Enhanced Robustness of the Mouse Retinal Circadian Clock Upon Inherited Retina Degeneration

Shumet T Gegnaw; Cristina Sandu; Nadia Mazzaro; Jorge Mendoza; Arthur A Bergen; Marie-Paule Felder-Schmittbuhl

doi:10.1177/07487304221112845

Enhanced Robustness of the Mouse Retinal Circadian Clock Upon Inherited Retina Degeneration

Shumet T Gegnaw, Cristina Sandu, Nadia Mazzaro, Jorge Mendoza, Arthur A Bergen, Marie-Paule Felder-Schmittbuhl

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Onderzoeksoutput: Bijdrage aan wetenschappelijk tijdschrift/periodieke uitgave › Artikel › Wetenschappelijk › peer review

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Daily biological rhythms are fundamental to retinal physiology and visual function. They are generated by a local circadian clock composed of a network of cell type/layer-specific, coupled oscillators. Animal models of retinal degeneration have been instrumental in characterizing the anatomical organization of the retinal clock. However, it is still unclear, among the multiple cell-types composing the retina, which ones are essential for proper circadian function. In this study, we used a previously well-characterized mouse model for autosomal dominant retinitis pigmentosa to examine the relationship between rod degeneration and the retinal circadian clock. This model carries the P23H mutation in rhodopsin, which induces mild rod degeneration in heterozygous and rapid loss of photoreceptors in homozygous genotypes. By measuring PER2::LUC bioluminescence rhythms, we show that the retinal clock in P23H/+ heterozygous mice displays circadian rhythms with significantly increased robustness and amplitude. By treating retinal explants with L-α aminoadipic acid, we further provide evidence that this enhanced rhythmicity might involve activation of Müller glial cells.

Originele taal-2	Engels
Pagina's (van-tot)	567-574
Tijdschrift	Journal of Biological Rhythms
Volume	37
DOI's	https://doi.org/10.1177/07487304221112845
Status	Gepubliceerd - jul. 2022

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10.1177/07487304221112845

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abstract = "Daily biological rhythms are fundamental to retinal physiology and visual function. They are generated by a local circadian clock composed of a network of cell type/layer-specific, coupled oscillators. Animal models of retinal degeneration have been instrumental in characterizing the anatomical organization of the retinal clock. However, it is still unclear, among the multiple cell-types composing the retina, which ones are essential for proper circadian function. In this study, we used a previously well-characterized mouse model for autosomal dominant retinitis pigmentosa to examine the relationship between rod degeneration and the retinal circadian clock. This model carries the P23H mutation in rhodopsin, which induces mild rod degeneration in heterozygous and rapid loss of photoreceptors in homozygous genotypes. By measuring PER2::LUC bioluminescence rhythms, we show that the retinal clock in P23H/+ heterozygous mice displays circadian rhythms with significantly increased robustness and amplitude. By treating retinal explants with L-α aminoadipic acid, we further provide evidence that this enhanced rhythmicity might involve activation of M{\"u}ller glial cells.",

author = "Gegnaw, {Shumet T} and Cristina Sandu and Nadia Mazzaro and Jorge Mendoza and Bergen, {Arthur A} and Marie-Paule Felder-Schmittbuhl",

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AU - Gegnaw, Shumet T

AU - Sandu, Cristina

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AU - Mendoza, Jorge

AU - Bergen, Arthur A

AU - Felder-Schmittbuhl, Marie-Paule

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AB - Daily biological rhythms are fundamental to retinal physiology and visual function. They are generated by a local circadian clock composed of a network of cell type/layer-specific, coupled oscillators. Animal models of retinal degeneration have been instrumental in characterizing the anatomical organization of the retinal clock. However, it is still unclear, among the multiple cell-types composing the retina, which ones are essential for proper circadian function. In this study, we used a previously well-characterized mouse model for autosomal dominant retinitis pigmentosa to examine the relationship between rod degeneration and the retinal circadian clock. This model carries the P23H mutation in rhodopsin, which induces mild rod degeneration in heterozygous and rapid loss of photoreceptors in homozygous genotypes. By measuring PER2::LUC bioluminescence rhythms, we show that the retinal clock in P23H/+ heterozygous mice displays circadian rhythms with significantly increased robustness and amplitude. By treating retinal explants with L-α aminoadipic acid, we further provide evidence that this enhanced rhythmicity might involve activation of Müller glial cells.

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Enhanced Robustness of the Mouse Retinal Circadian Clock Upon Inherited Retina Degeneration

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