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Significance In neurodegenerative disease, protein aggregates spread to neighboring cells to promote pathology. The in vivo regulation of toxic material transfer remains poorly understood, although mechanistic understanding should reveal previously unrecognized therapeutic targets. ProteostressedCaenorhabditis elegans neurons can concentrate protein aggregates and extrude them in membrane-encased vesicles called exophers. We identify specific systemic stress conditions that enhance exopher production, revealing stress-type, stress-level, and temporal constraints on the process. We identify three pathways that promote fasting-induced exophergenesis: lipid synthesis, FGF/RAS/MAPK, and EGF/RAS/MAPK. In establishing an initial molecular model for transtissue requirements for fasting-induced exopher elevation in neurons, we report molecular insights into the regulation of aggregate transfer biology, relevant to the fundamental mysteries of neurodegenerative disease.

Stress increases in exopher-mediated neuronal extrusion require lipid biosynthesis, FGF, and EGF RAS/MAPK signaling