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

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 ?-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.

SUBMITTER: Zong W 

PROVIDER: S-EPMC6126864 | biostudies-literature | 2018 Aug

REPOSITORIES: biostudies-literature