ArticlePLoS biology2018
Prd1 associates with the clathrin adaptor α-Adaptin and the kinesin-3 Imac/Unc-104 to govern dendrite pruning in Drosophila.
Article in PLoS biology, 2018. 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, 13 citations in OpenAlex.
- Modeling AP2M1 developmental and epileptic encephalopathy in Drosophila.Disease models & mechanisms · 2025Article
- Glial-derived TNF/Eiger signaling promotes somatosensory neurite sculpting.Cellular and molecular life sciences : CMLS · 2025Article
- Recent progress in dendritic pruning ofOpen biology · 2024Review
- Spatial regulation of endosomes in growing dendrites.Developmental biology · 2022Review
- Spatiotemporal Control of Neuronal Remodeling by Cell Adhesion Molecules: Insights FromFrontiers in neuroscience · 2022Review
- A systematic analysis of microtubule-destabilizing factors during dendrite pruning in Drosophila.EMBO reports · 2021Article
- Drosophila Rab39 Attenuates Lysosomal Degradation.International journal of molecular sciences · 2021Article
- Scrap and Build for Functional Neural Circuits: Spatiotemporal Regulation of Dendrite Degeneration and Regeneration in Neural Development and Disease.Frontiers in cellular neuroscience · 2020Review
- The Conserved IgSF9 Protein Borderless Regulates Axonal Transport of Presynaptic Components and Color Vision inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Refinement of the nervous system depends on selective removal of excessive axons/dendrites, a process known as pruning. Drosophila ddaC sensory neurons prune their larval dendrites via endo-lysosomal degradation of the L1-type cell adhesion molecule (L1-CAM), Neuroglian (Nrg). Here, we have identified a novel gene, pruning defect 1 (prd1), which governs dendrite pruning of ddaC neurons. We show that Prd1 colocalizes with the clathrin adaptor protein α-Adaptin (α-Ada) and the kinesin-3 immaculate connections (Imac)/Uncoordinated-104 (Unc-104) in dendrites. Moreover, Prd1 physically associates with α-Ada and Imac, which are both critical for dendrite pruning. Prd1, α-Ada, and Imac promote dendrite pruning via the regulation of endo-lysosomal degradation of Nrg. Importantly, genetic interactions among prd1, α-adaptin, and imac indicate that they act in the same pathway to promote dendrite pruning. Our findings indicate that Prd1, α-Ada, and Imac act together to regulate discrete distribution of α-Ada/clathrin puncta, facilitate endo-lysosomal degradation, and thereby promote dendrite pruning in sensory neurons.
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