Abstract
Cul3 belongs to the family of cullin proteins, which function as scaffold proteins of E3 ubiquitin ligase complexes. Here we show cell-autonomous involvement of Cul3 in axonal arborization and dendritic elaboration of Drosophila mushroom body neurons. Cul3 mutant neurons are defective in terminal morphogenesis of neurites. Interestingly, mutant axons often terminate around branching points. In addition, dendritic elaboration is severely affected in Cul3 mutant neurons. However, loss of Cul3 function does not affect extension of the axons that rarely arborize. Function of cullin-type proteins has been shown to require covalent attachment of Nedd8 (neural precursor cell-expressed developmentally downregulated), a ubiquitin-like protein. Consistent with this notion, Cul3 is inactivated by a mutation in its conserved neddylation site, and Nedd8 mutant neurons exhibit similar neuronal morphogenetic defects. Together, Cul3 plays an essential role in both axonal arborization and proper elaboration of dendrites and may require neddylation for its proper function.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
