Amyotrophic lateral sclerosis (ALS) is a well-known neurodegenerative disease caused by motor neuron death within the spinal cord and brain. Soon after the nerve cells die, the patient’s muscle cells degenerate resulting in paralysis and eventually death. Another debilitating human disease is primary open-angle glaucoma (POAG). POAG is an ocular disease triggered by the rise in internal eye pressure which damages the optic nerve, reducing image signals to the brain. Most cases of ALS are sporadic and the direct causes for the increase of internal eye pressure are questionable, meaning that a clear genetic and molecular understanding of the mechanisms leading to the diseases is not well understood. The gene optineurin (OPTN) has been identified and implicated as a contributor to the mechanisms leading to the onset of both of these diseases. To gain a better understanding of the cellular functions of OPTN, we are using TAL-effector nuclease (TALEN) facilitated mutagenesis. The TALEN specific for the OPTN gene in zebrafish has been generated, injected, and has produced mutations. The mutations are being characterized for their consequences on zebrafish eyes and motor neurons to hopefully allow us to create new zebrafish models for ALS and glaucoma.