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Endocytosis restricts dendrite branching via removing ectopically localized branching ligands

Author

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  • Jie Fang

    (Zhejiang University School of Medicine
    Zhejiang University
    Zhejiang University School of Medicine)

  • Wenli Jiang

    (University of Science and Technology of China
    University of Science and Technology of China)

  • Weixia Zhao

    (Zhejiang University School of Medicine
    Zhejiang University)

  • Jie Wang

    (Zhejiang University School of Medicine
    Zhejiang University)

  • Beibei Cao

    (Zhejiang University School of Medicine
    Zhejiang University)

  • Nan Wang

    (Zhejiang University School of Medicine
    Zhejiang University)

  • Baohui Chen

    (Zhejiang University School of Medicine)

  • Chao Wang

    (University of Science and Technology of China
    University of Science and Technology of China)

  • Wei Zou

    (Zhejiang University School of Medicine
    Zhejiang University)

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.

Suggested Citation

  • Jie Fang & Wenli Jiang & Weixia Zhao & Jie Wang & Beibei Cao & Nan Wang & Baohui Chen & Chao Wang & Wei Zou, 2024. "Endocytosis restricts dendrite branching via removing ectopically localized branching ligands," Nature Communications, Nature, vol. 15(1), pages 1-18, December.
    • Handle: RePEc:nat:natcom:v:15:y:2024:i:1:d:10.1038_s41467-024-53970-3
    DOI: 10.1038/s41467-024-53970-3
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    References listed on IDEAS

    as
    1. Jin Ye & Guichang Zou & Ruichi Zhu & Chao Kong & Chenjian Miao & Mingjie Zhang & Jianchao Li & Wei Xiong & Chao Wang, 2021. "Structural basis of GABARAP-mediated GABAA receptor trafficking and functions on GABAergic synaptic transmission," Nature Communications, Nature, vol. 12(1), pages 1-12, December.
    2. Caroline Mauvezin & Péter Nagy & Gábor Juhász & Thomas P. Neufeld, 2015. "Autophagosome–lysosome fusion is independent of V-ATPase-mediated acidification," Nature Communications, Nature, vol. 6(1), pages 1-14, November.
    3. Takahiro Kanamori & Jiro Yoshino & Kei-ichiro Yasunaga & Yusuke Dairyo & Kazuo Emoto, 2015. "Local endocytosis triggers dendritic thinning and pruning in Drosophila sensory neurons," Nature Communications, Nature, vol. 6(1), pages 1-14, May.
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