Prd1 associates with the clathrin adaptor α-Adaptin and the kinesin-3 Imac/Unc-104 to govern dendrite pruning in Drosophila.
PLoS Biol
; 16(8): e2004506, 2018 08.
Article
in En
| MEDLINE
| ID: mdl-30142146
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.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Cell Adhesion Molecules, Neuronal
/
Kinesins
/
Drosophila Proteins
/
Dendrites
/
Neural Cell Adhesion Molecule L1
/
Adaptor Protein Complex alpha Subunits
/
Drosophila melanogaster
/
Neuronal Plasticity
Type of study:
Prognostic_studies
/
Risk_factors_studies
Limits:
Animals
Language:
En
Journal:
PLoS Biol
Journal subject:
BIOLOGIA
Year:
2018
Document type:
Article
Affiliation country:
Singapore