{"id":{"repo_id":"utswmed","oai_identifier":"oai:utswmed-ir.tdl.org:2152.5/566"},"canonical_url":"https://search.dev.ndltd.org/etd/utswmed/oai:utswmed-ir.tdl.org:2152.5/566","repository":{"repo_id":"utswmed","name":"University of Texas Southwestern Medical Center","base_url":"https://utswmed-ir.tdl.org/server/oai/request"},"display":{"title":"The Study of Wnt Signaling Effector POP-1/TCF in C. Elegans Early Embryos","abstract":"In C. elegans embryos, the combined Wnt/MAPK pathway polarizes the founder cell of mesendoderm, EMS blastomere, such that EMS produces two daughters with distinct developmental fates. The posterior daughter E, whose fate is specified by Wnt/MAPK, generates intestinal tissues (endoderm), whereas the anterior daughter MS generates pharynx and muscle cells (mesoderm). The downstream Wnt/MAPK effector POP-1 is asymmetrically localized in the nuclei of A-P sisters including the MS/E pair, with a higher level in the anterior cells. This phenomenon is called POP-1 nuclear asymmetry. The Wnt/MAPK signaling is required for POP-1 nuclear asymmetry. It is believed that POP-1 represses endoderm fate in MS and Wnt/MAPK allows endoderm fate in E by downregulating the nuclear level of POP-1. In this study, the potential mechanisms for POP-1 nuclear asymmetry are presented. POP-1 nuclear asymmetry requires a 14-3-3 protein PAR-5 and at least three POP-1 potential phosphorylation sites for the MAPK LIT-1. LIT-1 activity is required for both POP-1/PAR-5 interaction and phosphorylation of at least two of the three potential LIT-1 sites in vivo. Nuclear export is also required for POP-1 nuclear asymmetry. The nuclear level of LIT-1 is higher in the E blastomere, which is regulated by the upstream kinase and Wnt signaling. All together, I propose that in the E blastomere, Wnt/MAPK signaling promotes PAR-5-mediated nuclear export of POP-1, thereby lowering its nuclear level. In addition to this differential nuclear export mechanism, POP-1 nuclear asymmetry may also be regulated by differential protein degradation. This study also shows that POP-1 functions to activate a Wnt/MAPK-responsive gene, sdz-23, in the E blastomere. This challenged the commonly accepted model of Wnt/MAPK-induced gene expression in E, which is based upon the alleviation of the repressive activity of POP-1. The activation of sdz-23 in E requires the ᭣atenin binding domain of POP-1 and a low nuclear level of POP-1. These results suggest that Wnt/MAPK converts the repressor POP-1 into a transcriptional activator and therefore, the non-canonical Wnt signaling in C. elegans early embryos is found to regulate its downstream effector POP-1 in a more canonical way than previously realized.","abstract_html":"In C. elegans embryos, the combined Wnt/MAPK pathway polarizes the founder cell of mesendoderm, EMS blastomere, such that EMS produces two daughters with distinct developmental fates. The posterior daughter E, whose fate is specified by Wnt/MAPK, generates intestinal tissues (endoderm), whereas the anterior daughter MS generates pharynx and muscle cells (mesoderm). The downstream Wnt/MAPK effector POP-1 is asymmetrically localized in the nuclei of A-P sisters including the MS/E pair, with a higher level in the anterior cells. This phenomenon is called POP-1 nuclear asymmetry. The Wnt/MAPK signaling is required for POP-1 nuclear asymmetry. It is believed that POP-1 represses endoderm fate in MS and Wnt/MAPK allows endoderm fate in E by downregulating the nuclear level of POP-1. In this study, the potential mechanisms for POP-1 nuclear asymmetry are presented. POP-1 nuclear asymmetry requires a 14-3-3 protein PAR-5 and at least three POP-1 potential phosphorylation sites for the MAPK LIT-1. LIT-1 activity is required for both POP-1/PAR-5 interaction and phosphorylation of at least two of the three potential LIT-1 sites in vivo. Nuclear export is also required for POP-1 nuclear asymmetry. The nuclear level of LIT-1 is higher in the E blastomere, which is regulated by the upstream kinase and Wnt signaling. All together, I propose that in the E blastomere, Wnt/MAPK signaling promotes PAR-5-mediated nuclear export of POP-1, thereby lowering its nuclear level. In addition to this differential nuclear export mechanism, POP-1 nuclear asymmetry may also be regulated by differential protein degradation. This study also shows that POP-1 functions to activate a Wnt/MAPK-responsive gene, sdz-23, in the E blastomere. This challenged the commonly accepted model of Wnt/MAPK-induced gene expression in E, which is based upon the alleviation of the repressive activity of POP-1. The activation of sdz-23 in E requires the ᭣atenin binding domain of POP-1 and a low nuclear level of POP-1. These results suggest that Wnt/MAPK converts the repressor POP-1 into a transcriptional activator and therefore, the non-canonical Wnt signaling in C. elegans early embryos is found to regulate its downstream effector POP-1 in a more canonical way than previously realized.","abstract_has_math":false,"creators":["Lo, Miao-Chia"],"institution":null,"degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":["Lin, Rueyling"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2010,"date_issued":"2010-07-12T18:28:10Z","date_published":"2010-07-12T18:28:10Z","updated_at":"2026-07-24T05:52:20Z","subjects":["Caenorhabditis elegans","DNA-Binding Proteins","Mitogen-Activated Protein Kinases"],"languages":["en"],"rights":[],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["60493338"],"render_values":[{"text":"60493338","href":null,"code":true}]}]},"links":{"outbound_url":"https://hdl.handle.net/2152.5/566","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Lin, Rueyling"]},{"key":"dc:creator","label":"Author","values":["Lo, Miao-Chia"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2010-07-12T18:28:10Z","2005-04-29"]},{"key":"dc:type","label":"Dc