Molecular components affecting ocular carotenoid and retinoid homeostasis

The photochemistry of vision employs opsins and geometric isomerization of their covalently bound retinylidine chromophores. In different animal classes, these light receptors associate with distinct G proteins that either hyperpolarize or depolarize photoreceptor membranes. Vertebrates also use the acidic form of chromophore, retinoic acid, as the ligand of nuclear hormone receptors that orchestrate eye development. To establish and sustain these processes, animals must acquire carotenoids from the diet, transport them, and metabolize them to chromophore and retinoic acid. The understanding of carotenoid metabolism, however, lagged behind our knowledge about the biology of their receptor molecules. In the past decades, much progress has been made in identifying the genes encoding proteins that mediate the transport and enzymatic transformations of carotenoids and their retinoid metabolites. Comparative analysis in different animal classes revealed how evolutionary tinkering with a limited number of genes evolved different biochemical strategies to supply photoreceptors with chromophore. Mutations in these genes impair carotenoid metabolism and induce various ocular pathologies. This review summarizes this advancement and introduces the involved proteins, including the homeostatic regulation of their activities.

Automated summary

The photochemistry of vision involves opsins and the isomerization of their retinylidine chromophores. Different animal classes use distinct G proteins to regulate the photoreceptor membranes. Vertebrates utilize retinoic acid as a ligand for nuclear hormone receptors, while obtaining carotenoids from diet and metabolizing them. Recent advancements have led to a better understanding of carotenoid metabolism and its impact on ocular pathologies.