Please use this identifier to cite or link to this item: https://doi.org/10.1371/journal.pbio.2004506
Title: Prd1 associates with the clathrin adaptor ?-Adaptin and the kinesin-3 Imac/Unc-104 to govern dendrite pruning in Drosophila
Authors: Zong W.
Wang Y. 
Tang Q.
Zhang H. 
Yu F. 
Issue Date: 2018
Publisher: Public Library of Science
Citation: Zong W., Wang Y., Tang Q., Zhang H., Yu F. (2018). Prd1 associates with the clathrin adaptor ?-Adaptin and the kinesin-3 Imac/Unc-104 to govern dendrite pruning in Drosophila. PLoS Biology 16 (8) : e2004506. ScholarBank@NUS Repository. https://doi.org/10.1371/journal.pbio.2004506
Rights: Attribution 4.0 International
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. © 2018 Zong et al. http://creativecommons.org/licenses/by/4.0/.
Source Title: PLoS Biology
URI: http://scholarbank.nus.edu.sg/handle/10635/152187
ISSN: 15449173
DOI: 10.1371/journal.pbio.2004506
Rights: Attribution 4.0 International
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