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dc.contributor.authorSoto, Ximena
dc.contributor.authorMayor, Roberto
dc.contributor.authorTorrejon, Marcela
dc.contributor.authorMontecino, Martin A.
dc.contributor.authorHinrichs, Maria Victoria
dc.contributor.authorOlate, Juan
dc.date2022-08-11T08:08:51.000
dc.date.accessioned2022-08-23T16:10:03Z
dc.date.available2022-08-23T16:10:03Z
dc.date.issued2007-07-27
dc.date.submitted2009-02-19
dc.identifier.citationJ Cell Physiol. 2008 Feb;214(2):483-90. <a href="http://dx.doi.org/10.1002/jcp.21228">Link to article on publisher's site</a>
dc.identifier.issn1097-4652 (Electronic)
dc.identifier.doi10.1002/jcp.21228
dc.identifier.pmid17654482
dc.identifier.urihttp://hdl.handle.net/20.500.14038/32846
dc.description.abstractThe 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.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=17654482&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1002/jcp.21228
dc.subjectAnimals; *Body Patterning; Embryo, Nonmammalian; Embryonic Development; GTP-Binding Protein alpha Subunits, Gq-G11; Gastrulation; *Gene Expression Regulation, Developmental; Wnt Proteins; Xenopus laevis; beta Catenin
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleGalphaq negatively regulates the Wnt-beta-catenin pathway and dorsal embryonic Xenopus laevis development
dc.typeJournal Article
dc.source.journaltitleJournal of cellular physiology
dc.source.volume214
dc.source.issue2
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/1400
dc.identifier.contextkey727653
html.description.abstract<p>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.</p>
dc.identifier.submissionpathgsbs_sp/1400
dc.contributor.departmentDepartment of Cell Biology
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.source.pages483-90


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