**Abstract**

Humans with mutations in photoreceptor-related genes develop forms of retinal degeneration, such as retinitis pigmentosa, cone dystrophy, or Leber congenital amaurosis. Similarly, numerous photoreceptor mutant animal models present phenotypes that resemble retinal degeneration. Zebrafish retina manifests anatomical organization and development remarkably conserved in humans, making these fish a good model to study photoreceptor development and disease. Zebrafish are ideal for forward genetic screens to isolate mutants with visual defects. More recently, CRISPR/Cas system-mediated genome editing has enabled establishment of specific zebrafish photoreceptor mutants. Here, I review zebrafish models of inherited retinal diseases, focusing on rod versus cone photoreceptor mutants. Because zebrafish possess robust regeneration capacity to replace the lost photoreceptors, here I review the current understanding of molecular mechanisms underlying this response.

**Keywords:** photoreceptor, degeneration, genetic mutant, regeneration, Müller glia, genome editing, CRISPR/Cas9 system, zebrafish