Type","values":["Thesis","Text","dissertation"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Caenorhabditis elegans","DNA-Binding Proteins","Mitogen-Activated Protein Kinases"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["en"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://hdl.handle.net/2152.5/566","60493338"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["In C. elegans embryos, the combined Wnt/MAPK pathway polarizes the founder cell of mesendoderm, EMS blastomere, such that EMS produces two daughters with distinct developmental fates. The posterior daughter E, whose fate is specified by Wnt/MAPK, generates intestinal tissues (endoderm), whereas the anterior daughter MS generates pharynx and muscle cells (mesoderm). The downstream Wnt/MAPK effector POP-1 is asymmetrically localized in the nuclei of A-P sisters including the MS/E pair, with a higher level in the anterior cells. This phenomenon is called POP-1 nuclear asymmetry. The Wnt/MAPK signaling is required for POP-1 nuclear asymmetry. It is believed that POP-1 represses endoderm fate in MS and Wnt/MAPK allows endoderm fate in E by downregulating the nuclear level of POP-1. In this study, the potential mechanisms for POP-1 nuclear asymmetry are presented. POP-1 nuclear asymmetry requires a 14-3-3 protein PAR-5 and at least three POP-1 potential phosphorylation sites for the MAPK LIT-1. LIT-1 activity is required for both POP-1/PAR-5 interaction and phosphorylation of at least two of the three potential LIT-1 sites in vivo. Nuclear export is also required for POP-1 nuclear asymmetry. The nuclear level of LIT-1 is higher in the E blastomere, which is regulated by the upstream kinase and Wnt signaling. All together, I propose that in the E blastomere, Wnt/MAPK signaling promotes PAR-5-mediated nuclear export of POP-1, thereby lowering its nuclear level. In addition to this differential nuclear export mechanism, POP-1 nuclear asymmetry may also be regulated by differential protein degradation. This study also shows that POP-1 functions to activate a Wnt/MAPK-responsive gene, sdz-23, in the E blastomere. This challenged the commonly accepted model of Wnt/MAPK-induced gene expression in E, which is based upon the alleviation of the repressive activity of POP-1. The activation of sdz-23 in E requires the ᭣atenin binding domain of POP-1 and a low nuclear level of POP-1. These results suggest that Wnt/MAPK converts the repressor POP-1 into a transcriptional activator and therefore, the non-canonical Wnt signaling in C. elegans early embryos is found to regulate its downstream effector POP-1 in a more canonical way than previously realized."]},{"key":"dc:format","label":"Dc Format","values":["Electronic","application/pdf","born digital"]},{"key":"dc:title","label":"Title","values":["The Study of Wnt Signaling Effector POP-1/TCF in C. Elegans Early Embryos"]}]}],"canonical_facts":{"dc:contributor":["Lin, Rueyling"],"dc:creator":["Lo, Miao-Chia"],"dc:date":["2010-07-12T18:28:10Z","2005-04-29"],"dc:description":["In C. elegans embryos, the combined Wnt/MAPK pathway polarizes the founder cell of mesendoderm, EMS blastomere, such that EMS produces two daughters with distinct developmental fates. The posterior daughter E, whose fate is specified by Wnt/MAPK, generates intestinal tissues (endoderm), whereas the anterior daughter MS generates pharynx and muscle cells (mesoderm). The downstream Wnt/MAPK effector POP-1 is asymmetrically localized in the nuclei of A-P sisters including the MS/E pair, with a higher level in the anterior cells. This phenomenon is called POP-1 nuclear asymmetry. The Wnt/MAPK signaling is required for POP-1 nuclear asymmetry. It is believed that POP-1 represses endoderm fate in MS and Wnt/MAPK allows endoderm fate in E by downregulating the nuclear level of POP-1. In this study, the potential mechanisms for POP-1 nuclear asymmetry are presented. POP-1 nuclear asymmetry requires a 14-3-3 protein PAR-5 and at least three POP-1 potential phosphorylation sites for the MAPK LIT-1. LIT-1 activity is required for both POP-1/PAR-5 interaction and phosphorylation of at least two of the three potential LIT-1 sites in vivo. Nuclear export is also required for POP-1 nuclear asymmetry. The nuclear level of LIT-1 is higher in the E blastomere, which is regulated by the upstream kinase and Wnt signaling. All together, I propose that in the E blastomere, Wnt/MAPK signaling promotes PAR-5-mediated nuclear export of POP-1, thereby lowering its nuclear level. In addition to this differential nuclear export mechanism, POP-1 nuclear asymmetry may also be regulated by differential protein degradation. This study also shows that POP-1 functions to activate a Wnt/MAPK-responsive gene, sdz-23, in the E blastomere. This challenged the commonly accepted model of Wnt/MAPK-induced gene expression in E, which is based upon the alleviation of the repressive activity of POP-1. The activation of sdz-23 in E requires the ᭣atenin binding domain of POP-1 and a low nuclear level of POP-1. These results suggest that Wnt/MAPK converts the repressor POP-1 into a transcriptional activator and therefore, the non-canonical Wnt signaling in C. elegans early embryos is found to regulate its downstream effector POP-1 in a more canonical way than previously realized."],"dc:format":["Electronic","application/pdf","born digital"],"dc:identifier":["https://hdl.handle.net/2152.5/566","60493338"],"dc:language":["en"],"dc:subject":["Caenorhabditis elegans","DNA-Binding Proteins","Mitogen-Activated Protein Kinases"],"dc:title":["The Study of Wnt Signaling Effector POP-1/TCF in C. Elegans Early Embryos"],"dc:type":["Thesis","Text","dissertation"]},"updated_at":"2026-07-24T05:52:20Z"}