Juvenile-onset visual impairment in zebrafish rlbp1b mutants highlights Müller glia contributions to cone vision.

Vision depends on the continuous recycling of the visual pigment chromophore 11-cis-retinal, which is converted by light into all-trans-retinal at the onset of the phototransduction cascade. Cellular retinaldehyde-binding protein 1 (CRALBP1) is a key component of both the canonical visual cycle in the retinal pigment epithelium (RPE) and the cone-specific recycling pathway mediated by Müller glia (MG) cells. Previous studies demonstrated that knockout of the RPE-specific gene rlbp1a (encoding CRALBP1) results in severe physiological and morphological defects that are evident already at cone dominant larval stages in zebrafish. In contrast, mutants lacking the MG-specific paralog rlbp1b showed no obvious phenotype during early development. Here, we show that juvenile rlbp1b mutants, when the retina has incorporated rod photoreceptors, exhibit reduced b-wave amplitudes in the electroretinogram under dark-adapted conditions, accompanied by a progressively prolonged time-to-peak at higher light intensities. These results underscore the importance of both illumination conditions and retinal maturation when investigating visual pigment recycling dynamics in cone vision.