Sensory organ glia surround neuronal receptive endings (NREs), forming a specialized extracellular space, or compartment, important for neuronal activity, and reminiscent of glia-ensheathed synapses in the central nervous system. Sensory organ glia are conserved across organisms, but our current understanding of how they form sensory compartments is generally lacking. To date, the Caenorhabditis elegans amphid sensory organ has provided critical insight into some of these developmental processes. DAF-6, a Patched-related protein, was previously shown to be required in amphid glia to restrict sensory compartment size. LIT-1, a Nemo-like kinase, and SNX-1, a retromer component, antagonize DAF-6 and promote compartment expansion. My work here further explores the machinery underlying compartment size control. In seeking genes whose inactivation restores normal compartment size to daf-6 mutants, I identify two novel regulators: IGDB-2, an Ig/FNIII protein, and LGC-34, a ligand-gated ion channel. First, igdb-2 mutations suppress daf-6 mutant defects. IGDB-2 acts in glia, where it localizes to glial membranes surrounding NREs, and, together with LIT-1 and SNX-1, regulates compartment morphogenesis. Second, immunoprecipitation followed by mass spectrometry demonstrates that IGDB-2 binds to LGC-34, and lgc-34 mutations inhibit igdb-2 suppression of daf-6. My findings thus reveal the novel IGDB-2/LGC-34 membrane protein complex and suggest new molecular mechanisms for how sensory compartment size is controlled.
","abstract_html":"<p>Sensory organ glia surround neuronal receptive endings (NREs), forming a specialized extracellular space, or compartment, important for neuronal activity, and reminiscent of glia-ensheathed synapses in the central nervous system. Sensory organ glia are conserved across organisms, but our current understanding of how they form sensory compartments is generally lacking. To date, the Caenorhabditis elegans amphid sensory organ has provided critical insight into some of these developmental processes. DAF-6, a Patched-related protein, was previously shown to be required in amphid glia to restrict sensory compartment size. LIT-1, a Nemo-like kinase, and SNX-1, a retromer component, antagonize DAF-6 and promote compartment expansion. My work here further explores the machinery underlying compartment size control. In seeking genes whose inactivation restores normal compartment size to daf-6 mutants, I identify two novel regulators: IGDB-2, an Ig/FNIII protein, and LGC-34, a ligand-gated ion channel. First, igdb-2 mutations suppress daf-6 mutant defects. IGDB-2 acts in glia, where it localizes to glial membranes surrounding NREs, and, together with LIT-1 and SNX-1, regulates compartment morphogenesis. Second, immunoprecipitation followed by mass spectrometry demonstrates that IGDB-2 binds to LGC-34, and lgc-34 mutations inhibit igdb-2 suppression of daf-6. My findings thus reveal the novel IGDB-2/LGC-34 membrane protein complex and suggest new molecular mechanisms for how sensory compartment size is controlled.</p>","abstract_has_math":false,"creators":["Wang, Wendy"],"institution":null,"degree_name":"Doctor of Philosophy (PhD)","degree_level":"Thesis","degree_discipline":null,"degree_department":null,"school":null,"contributors":["Shai Shaham"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2018,"date_issued":"2018-01-01T08:00:00Z","date_published":"2018-01-01T08:00:00Z","updated_at":"2026-07-24T04:11:11Z","subjects":["sensory organ glia","neuronal receptive endings (NREs)","C. elegans","amphid sensory organ","sensory compartment size","DAF-6","Life Sciences"],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"https://digitalcommons.rockefeller.edu/student_theses_and_dissertations/468","outbound_label":"Repository record","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Shai Shaham"]},{"key":"dc:creator","label":"Author","values":["Wang, Wendy"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"thesis:degree_level","label":"Degree Level","values":["Thesis"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Doctor of Philosophy (PhD)"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["sensory