Presentation/Session Information

Session Information

Session Title: Neuronal Development Session Type: Parallel
Session Location: Grand Horizon Ballroom Session Time: Fri, Jun 26 8:30AM - 11:30AM

Presentation Information

Program Number: 94 Presentation Time: 10:30AM - 10:42AM

Presentation Content

Autophagy is required for Axon Outgrowth and the Specification of Presynaptic Sites during Neurodevelopment.Sarah Hill 1,2, Andrea Stavoe 1,2, Daniel Colon-Ramos 1,2. 1)Cell Biology, Yale University, New Haven, CT; 2)Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University, New Haven, CT

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.

Please note: Abstract shown here should NOT be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.

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