Down syndrome cell adhesion molecule (Dscam) family genes play diverse roles across many species. The Drosophila dscam is alternatively spliced and serves as intra- and intercellular recognition cues for repulsive interactions between axons and dendrites. In mice and chicken, Dscam and Dscam-like 1 (Dscaml1) are involved in promoting cell death, maintain cellular spacing, and laminar targeting of neurites in the developing visual system. The functional and behavioral importance of Dscam and Dscaml1, however, are less clear. In this study, we generated a TALEN-mediated dscaml1 mutant in Zebrafish (Danio rerio) and investigated how loss of dscaml1 affects visual system development and visual behaviors. The small size, translucent brain, powerful genetics, and robust visual behaviors of zebrafish make it an ideal vertebrate model system. Consistent with dscaml1’s function in mammals, we found significant aggregation and misplacement of retinal cell types, particularly the serotonergic amacrine cells and muller glia. The mutant brain was narrower, with increased neuropil thickness and reduced width. Despite these abnormalities, dscaml1 have normal light-on and light-off induced locomotor response and can respond to moving vertical bars while performing the optokinetic response (OKR), suggesting that perception of visual stimulus is grossly normal, though light sensitivity is reduced. However, when challenged with a faster or more prolonged moving stimulus, the dscaml1 mutants display severe deficits in saccadic (fast-resetting) eye movements and the eyes eventually become fixated at eccentric positions. These results suggest that dscaml1 is required for the development or function of the motor systems downstream of saccade generation centers. Work is currently in progress to investigate the neural correlates of the saccade deficits and the temporal requirements of dscaml1.