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dc.contributor.authorGarriock, Robert John
dc.creatorGarriock, Robert Johnen_US
dc.date.accessioned2011-12-06T14:10:19Z
dc.date.available2011-12-06T14:10:19Z
dc.date.issued2006en_US
dc.identifier.urihttp://hdl.handle.net/10150/195854
dc.description.abstractThis dissertation is composed of five major chapters. The first is a review of the literature discussing the secreted growth factor Wnt11 with particular interest in the Wnt11-dependent signaling cascades that regulate cell movements, followed by three chapters of research findings, and a final concluding chapter. Wnts are encoded by a family of 19 genes that play roles in development and disease. Homologs of Wnt11 are important regulators of cell movements in gastrulating embryos. In addition to gastrulation, Wnt11 genes show expression in other embryonic tissue including neural crest cells, the heart and the somite. Following the literature review, the first three chapters describe research that studies the roles of Wnt11-signaling during the development of the heart and neural crest. The first one demonstrates that Wnt11-signaling is required for heart morphogenesis. This work also refutes a proposed role for Wnt11 as a heart inducer. Next, the role of Wnt11 homologs is studied in the regulation of cranial and trunk neural crest cell migration. During neural crest development two Wnt genes are redundantly required to regulate cell migration Wnt11 and Wnt11-related (Wnt11-R). Trunk neural crest migration requires Wnt11-R for migration into the dorsal fin. Alternatively, cranial neural crest development predominantly requires Wnt11 while more severe migratory defects are observed when Wnt11 and Wnt11-R are co-inhibited. A final chapter discusses the overall conclusions about the general role that Wnt11 genes play during embryonic development.
dc.language.isoenen_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.titleWnt11-Signaling Regulates Cardiac and Neural Crest Developmenten_US
dc.typetexten_US
dc.typeElectronic Dissertationen_US
dc.contributor.chairKrieg, Paul A.en_US
dc.identifier.oclc137356715en_US
thesis.degree.grantorUniversity of Arizonaen_US
thesis.degree.leveldoctoralen_US
dc.contributor.committeememberKrieg, Paul A.en_US
dc.contributor.committeememberAntin, Parker B.en_US
dc.contributor.committeememberBoitano, Scotten_US
dc.identifier.proquest1655en_US
thesis.degree.disciplineCell Biology & Anatomyen_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.namePh.D.en_US
refterms.dateFOA2018-08-25T11:39:38Z
html.description.abstractThis dissertation is composed of five major chapters. The first is a review of the literature discussing the secreted growth factor Wnt11 with particular interest in the Wnt11-dependent signaling cascades that regulate cell movements, followed by three chapters of research findings, and a final concluding chapter. Wnts are encoded by a family of 19 genes that play roles in development and disease. Homologs of Wnt11 are important regulators of cell movements in gastrulating embryos. In addition to gastrulation, Wnt11 genes show expression in other embryonic tissue including neural crest cells, the heart and the somite. Following the literature review, the first three chapters describe research that studies the roles of Wnt11-signaling during the development of the heart and neural crest. The first one demonstrates that Wnt11-signaling is required for heart morphogenesis. This work also refutes a proposed role for Wnt11 as a heart inducer. Next, the role of Wnt11 homologs is studied in the regulation of cranial and trunk neural crest cell migration. During neural crest development two Wnt genes are redundantly required to regulate cell migration Wnt11 and Wnt11-related (Wnt11-R). Trunk neural crest migration requires Wnt11-R for migration into the dorsal fin. Alternatively, cranial neural crest development predominantly requires Wnt11 while more severe migratory defects are observed when Wnt11 and Wnt11-R are co-inhibited. A final chapter discusses the overall conclusions about the general role that Wnt11 genes play during embryonic development.


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