{"id":{"repo_id":"uiuc","oai_identifier":"oai:www.ideals.illinois.edu:2142/82488"},"canonical_url":"https://search.dev.ndltd.org/etd/uiuc/oai:www.ideals.illinois.edu:2142/82488","repository":{"repo_id":"uiuc","name":"University of Illinois - Urbana-Champaign","base_url":"https://www.ideals.illinois.edu/oai-pmh"},"display":{"title":"Mechanisms of Asymmetric Protein Localization in Drosophila Embryonic Neural Stem Cells","abstract":"By screening a collection of deficiency lines and testing candidate gene involved in cell polarity, we identified lethal giant larvae (lgl) and discs large (dlg) to play key roles in the basal targeting of Prospero and Miranda. In embryonic and larval neuroblasts of lgl and dlg mutants, all basal targeted proteins become uniformly localized but distributions of the apical proteins are unaffected. In neuroblasts, Lgl protein is uniformly distributed at the cell cortex, and its cortical attachment is dependent on Dlg's apically enriched localization. Pharmacological studies suggest Lgl mediated basal targeting occur via a myosin-based transport mechanism, which is supported by genetic studies that show loss of Myosin II suppresses Lgl phenotype in neuroblasts. Taken together, we conclude that Lgl may function to suppress Myosin II activity and allow/promote positive Myosin dependent asymmetric localization in neuroblasts.","abstract_html":"By screening a collection of deficiency lines and testing candidate gene involved in cell polarity, we identified lethal giant larvae (lgl) and discs large (dlg) to play key roles in the basal targeting of Prospero and Miranda. In embryonic and larval neuroblasts of lgl and dlg mutants, all basal targeted proteins become uniformly localized but distributions of the apical proteins are unaffected. In neuroblasts, Lgl protein is uniformly distributed at the cell cortex, and its cortical attachment is dependent on Dlg's apically enriched localization. Pharmacological studies suggest Lgl mediated basal targeting occur via a myosin-based transport mechanism, which is supported by genetic studies that show loss of Myosin II suppresses Lgl phenotype in neuroblasts. Taken together, we conclude that Lgl may function to suppress Myosin II activity and allow/promote positive Myosin dependent asymmetric localization in neuroblasts.","abstract_has_math":false,"creators":["Peng, Chian-Yu"],"institution":"University of Illinois at Urbana-Champaign","degree_name":"Ph.D.","degree_level":"Dissertation","degree_discipline":"Neuroscience","degree_department":null,"school":null,"contributors":["Chris Doe"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2015,"date_issued":"2015-09-25T20:45:31Z","date_published":"2015-09-25T20:45:31Z","updated_at":"2026-07-22T22:26:18Z","subjects":["Biology, Neuroscience"],"languages":["eng"],"rights":[],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["(MiAaPQ)AAI3017180"],"render_values":[{"text":"(MiAaPQ)AAI3017180","href":null,"code":true}]}]},"links":{"outbound_url":"http://hdl.handle.net/2142/82488","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Chris Doe"]},{"key":"dc:creator","label":"Author","values":["Peng, Chian-Yu"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2015-09-25T20:45:31Z","10000-01-01","2001"]},{"key":"dc:type","label":"Dc Type","values":["text"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Neuroscience"]},{"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, Neuroscience"]}]},{"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/2142/82488","(MiAaPQ)AAI3017180"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["By screening a collection of deficiency lines and testing candidate gene involved in cell polarity, we identified lethal giant larvae (lgl) and discs large (dlg) to play key roles in the basal targeting of Prospero and Miranda. In embryonic and larval neuroblasts of lgl and dlg mutants, all basal targeted proteins become uniformly localized but distributions of the apical proteins are unaffected. In neuroblasts, Lgl protein is uniformly distributed at the cell cortex, and its cortical attachment is dependent on Dlg's apically enriched localization. Pharmacological studies suggest Lgl mediated basal targeting occur via a myosin-based transport mechanism, which is supported by genetic studies that show loss of Myosin II suppresses Lgl phenotype in neuroblasts. Taken together, we conclude that Lgl may function to suppress Myosin II activity and allow/promote positive Myosin dependent asymmetric localization in neuroblasts.","Made available in DSpace on 2015-09-25T20:45:31Z (GMT). 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In embryonic and larval neuroblasts of lgl and dlg mutants, all basal targeted proteins become uniformly localized but distributions of the apical proteins are unaffected. In neuroblasts, Lgl protein is uniformly distributed at the cell cortex, and its cortical attachment is dependent on Dlg's apically enriched localization. Pharmacological studies suggest Lgl mediated basal targeting occur via a myosin-based transport mechanism, which is supported by genetic studies that show loss of Myosin II suppresses Lgl phenotype in neuroblasts. Taken together, we conclude that Lgl may function to suppress Myosin II activity and allow/promote positive Myosin dependent asymmetric localization in neuroblasts.","Made available in DSpace on 2015-09-25T20:45:31Z (GMT). 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