Sleep is an essential phylogenetically conserved behavioral state, whose regulation remains poorly understood. Several lines of evidence suggest that epidermal growth factor (EGFR) signaling may play an evolutionarily conserved and important role in regulating sleep. Genetic studies in Drosophila and C. elegans have demonstrated that EGFR signaling is required for invertebrate sleep. However, vertebrate studies have been inconclusive. To address this, we use the diurnal zebrafish to test the hypothesis that EGFR signaling is required for vertebrate sleep. We reveal that heat shock-induced overexpression of the EGFR ligand transforming growth factor alpha (TGFa) decreases locomotor activity and increases sleep, and that this phenotype is abrogated by small molecule inhibitors of MAPK, an EGFR effector pathway. We further observe that zebrafish containing mutations in EGFR ligands exhibit a dose dependent decrease in sleep. Corroborating this, animals with pharmacological inhibition and genetic loss-of-function of EGFR, demonstrate increased locomotor activity and decreased sleep during the day and night. Moreover, site of action analysis demonstrate that TGFa-induced sleep is centrally mediated. Similar to rodents and humans, EGFR is expressed in cells lining the brain ventricle of zebrafish. Following TGFa overexpressing, c-fos coexpresses with these egfra cells, suggesting that neural activity in this cell population is critical in mediating TGFa/EGFR-induced sleep. Taken together, these results indicate that EGFR signaling is both necessary and sufficient for normal vertebrate sleep, suggesting it participates in an ancient and central aspect of sleep control.