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dc.contributor.advisorHabibi, Hamid R.
dc.contributor.authorKlausen, Christian
dc.date.accessioned2005-08-16T17:06:36Z
dc.date.available2005-08-16T17:06:36Z
dc.date.issued2004
dc.identifier.citationKlausen, C. (2004). Signal transduction of gonadotropin-releasing hormone-induced gonadotropin subunit and growth hormone gene expression in the goldfish pituitary (Unpublished doctoral thesis). University of Calgary, Calgary, AB. doi:10.11575/PRISM/17619en_US
dc.identifier.isbn061297748Xen
dc.identifier.urihttp://hdl.handle.net/1880/41674
dc.descriptionBibliography: p. 129-145en
dc.description.abstractBest known for its regulation of the production and secretion of pituitary gonadotropin hormones (GtHs), gonadotropin-releasing hormone (GnRH) is the central regulator of reproduction in all vertebrates. In mammalian and non-mammalian systems, the signaling pathways mediating GnRH-induced GtH and growth hormone (GH, fish only) secretion have been extensively studied. In contrast, much less is known about the mechanisms mediating GnRH-induced GtH subunit gene expression, especially in non­mammalian vertebrates. Moreover, the signaling pathways coupling GnRH receptor activation to increases in GH gene expression have not been investigated in any model system. The purpose of the present study was to investigate the signal transduction pathways that mediate GnRH-induced increases in GtH subunit and GH mRNA levels, with emphasis on the roles of protein kinase C (PKC) and extracellular signal-regulated kinase (ERK). The main hypothesis of this study was that the two native GnRHs use similar signal transduction pathways coupling GnRH receptors to GtH subunit and GH gene expression and release in the goldfish pituitary. Initial experiments revealed significant differences in the time- and dose-related effects of the two GnRHs in vivo and in vitro. Studies were then carried out to investigate the role of PKC in GnRH-induced GtH and GH gene expression in goldfish pituitary cells. Western blot analysis confirmed the presence of conventional, novel and atypical PK Cs in the goldfish pituitary. The results presented in this dissertation suggest a dual role for PKC in the regulation of GtH, but not GH, gene expression. Moreover, the data would appear to refute the hypothesis that conventional and novel PKCs are involved in GnRH-induced GtH and GH gene expression. The involvement of the ERK pathway in GnRH-stimulated GtH and GH gene expression was demonstrated using a combination of Northern and Western blot analysis. Although GnRH-induced GtH and GH gene expression is ERK-dependent, the data suggest a PKC-independent mechanism of activation. Together these results provide novel insights into the complexity and functional-specificity of GnRH signaling with respect to the regulation of secretion and gene expression in gonadotropes and somatotropes.en
dc.format.extentxxi, 187 leaves : ill. ; 30 cm.en
dc.language.isoeng
dc.rightsUniversity of Calgary graduate students retain copyright ownership and moral rights for their thesis. You may use this material in any way that is permitted by the Copyright Act or through licensing that has been assigned to the document. For uses that are not allowable under copyright legislation or licensing, you are required to seek permission.
dc.titleSignal transduction of gonadotropin-releasing hormone-induced gonadotropin subunit and growth hormone gene expression in the goldfish pituitary
dc.typedoctoral thesis
dc.publisher.institutionUniversity of Calgaryen
dc.identifier.doihttp://dx.doi.org/10.11575/PRISM/17619
thesis.degree.nameDoctor of Philosophy
thesis.degree.namePhD
thesis.degree.disciplineBiological Sciences
thesis.degree.grantorUniversity of Calgary
dc.identifier.lccAC1 .T484 2004 K53en
dc.publisher.placeCalgaryen
ucalgary.thesis.notesUARCen
ucalgary.thesis.uarcreleaseyen
ucalgary.item.requestcopytrue
ucalgary.thesis.accessionTheses Collection 58.002:Box 1512 520492029


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University of Calgary graduate students retain copyright ownership and moral rights for their thesis. You may use this material in any way that is permitted by the Copyright Act or through licensing that has been assigned to the document. For uses that are not allowable under copyright legislation or licensing, you are required to seek permission.