The eye is a complex organ, formed by many coordinated developmental processes. When these processes go wrong, clinically significant eye disorders can result. One such case is modeled by a zebrafish mutant in mab21l2. This gene is highly conserved amongst vertebrates, but very little is known about its function. No structural motifs are predicted for the protein, and its biological activity is unknown. mab21l2 mutants present with lens defects and coloboma. Humans with mutations in MAB21L2 possess colobomas and associated eye defects, but the molecular and cellular underpinnings of these defects are unknown. The goal of this project is to discover the mechanisms by which MAB21L2 mutations result in developmental abnormalities in the eye. Evidence suggests mab21l2 may be a transcriptional regulator required to maintain proliferation during lens development and choroid fissure closure. Preliminary evidence supports chromatin association of mab21l2, where it could indeed be involved in transcriptional regulation. Preliminary work has also begun to explore the phenotypes and progression of defects in the mutant zebrafish eye. Some mutants appear to completely fail to begin lens morphogenesis, while others begin morphogenesis with a slight delay and slower rate of growth, leading to dramatic differences in lens size at later ages. Identifying the functions of mab21l2 and the pathways it is involved with will increase the understanding of this enigmatic protein as well as conserved mechanisms governing eye development in humans.