biostudies-literatureGegnaw STCentre National de la Recherche Scientifique (CNRS)EC | Chafea | Consumer Programme (Consumer Programme - European Commission)Consumer ProgrammeCentre National de la Recherche Scientifiquee70507https://www.ebi.ac.uk/biostudies/studies/S-EPMC11962828biostudies-literatureUnknown39(7)Daily rhythms are a central hallmark of vision, in particular by adapting retinal physiology and light response to the day-night cycle. These cyclic processes are regulated by retinal circadian clocks, molecular machineries regulating gene expression across the 24-h cycle. Although hundreds of genes associated with genetic retinal disorders have been identified, no direct link has been established with the clock. Hence, we investigated the hypothesis that a poorly functioning circadian clock aggravates retinal photoreceptor disease. We performed this study in the P23H rhodopsin-mutated mouse model (P23H Rho) that mimics one major cause of human autosomal dominant retinitis pigmentosa. We also used the rod-specific knockout (rod-Bmal1KO) of Bmal1, a key clock component. More specifically, wFASEB journal : official publication of the Federation of American Societies for Experimental BiologyCircadian clock disruption promotes retinal photoreceptor degeneration.PMC11962828NeuroTime Erasmus+ grantCore fundingMoerland PDFelder-Schmittbuhl MPGegnaw STTen Brink JBMilicevic NJongejan ABergen AASandu CBery AfalseCircadian clock disruption promotes retinal photoreceptor degeneration.Daily rhythms are a central hallmark of vision, in particular by adapting retinal physiology and light response to the day-night cycle. These cyclic processes are regulated by retinal circadian clocks, molecular machineries regulating gene expression across the 24-h cycle. Although hundreds of genes associated with genetic retinal disorders have been identified, no direct link has been established with the clock. Hence, we investigated the hypothesis that a poorly functioning circadian clock aggravates retinal photoreceptor disease. We performed this study in the P23H rhodopsin-mutated mouse model (P23H Rho) that mimics one major cause of human autosomal dominant retinitis pigmentosa. We also used the rod-specific knockout (rod-Bmal1KO) of Bmal1, a key clock component. More specifically, w2025-01-01T00:00:00Z2025 Apr2026-07-15T11:10:29.017Z2025-07-11T03:03:53.224ZS-EPMC119628284017179510.1096/fj.202401967R