{"id":{"repo_id":"ecu","oai_identifier":"oai:thescholarship.ecu.edu:10342/7078"},"canonical_url":"https://search.dev.ndltd.org/etd/ecu/oai:thescholarship.ecu.edu:10342/7078","repository":{"repo_id":"ecu","name":"East Carolina University","base_url":"https://thescholarship.ecu.edu/server/oai/request"},"display":{"title":"The Role of Differential Sensitivity to Retinoic Acid (RA) in Regulating Spermatogonial Fate","abstract":"In the mammalian testis, the foundation of spermatogenesis is provided by spermatogonial stem cells (SSCs); their progeny either remain as stem cells (following a self-renewal division) or proliferate as undifferentiated progenitors prior to differentiating in response to retinoic acid (RA) and later entering meiosis. The mechanisms regulating spermatogonial response to RA are undefined, and their identification would represent a key advance in our understanding of how spermatogonial fate is determined both at the beginning of spermatogenesis and throughout the male reproductive lifespan. This dissertation summarizes the results of an investigation into elusive mechanisms regulating a key switch fundamental to spermatogonial fate, the capacity of spermatogonia to respond to RA. The results support a novel model by which mammalian prospermatogonial and spermatogonial fates are regulated by intrinsic capacity to respond (or not) to the differentiation signal provided by RA prior to and concurrent with the initiation of spermatogenesis.","abstract_html":"In the mammalian testis, the foundation of spermatogenesis is provided by spermatogonial stem cells (SSCs); their progeny either remain as stem cells (following a self-renewal division) or proliferate as undifferentiated progenitors prior to differentiating in response to retinoic acid (RA) and later entering meiosis. The mechanisms regulating spermatogonial response to RA are undefined, and their identification would represent a key advance in our understanding of how spermatogonial fate is determined both at the beginning of spermatogenesis and throughout the male reproductive lifespan. This dissertation summarizes the results of an investigation into elusive mechanisms regulating a key switch fundamental to spermatogonial fate, the capacity of spermatogonia to respond to RA. The results support a novel model by which mammalian prospermatogonial and spermatogonial fates are regulated by intrinsic capacity to respond (or not) to the differentiation signal provided by RA prior to and concurrent with the initiation of spermatogenesis.","abstract_has_math":false,"creators":["Velte, Ellen Kay"],"institution":"East Carolina University","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":"Anatomy and Cell Biology","school":null,"contributors":[],"advisors":["Geyer, Christopher B"],"committee_chairs":[],"committee_members":[],"year":2018,"date_issued":"2018-12-10","date_published":"2018-12-10","updated_at":"2026-07-24T02:13:47Z","subjects":["retinoic acid","CYP26","talarozole"],"languages":["en"],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"http://hdl.handle.net/10342/7078","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor.advisor","label":"Advisor","values":["Geyer, Christopher B"]},{"key":"dc:contributor.department","label":"Department","values":["Anatomy and Cell Biology"]},{"key":"dc:creator","label":"Author","values":["Velte, Ellen Kay"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2019-02-15T13:32:57Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2020-12-01T09:01:54Z"]},{"key":"dc:date.issued","label":"Date","values":["2018-12-10"]},{"key":"dc:publisher","label":"Institution","values":["East Carolina University"]},{"key":"dc:type","label":"Dc Type","values":["Doctoral Dissertation"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["retinoic acid","CYP26","talarozole"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language.iso","label":"Language (ISO)","values":["en"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.uri","label":"Identifier URI","values":["http://hdl.handle.net/10342/7078"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["In the mammalian testis, the foundation of spermatogenesis is provided by spermatogonial stem cells (SSCs); their progeny either remain as stem cells (following a self-renewal division) or proliferate as undifferentiated progenitors prior to differentiating in response to retinoic acid (RA) and later entering meiosis. The mechanisms regulating spermatogonial response to RA are undefined, and their identification would represent a key advance in our understanding of how spermatogonial fate is determined both at the beginning of spermatogenesis and throughout the male reproductive lifespan. This dissertation summarizes the results of an investigation into elusive mechanisms regulating a key switch fundamental to spermatogonial fate, the capacity of spermatogonia to respond to RA. The results support a novel model by which mammalian prospermatogonial and spermatogonial fates are regulated by intrinsic capacity to respond (or not) to the differentiation signal provided by RA prior to and concurrent with the initiation of spermatogenesis."]},{"key":"dc:format.mimetype","label":"Dc Format Mimetype","values":["application/pdf"]},{"key":"dc:title","label":"Title","values":["The Role of Differential Sensitivity to Retinoic Acid (RA) in Regulating Spermatogonial Fate"]}]}],"canonical_facts":{"dc:contributor.advisor":["Geyer, Christopher B"],"dc:contributor.department":["Anatomy and Cell Biology"],"dc:creator":["Velte, Ellen Kay"],"dc:date.accessioned":["2019-02-15T13:32:57Z"],"dc:date.available":["2020-12-01T09:01:54Z"],"dc:date.issued":["2018-12-10"],"dc:description.abstract":["In the mammalian testis, the foundation of spermatogenesis is provided by spermatogonial stem cells (SSCs); their progeny either remain as stem cells (following a self-renewal division) or proliferate as undifferentiated progenitors prior to differentiating in response to retinoic acid (RA) and later entering meiosis. The mechanisms regulating spermatogonial response to RA are undefined, and their identification would represent a key advance in our understanding of how spermatogonial fate is determined both at the beginning of spermatogenesis and throughout the male reproductive lifespan. This dissertation summarizes the results of an investigation into elusive mechanisms regulating a key switch fundamental to spermatogonial fate, the capacity of spermatogonia to respond to RA. The results support a novel model by which mammalian prospermatogonial and spermatogonial fates are regulated by intrinsic capacity to respond (or not) to the differentiation signal provided by RA prior to and concurrent with the initiation of spermatogenesis."],"dc:format.mimetype":["application/pdf"],"dc:identifier.uri":["http://hdl.handle.net/10342/7078"],"dc:language.iso":["en"],"dc:publisher":["East Carolina University"],"dc:subject":["retinoic acid","CYP26","talarozole"],"dc:title":["The Role of Differential Sensitivity to Retinoic Acid (RA) in Regulating Spermatogonial Fate"],"dc:type":["Doctoral Dissertation"]},"updated_at":"2026-07-24T02:13:47Z"}