Abstract
Pigment regeneration is critical for the function of cone photoreceptors in bright and rapidly-changing light conditions. This process is facilitated by the recently-characterized retina visual cycle, in which Müller cells recycle spent all-trans-retinol visual chromophore back to 11-cis-retinol. This 11-cis-retinol is oxidized selectively in cones to the 11-cis-retinal used for pigment regeneration. However, the enzyme responsible for the oxidation of 11-cis-retinol remains unknown. Here, we sought to determine whether retinol dehydrogenase 10 (RDH10), upregulated in rod/cone hybrid retinas and expressed abundantly in Müller cells, is the enzyme that drives this reaction. We created mice lacking RDH10 either in cone photoreceptors, Müller cells, or the entire retina. In vivo electroretinography and transretinal recordings revealed normal cone photoresponses in all RDH10-deficient mouse lines. Notably, their cone-driven dark adaptation both in vivo and in isolated retina was unaffected, indicating that RDH10 is not required for the function of the retina visual cycle. We also generated transgenic mice expressing RDH10 ectopically in rod cells. However, rod dark adaptation was unaffected by the expression of RDH10 and transgenic rods were unable to use cis-retinol for pigment regeneration. We conclude that RDH10 is not the dominant retina 11-cis-RDH, leaving its primary function in the retina unknown.
Highlights
Absorption of light by the chromophore of visual pigments in vertebrate photoreceptor cells results in its conversion from 11-cis- to all-trans-retinal
We examined whether overall cone dark adaptation in vivo, driven by both the retinal pigmented epithelium (RPE) and intraretinal visual cycles, is affected by the deletion of Rdh[10] in cones
In addition to the faster decay and regeneration of cone visual pigments compared to rhodopsin[39], such rapid dark adaptation could be facilitated by the ability of cone cells to oxidize 11-cis-retinol produced by Müller cells[9, 16]
Summary
Absorption of light by the chromophore of visual pigments in vertebrate photoreceptor cells results in its conversion from 11-cis- to all-trans-retinal. The supply of recycled chromophore appears to be the rate-limiting step of visual pigment regeneration that controls the kinetics of dark adaptation[4,5,6] This canonical visual cycle involves light-independent processing of the all-trans-chromophore by the retinal pigmented epithelium (RPE) followed by transfer of the recycled 11-cis-retinal to both rod and cone photoreceptors in the adjacent retina (reviewed in refs 3, 7 and 8). Unlike wild-type rods, hybrid rod photoreceptors in the rd[7] mouse retina can employ the typically cone-specific retina visual cycle[5] These hybrid rods can use 11-cis-retinol for pigment regeneration and dark adaptation, suggesting that rd[7] rods might express the unidentified cone-specific 11-cis-RDH. The possible involvement of RDH in the retina visual cycle and its function in the retina have not been investigated
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