Meeting Abstract
A central tenet of retinal neurobiology holds that the “duplex” mammalian retina functionally requires both rod and cone photoreceptors. The implications of cone photoreceptor loss on the mammalian retina is completely unknown outside of retinal disease and induced mutations in model organisms, but the recent observation of cone opsin mutation in some cetacean lineages provides a novel opportunity to investigate the effects of a natural, photoreceptor-specific mutation on retinal organization. We sequenced right whale (Eubalaena glacialis) cDNA derived from cone opsin mRNA and found an early nonsense mutation of their single cone opsin gene, suggesting loss of cone cell function but maintenance of non-photosensitive, opsin mRNA-expressing cells in the retina (i.e., cone soma). Therefore, we investigated the Balaenid whale retina to determine how the unprecedented loss of an entire photoreceptor class affects light signaling pathways. Anti-opsin immunofluorescence demonstrated the total loss of cone opsin expression in the bowhead whale (Balaena mysticetus), while light microscopy, transmission electron microscopy and bipolar cell immunofluorescence (against PKC-α and recoverin) revealed the loss of cone photoreceptor outer segments but maintenance of both rod and cone bipolar cell types. These findings demonstrate for the first time a naturally rod-monochromatic retina in mammals and suggest that despite the loss of cone-mediated photoreception, the associated cone signaling machinery may be functionally maintained for multi-channel rod-based signaling in Balaenid whales.
