RRC ID 84120
著者 Fang J, Jiang W, Zhao W, Wang J, Cao B, Wang N, Chen B, Wang C, Zou W.
タイトル Endocytosis restricts dendrite branching via removing ectopically localized branching ligands.
ジャーナル Nat Commun
Abstract Neurons often grow highly branched and cell-type specific dendrite morphologies to receive and integrate information, which is the basis of precise neural circuit formation. Previous studies have identified numerous mechanisms that promote dendrite branching. In contrast, it is much less understood how this process is negatively regulated. Here we show that EAT-17/EVI5 acts together with the dynein adaptor protein BICD-1 and the motor protein dynein in C. elegans epidermal cells to restrict branching of PVD sensory dendrites. Loss-of-function mutants of these genes cause both ectopic branching and accumulation of the dendrite branching ligand SAX-7/L1CAM on epidermal plasma membranes. Mutants of genes regulating endo-lysosomal trafficking, including rab-5/RAB5 and dyn-1/DNM1, show similar defects. Biochemical characterization, genetic analysis, and imaging results support that EAT-17 and BICD-1 directly interact with each other and function in the endocytic degradation pathway to remove ectopically localized dendrite branching ligands to restrict abnormal branching.
巻・号 15(1)
ページ 9651
公開日 2024-11-7
DOI 10.1038/s41467-024-53970-3
PII 10.1038/s41467-024-53970-3
PMID 39511227
PMC PMC11544243
MeSH Animals Caenorhabditis elegans* / genetics Caenorhabditis elegans* / metabolism Caenorhabditis elegans Proteins* / genetics Caenorhabditis elegans Proteins* / metabolism Cell Membrane / metabolism Dendrites* / metabolism Dyneins / metabolism Endocytosis* Ligands Mutation Neural Cell Adhesion Molecule L1 / genetics Neural Cell Adhesion Molecule L1 / metabolism Neural Cell Adhesion Molecules Vesicular Transport Proteins rab5 GTP-Binding Proteins / genetics rab5 GTP-Binding Proteins / metabolism
リソース情報
線虫 tm5159