Autophagy is a highly conserved multi-step pathway used by cells to degrade substrates. Autophagy is important for maintaining homeostasis in neurons, and disruption of autophagy contributes to neuronal diseases. However, the role of autophagy in neurodevelopment is not well understood. Through a forward genetic screen in C. elegans, we identified the autophagy gene, atg-9, as required for specifying presynaptic sites. Atg-9 mutant animals have disrupted synaptic vesicle clusters at presynaptic sites in the interneuron AIY and elongated axons in the sensory neuron PVD. We determined that each step of autophagosome biogenesis: initiation, nucleation, elongation, and recycling, is required for these two distinct phenotypes. Presynaptic assembly and axon outgrowth both rely on appropriate actin organization. Cell-specific disruption of F-actin phenocopied autophagy mutants. Additionally, we observed disordered F-actin localization in autophagy mutants. Our results demonstrate that autophagy is required cell-autonomously, during development, and likely acts through actin to control precise neurodevelopment.
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