Publication Date
3-1-2022
Journal
Proceedings of the National Academy of Sciences of the United States of America
DOI
10.1073/pnas.2115138119
PMID
35197287
PMCID
PMC8892328
PubMedCentral® Posted Date
2-23-2022
PubMedCentral® Full Text Version
Post-print
Published Open-Access
yes
Keywords
Animals, Cone Opsins, Electroretinography, Light Signal Transduction, Loss of Function Mutation, Mice, Retinal Cone Photoreceptor Cells, Retinal Pigments, Signal Transduction, cone opsin, rod–cone gap junction, cone photoreceptor, rod photoreceptor
Abstract
Rhodopsin and cone opsins are essential for light detection in vertebrate rods and cones, respectively. It is well established that rhodopsin is required for rod phototransduction, outer segment disk morphogenesis, and rod viability. However, the roles of cone opsins are less well understood. In this study, we adopted a loss-of-function approach to investigate the physiological roles of cone opsins in mice. We showed that cones lacking cone opsins do not form normal outer segments due to the lack of disk morphogenesis. Surprisingly, cone opsin-deficient cones survive for at least 12 mo, which is in stark contrast to the rapid rod degeneration observed in rhodopsin-deficient mice, suggesting that cone opsins are dispensable for cone viability. Although the mutant cones do not respond to light directly, they maintain a normal dark current and continue to mediate visual signaling by relaying the rod signal through rod-cone gap junctions. Our work reveals a striking difference between the role of rhodopsin and cone opsins in photoreceptor viability.