organ glia","neuronal receptive endings (NREs)","C. elegans","amphid sensory organ","sensory compartment size","DAF-6","Life Sciences"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://digitalcommons.rockefeller.edu/student_theses_and_dissertations/468"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Sensory organ glia surround neuronal receptive endings (NREs), forming a specialized extracellular space, or compartment, important for neuronal activity, and reminiscent of glia-ensheathed synapses in the central nervous system. Sensory organ glia are conserved across organisms, but our current understanding of how they form sensory compartments is generally lacking. To date, the Caenorhabditis elegans amphid sensory organ has provided critical insight into some of these developmental processes. DAF-6, a Patched-related protein, was previously shown to be required in amphid glia to restrict sensory compartment size. LIT-1, a Nemo-like kinase, and SNX-1, a retromer component, antagonize DAF-6 and promote compartment expansion. My work here further explores the machinery underlying compartment size control. In seeking genes whose inactivation restores normal compartment size to daf-6 mutants, I identify two novel regulators: IGDB-2, an Ig/FNIII protein, and LGC-34, a ligand-gated ion channel. First, igdb-2 mutations suppress daf-6 mutant defects. IGDB-2 acts in glia, where it localizes to glial membranes surrounding NREs, and, together with LIT-1 and SNX-1, regulates compartment morphogenesis. Second, immunoprecipitation followed by mass spectrometry demonstrates that IGDB-2 binds to LGC-34, and lgc-34 mutations inhibit igdb-2 suppression of daf-6. My findings thus reveal the novel IGDB-2/LGC-34 membrane protein complex and suggest new molecular mechanisms for how sensory compartment size is controlled.
"]},{"key":"dc:title","label":"Title","values":["IGDB-2, an IG/FNIII Protein, Binds the ION Channel LGC-34 and Controls Sensory Compartment Morphogenesis in C. Elegans"]}]}],"canonical_facts":{"dc:contributor":["Shai Shaham"],"dc:creator":["Wang, Wendy"],"dc:description.abstract":["Sensory organ glia surround neuronal receptive endings (NREs), forming a specialized extracellular space, or compartment, important for neuronal activity, and reminiscent of glia-ensheathed synapses in the central nervous system. Sensory organ glia are conserved across organisms, but our current understanding of how they form sensory compartments is generally lacking. To date, the Caenorhabditis elegans amphid sensory organ has provided critical insight into some of these developmental processes. DAF-6, a Patched-related protein, was previously shown to be required in amphid glia to restrict sensory compartment size. LIT-1, a Nemo-like kinase, and SNX-1, a retromer component, antagonize DAF-6 and promote compartment expansion. My work here further explores the machinery underlying compartment size control. In seeking genes whose inactivation restores normal compartment size to daf-6 mutants, I identify two novel regulators: IGDB-2, an Ig/FNIII protein, and LGC-34, a ligand-gated ion channel. First, igdb-2 mutations suppress daf-6 mutant defects. IGDB-2 acts in glia, where it localizes to glial membranes surrounding NREs, and, together with LIT-1 and SNX-1, regulates compartment morphogenesis. Second, immunoprecipitation followed by mass spectrometry demonstrates that IGDB-2 binds to LGC-34, and lgc-34 mutations inhibit igdb-2 suppression of daf-6. My findings thus reveal the novel IGDB-2/LGC-34 membrane protein complex and suggest new molecular mechanisms for how sensory compartment size is controlled.
"],"dc:identifier":["https://digitalcommons.rockefeller.edu/student_theses_and_dissertations/468"],"dc:subject":["sensory organ glia","neuronal receptive endings (NREs)","C. elegans","amphid sensory organ","sensory compartment size","DAF-6","Life Sciences"],"dc:title":["IGDB-2, an IG/FNIII Protein, Binds the ION Channel LGC-34 and Controls Sensory Compartment Morphogenesis in C. Elegans"],"thesis:degree_level":["Thesis"],"thesis:degree_name":["Doctor of Philosophy (PhD)"]},"updated_at":"2026-07-24T04:11:11Z"}