{"id":{"repo_id":"uiuc","oai_identifier":"oai:www.ideals.illinois.edu:2142/86327"},"canonical_url":"https://search.dev.ndltd.org/etd/uiuc/oai:www.ideals.illinois.edu:2142/86327","repository":{"repo_id":"uiuc","name":"University of Illinois - Urbana-Champaign","base_url":"https://www.ideals.illinois.edu/oai-pmh"},"display":{"title":"Dissecting the Role of Hedgehog Pathway in Murine Gonadal Development","abstract":"\"The main hypothesis of this dissertation was that gonadal Hh signaling, through the putative mammalian GLI proteins, is alone essential and sufficient to induce FLC differentiation. My objective was to address three main questions concerning the role of Hh signaling in gonadal development. In chapter III, I addressed the first question on whether Hh signaling is sufficient to induce FLC differentiation. Indeed, Hh activation led to appearance of ectopic functional FLCs in the ovary. In chapter IV, I addressed the second question on the essential role of GLI and GLI2, as Hh transcriptional activators, to induce FLC development. My data showed that both GLI1 and GLI2 were modulators of Hh to establish FLCs. In chapter V, I addressed the third question on the possible role of GLI3 (as a transcriptional repressor) to silence the Hh pathway in the fetal ovary, which expresses other mammalian Hh genes, such as Shh. The repressor form of GLI3 was expressed in the fetal ovary, and null mutation of Gli3 led to Hh activation and steroidogenic cell appearance. In chapter VI, I used the Hh signaling over-activation as a tool to identify the progenitors of FLCs in the mouse fetal testis. In the appendix, I compiled the data that are not included in chapters III to VI. In the \"\"future directions\"\" section, I provided speculations and ways to further investigate the questions that have been raised though the course my research.\"","abstract_html":""The main hypothesis of this dissertation was that gonadal Hh signaling, through the putative mammalian GLI proteins, is alone essential and sufficient to induce FLC differentiation. My objective was to address three main questions concerning the role of Hh signaling in gonadal development. In chapter III, I addressed the first question on whether Hh signaling is sufficient to induce FLC differentiation. Indeed, Hh activation led to appearance of ectopic functional FLCs in the ovary. In chapter IV, I addressed the second question on the essential role of GLI and GLI2, as Hh transcriptional activators, to induce FLC development. My data showed that both GLI1 and GLI2 were modulators of Hh to establish FLCs. In chapter V, I addressed the third question on the possible role of GLI3 (as a transcriptional repressor) to silence the Hh pathway in the fetal ovary, which expresses other mammalian Hh genes, such as Shh. The repressor form of GLI3 was expressed in the fetal ovary, and null mutation of Gli3 led to Hh activation and steroidogenic cell appearance. In chapter VI, I used the Hh signaling over-activation as a tool to identify the progenitors of FLCs in the mouse fetal testis. In the appendix, I compiled the data that are not included in chapters III to VI. In the ""future directions"" section, I provided speculations and ways to further investigate the questions that have been raised though the course my research."","abstract_has_math":false,"creators":["Barsoum, Ivraym Boshra"],"institution":"University of Illinois at Urbana-Champaign","degree_name":"Ph.D.","degree_level":"Dissertation","degree_discipline":"Cell and Developmental Biology","degree_department":null,"school":null,"contributors":["Henry, Jonathan J."],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2015,"date_issued":"2015-09-28T15:03:21Z","date_published":"2015-09-28T15:03:21Z","updated_at":"2026-07-22T22:26:27Z","subjects":["Biology, Molecular"],"languages":["eng"],"rights":[],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["(MiAaPQ)AAI3391882"],"render_values":[{"text":"(MiAaPQ)AAI3391882","href":null,"code":true}]}]},"links":{"outbound_url":"http://hdl.handle.net/2142/86327","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Henry, Jonathan J."]},{"key":"dc:creator","label":"Author","values":["Barsoum, Ivraym Boshra"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2015-09-28T15:03:21Z","10000-01-01","2009"]},{"key":"dc:type","label":"Dc Type","values":["text"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Cell and Developmental Biology"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Dissertation"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Ph.D."]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["University of Illinois at Urbana-Champaign"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Biology, Molecular"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["eng"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["http://hdl.handle.net/2142/86327","(MiAaPQ)AAI3391882"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["\"The main hypothesis of this dissertation was that gonadal Hh signaling, through the putative mammalian GLI proteins, is alone essential and sufficient to induce FLC differentiation. My objective was to address three main questions concerning the role of Hh signaling in gonadal development. In chapter III, I addressed the first question on whether Hh signaling is sufficient to induce FLC differentiation. Indeed, Hh activation led to appearance of ectopic functional FLCs in the ovary. In chapter IV, I addressed the second question on the essential role of GLI and GLI2, as Hh transcriptional activators, to induce FLC development. My data showed that both GLI1 and GLI2 were modulators of Hh to establish FLCs. In chapter V, I addressed the third question on the possible role of GLI3 (as a transcriptional repressor) to silence the Hh pathway in the fetal ovary, which expresses other mammalian Hh genes, such as Shh. The repressor form of GLI3 was expressed in the fetal ovary, and null mutation of Gli3 led to Hh activation and steroidogenic cell appearance. In chapter VI, I used the Hh signaling over-activation as a tool to identify the progenitors of FLCs in the mouse fetal testis. In the appendix, I compiled the data that are not included in chapters III to VI. In the \"\"future directions\"\" section, I provided speculations and ways to further investigate the questions that have been raised though the course my research.\"","Made available in DSpace on 2015-09-28T15:03:21Z (GMT). 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My objective was to address three main questions concerning the role of Hh signaling in gonadal development. In chapter III, I addressed the first question on whether Hh signaling is sufficient to induce FLC differentiation. Indeed, Hh activation led to appearance of ectopic functional FLCs in the ovary. In chapter IV, I addressed the second question on the essential role of GLI and GLI2, as Hh transcriptional activators, to induce FLC development. My data showed that both GLI1 and GLI2 were modulators of Hh to establish FLCs. In chapter V, I addressed the third question on the possible role of GLI3 (as a transcriptional repressor) to silence the Hh pathway in the fetal ovary, which expresses other mammalian Hh genes, such as Shh. The repressor form of GLI3 was expressed in the fetal ovary, and null mutation of Gli3 led to Hh activation and steroidogenic cell appearance. In chapter VI, I used the Hh signaling over-activation as a tool to identify the progenitors of FLCs in the mouse fetal testis. In the appendix, I compiled the data that are not included in chapters III to VI. In the \"\"future directions\"\" section, I provided speculations and ways to further investigate the questions that have been raised though the course my research.\"","Made available in DSpace on 2015-09-28T15:03:21Z (GMT). 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