Prd1 associates with the clathrin adaptor ?-Adaptin and the kinesin-3 Imac/Unc-104 to govern dendrite pruning in Drosophila.

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 ?-Adaptin (?-Ada) and the kinesin-3 immaculate connections (Imac)/Uncoordinated-104 (Unc-104) in dendrites. Moreover, Prd1 physically associates with ?-Ada and Imac, which are both critical for dendrite pruning. Prd1, ?-Ada, and Imac promote dendrite pruning via the regulation of endo-lysosomal degradation of Nrg. Importantly, genetic interactions among prd1, ?-adaptin, and imac indicate that they act in the same pathway to promote dendrite pruning. Our findings indicate that Prd1, ?-Ada, and Imac act together to regulate discrete distribution of ?-Ada/clathrin puncta, facilitate endo-lysosomal degradation, and thereby promote dendrite pruning in sensory neurons.
Mesh Terms:
Adaptor Protein Complex alpha Subunits, Animals, Brain, Cell Adhesion Molecules, Neuronal, Dendrites, Drosophila Proteins, Drosophila melanogaster, Endosomes, Gene Expression Regulation, Developmental, Kinesin, Larva, Lysosomes, Metamorphosis, Biological, Neural Cell Adhesion Molecule L1, Neuronal Plasticity, Protein Binding, Proteolysis, Sensory Receptor Cells, Signal Transduction
PLoS Biol
Date: Dec. 01, 2017
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