Cul4 ubiquitin ligase cofactor DCAF12 promotes neurotransmitter release and homeostatic plasticity
AuthorPatrón, Lilian A
Eves, David Tyler
Rogers, Gregory C
Zinsmaier, Konrad E
AffiliationUniv Arizona, Dept Neurosci
Univ Arizona, Grad Interdisciplinary Program Neurosci
Univ Arizona, Dept Mol & Cellular Biol
Univ Arizona, Dept Cellular & Mol Med
MetadataShow full item record
PublisherROCKEFELLER UNIV PRESS
CitationPatrón, L. A., Nagatomo, K., Eves, D. T., Imad, M., Young, K., Torvund, M., ... & Zinsmaier, K. E. (2019). Cul4 ubiquitin ligase cofactor DCAF12 promotes neurotransmitter release and homeostatic plasticity. J Cell Biol, 218(3), 993-1010.
JournalJOURNAL OF CELL BIOLOGY
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AbstractWe genetically characterized the synaptic role of the Drosophila homologue of human DCAF12, a putative cofactor of Cullin4 (Cul4) ubiquitin ligase complexes. Deletion of Drosophila DCAF12 impairs larval locomotion and arrests development. At larval neuromuscular junctions (NMJs), DCAF12 is expressed presynaptically in synaptic boutons, axons, and nuclei of motor neurons. Postsynaptically, DCAF12 is expressed in muscle nuclei and facilitates Cul4-dependent ubiquitination. Genetic experiments identified several mechanistically independent functions of DCAF12 at larval NMJs. First, presynaptic DCAF12 promotes evoked neurotransmitter release. Second, postsynaptic DCAF12 negatively controls the synaptic levels of the glutamate receptor subunits GluRIIA, GluRIIC, and GluRIID. The down-regulation of synaptic GluRIIA subunits by nuclear DCAF12 requires Cul4. Third, presynaptic DCAF12 is required for the expression of synaptic homeostatic potentiation. We suggest that DCAF12 and Cul4 are critical for normal synaptic function and plasticity at larval NMJs.
Note6 month embargo; published online: 22 January 2019
VersionFinal published version
SponsorsNational Institutes of Health [2P40OD010949]; National Institute of Neurological Disorders and Stroke [R03 NS057215]; National Science Foundation [IOS-1121054]
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