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Published October 1, 2017 | Published + Supplemental Material
Journal Article Open

IGDB-2, an Ig/FNIII protein, binds the ion channel LGC-34 and controls sensory compartment morphogenesis in C. elegans

Abstract

Sensory organ glia surround neuronal receptive endings (NREs), forming a specialized compartment important for neuronal activity, and reminiscent of glia-ensheathed synapses in the central nervous system. We previously showed that DAF-6, a Patched-related protein, is required in glia of the C. elegans amphid sensory organ to restrict sensory compartment size. LIT-1, a Nemo-like kinase, and SNX-1, a retromer component, antagonize DAF-6 and promote compartment expansion. To further explore the machinery underlying compartment size control, we sought genes whose inactivation restores normal compartment size to daf-6 mutants. We found that mutations in igdb-2, encoding a single-pass transmembrane protein containing Ig-like and fibronectin type III domains, 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. Immunoprecipitation followed by mass spectrometry demonstrates that IGDB-2 binds to LGC-34, a predicted ligand-gated ion channel, and lgc-34 mutations inhibit igdb-2 suppression of daf-6. Our findings reveal a novel membrane protein complex and suggest possible mechanisms for how sensory compartment size is controlled.

Additional Information

© 2017 Elsevier Inc. Received 5 June 2017, Revised 4 August 2017, Accepted 7 August 2017, Available online 10 August 2017. We thank Shaham lab members for discussions and comments. We thank the Rockefeller University Proteomics and Bio-Imaging Resource Centers for technical support, and Baolin Wang and Howard Baylis for reagents. Some strains were provided by the Caenorhabditis Genetics Center, which is funded by NIH Office of Research Infrastructure Programs (P40 OD010440). W.W. was supported by NIH Medical Scientist Training Program grant T32GM07739. S.S. was supported by NIH grants HD078703, NS064273 and NS081490.

Attached Files

Published - 1-s2.0-S0012160617303871-main.pdf

Supplemental Material - mmc1.pdf

Supplemental Material - mmc2.pdf

Supplemental Material - mmc3.xlsx

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Additional details

Created:
August 19, 2023
Modified:
October 17, 2023