Forebrain pathways of the mammalian visual system are organized into topographic maps during development. Early patterning cues likely translate regional gradients of gene expression into precise diagrams of retinogeniculate and geniculocortical wiring, though the molecular mechanisms of these processes are not well understood. Here we examine the role of Zic4 and Zic1, two transcription factors currently known to control aspects of cerebellar differentiation, in specifying retinotopic organization within the dorsal lateral geniculate nucleus (dLG) and primary visual cortex (V1). Zic4 and Zic1 are both highly expressed in gradients of the embryonic and perinatal retina, dLG and posterior cortex. Mice with null mutations in Zic4 and Zic1/4 were used to investigate whether these genes are necessary for the proper formation of retinotopic maps. Retinal cholera toxin-B (CTB) injections at postnatal day 28 (P28) were used to assay retinogeniculate targeting in its mature state. We found that ipsilateral retinal projections to the dLG are disordered in Zic4 mutants, with abnormal increases in clustering, compression in the medial-lateral axis and ectopic projections to the lateral edge of the dLG. Eye specific segregation is normal, suggesting no disruptions in activity-dependent refinement of retinogeniculate terminals. Intrinsic signal optical imaging of V1 in Zic4 mutant and control mice at P28 was performed to examine functional maps of retinotopy in the cortex. Zic4 mutants exhibit a compression in size of the binocular zone, while the total size of V1 remains unchanged. Mice with Zic4 mutations demonstrate deficits in visually mediated behavior using a visual cliff test, including the number of crossing over a presumptive cliff. These data indicate that Zic4 is necessary for the proper patterning of ipsilateral axons in the dLG, the formation of normal binocular maps in V1, and the detection of behaviorally relevant landmarks in visual space.