ArticleDevelopmental cell2022
Neurexin and frizzled intercept axonal transport at microtubule minus ends to control synapse formation.
Article in Developmental cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Markers and Enrichment Strategies for Brain-Derived Extracellular Vesicles: Current Evidence, Limitations and Future Directions.Neuromolecular medicine · 2026Review
- Kinesins inOpen biology · 2025Review
- VAB-8/KIF26, LIN-17/Frizzled, and EFN-4/Ephrin control distinct stages of posterior neuroblast migration downstream of the MAB-5/Hox transcription factor in Caenorhabditis elegans.PLoS genetics · 2025Article
- Transgenic expression of endoplasmic reticulum proteins inmicroPublication biology · 2025Article
- Patronin regulates presynaptic microtubule organization and neuromuscular junction development iniScience · 2024Article
- Article
- Recently recycled synaptic vesicles use multi-cytoskeletal transport and differential presynaptic capture probability to establish a retrograde net flux during ISVE in central neurons.Frontiers in cell and developmental biology · 2023Article
- Contributions of microtubule dynamics and transport to presynaptic and postsynaptic functions.Molecular and cellular neurosciences · 2022Article
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10 authors at 2 institutions in 1 country.
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Abstract
Synapse formation is locally determined by transmembrane proteins, yet synaptic material is synthesized remotely and undergoes processive transport in axons. How local synaptogenic signals intercept synaptic cargo in transport to promote its delivery and synapse formation is unknown. We found that the control of synaptic cargo delivery at microtubule (MT) minus ends mediates pro- and anti-synaptogenic activities of presynaptic neurexin and frizzled in C. elegans and identified the atypical kinesin VAB-8/KIF26 as a key molecule in this process. VAB-8/KIF26 levels at synaptic MT minus ends are controlled by frizzled and neurexin; loss of VAB-8 mimics neurexin mutants or frizzled hyperactivation, and its overexpression can rescue synapse loss in these backgrounds. VAB-8/KIF26 is required for the synaptic localization of other minus-end proteins and promotes the pausing of retrograde transport to allow delivery to synapses. Consistently, reducing retrograde transport rescues synapse loss in vab-8 and neurexin mutants. These results uncover a mechanistic link between synaptogenic signaling and axonal transport.
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