228
    Abstract
    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.
    Source
    J Cell Physiol. 2008 Feb;214(2):483-90. Link to article on publisher's site
    DOI
    10.1002/jcp.21228
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/32846
    PubMed ID
    17654482
    Related Resources
    Link to Article in PubMed
    ae974a485f413a2113503eed53cd6c53
    10.1002/jcp.21228
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    Morningside Graduate School of Biomedical Sciences Scholarly Publications

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