![]() ![]() Received: MaAccepted: OctoPublished: November 5, 2018Ĭopyright: © 2018 Clark et al. PLoS ONE 13(11):Įditor: Udai Pandey, Children's Hospital of Pittsburgh, University of Pittsburgh Medical Center, UNITED STATES Collectively, these studies implicate transcriptional control of basal autophagy in directing dendritic terminal branching and demonstrate the importance of homeostatic control of autophagic levels for dendritic arbor complexity under native or cellular stress conditions.Ĭitation: Clark SG, Graybeal LL, Bhattacharjee S, Thomas C, Bhattacharya S, Cox DN (2018) Basal autophagy is required for promoting dendritic terminal branching in Drosophila sensory neurons. Finally, autophagic induction partially rescues dendritic atrophy defects observed in a model of polyglutamine toxicity. We demonstrate that the Atg1 initiator kinase interacts with the dual leucine zipper kinase (DLK) pathway by negatively regulating the E3 ubiquitin ligase Highwire and positively regulating the MAPKKK Wallenda. Further, loss of function analyses implicate Atg genes in promoting cell type-specific dendritic arborization and terminal branching, while gain of function studies suggest that excessive autophagy leads to dramatic reductions in dendritic complexity. We demonstrate that autophagy-related ( Atg) genes are positively regulated by the homeodomain transcription factor Cut, and that basal autophagy functions as a downstream effector pathway for Cut-mediated dendritic terminal branching in Drosophila multidendritic (md) sensory neurons. However, relatively little is known regarding the developmental role of basal autophagy in directing aspects of dendritic arborization or the mechanisms by which the autophagic machinery may be transcriptionally regulated to promote dendritic diversification. Post-mitotic neurons require high levels of basal autophagy to clear cytotoxic materials and autophagic dysfunction under native or cellular stress conditions has been linked to neuronal cell death as well as axo-dendritic degeneration. Dendrites function as the primary sites for synaptic input and integration with impairments in dendritic arborization being associated with dysfunctional neuronal circuitry.
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