Rhodopsin light activation produces all-trans retinal, a toxic byproduct. As a result, animals with enhanced dim light sensitivity are at higher risk of retinal degeneration when exposed to bright light conditions. Rod arrestin (Arr-1) binds to rhodopsin and promotes sequestration of excess all-trans retinal, potentially protecting against photoreceptor cell death.
Recently, Castiglione et al. have discovered a rare rod arrestin (Arr-1) mutation in owls and deep-diving whales that significantly enhances the sequestration of all-trans retinal in vitro. This exciting functional convergence in animals at risk of retinal damage suggests Arr-1’s underappreciated role in the photoprotection of the eye and has important implications for visual disease.