Endocytosis restricts dendrite branching via removing ectopically localized branching ligands
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 un...
Saved in:
| Main Authors: | , , , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Nature Portfolio
2024-11-01
|
| Series: | Nature Communications |
| Online Access: | https://doi.org/10.1038/s41467-024-53970-3 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1846171850827104256 |
|---|---|
| author | Jie Fang Wenli Jiang Weixia Zhao Jie Wang Beibei Cao Nan Wang Baohui Chen Chao Wang Wei Zou |
| author_facet | Jie Fang Wenli Jiang Weixia Zhao Jie Wang Beibei Cao Nan Wang Baohui Chen Chao Wang Wei Zou |
| author_sort | Jie Fang |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-d970d06366744db9acdcad9bee3bb9bb |
| institution | Kabale University |
| issn | 2041-1723 |
| language | English |
| publishDate | 2024-11-01 |
| publisher | Nature Portfolio |
| record_format | Article |
| series | Nature Communications |
| spelling | doaj-art-d970d06366744db9acdcad9bee3bb9bb2024-11-10T12:33:31ZengNature PortfolioNature Communications2041-17232024-11-0115111810.1038/s41467-024-53970-3Endocytosis restricts dendrite branching via removing ectopically localized branching ligandsJie Fang0Wenli Jiang1Weixia Zhao2Jie Wang3Beibei Cao4Nan Wang5Baohui Chen6Chao Wang7Wei Zou8The Fourth Affiliated Hospital, Zhejiang University School of MedicineMOE Key Laboratory for Membraneless Organelles & Cellular Dynamics, Hefei National Research Center for Physical Sciences at the Microscale, Biomedical Sciences and Health Laboratory of Anhui Province, School of Life Sciences, Division of Life Sciences and Medicine, University of Science and Technology of ChinaThe Fourth Affiliated Hospital, Zhejiang University School of MedicineThe Fourth Affiliated Hospital, Zhejiang University School of MedicineThe Fourth Affiliated Hospital, Zhejiang University School of MedicineThe Fourth Affiliated Hospital, Zhejiang University School of MedicineDepartment of Cell Biology, and Bone Marrow Transplantation Center of the First Affiliated Hospital, Zhejiang University School of MedicineMOE Key Laboratory for Membraneless Organelles & Cellular Dynamics, Hefei National Research Center for Physical Sciences at the Microscale, Biomedical Sciences and Health Laboratory of Anhui Province, School of Life Sciences, Division of Life Sciences and Medicine, University of Science and Technology of ChinaThe Fourth Affiliated Hospital, Zhejiang University School of MedicineAbstract 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.https://doi.org/10.1038/s41467-024-53970-3 |
| spellingShingle | Jie Fang Wenli Jiang Weixia Zhao Jie Wang Beibei Cao Nan Wang Baohui Chen Chao Wang Wei Zou Endocytosis restricts dendrite branching via removing ectopically localized branching ligands Nature Communications |
| title | Endocytosis restricts dendrite branching via removing ectopically localized branching ligands |
| title_full | Endocytosis restricts dendrite branching via removing ectopically localized branching ligands |
| title_fullStr | Endocytosis restricts dendrite branching via removing ectopically localized branching ligands |
| title_full_unstemmed | Endocytosis restricts dendrite branching via removing ectopically localized branching ligands |
| title_short | Endocytosis restricts dendrite branching via removing ectopically localized branching ligands |
| title_sort | endocytosis restricts dendrite branching via removing ectopically localized branching ligands |
| url | https://doi.org/10.1038/s41467-024-53970-3 |
| work_keys_str_mv | AT jiefang endocytosisrestrictsdendritebranchingviaremovingectopicallylocalizedbranchingligands AT wenlijiang endocytosisrestrictsdendritebranchingviaremovingectopicallylocalizedbranchingligands AT weixiazhao endocytosisrestrictsdendritebranchingviaremovingectopicallylocalizedbranchingligands AT jiewang endocytosisrestrictsdendritebranchingviaremovingectopicallylocalizedbranchingligands AT beibeicao endocytosisrestrictsdendritebranchingviaremovingectopicallylocalizedbranchingligands AT nanwang endocytosisrestrictsdendritebranchingviaremovingectopicallylocalizedbranchingligands AT baohuichen endocytosisrestrictsdendritebranchingviaremovingectopicallylocalizedbranchingligands AT chaowang endocytosisrestrictsdendritebranchingviaremovingectopicallylocalizedbranchingligands AT weizou endocytosisrestrictsdendritebranchingviaremovingectopicallylocalizedbranchingligands |