Visual
opsins are
proteins expressed by retinal photoreceptors that capture light to begin the process of phototransduction. In vertebrates, the two types of photoreceptors (rods and cones) express one or multiple
opsins and are distributed in variable patterns across the retina. Some cones form
opsin retinal gradients, as in the mouse, whereas others form more demarcated
opsin domains, as in the lattice-like mosaic retinas of teleost fishes. Reduced
rod opsin (rh1) expression in mouse, zebrafish, and African clawed frog results in lack of photoreceptor outer segments (i.e., the cilium that houses the
opsins) and, in the case of the mouse, to
retinal degeneration. The effects of diminished
cone opsin expression have only been studied in the mouse where knockout of the short-wavelength sensitive 1 (sws1)
opsin leads to ventral retinal cones lacking outer segments, but no
retinal degeneration. Here we show that, following CRISPR/Cas9
injections that targeted knockout of the sws1
opsin in rainbow trout, fish with diminished sws1
opsin expression exhibited a variety of developmental defects including head and eye malformations, underdeveloped outer retina, mislocalized
opsin expression, cone degeneration, and mosaic irregularity. All photoreceptor types were affected even though sws1 is only expressed in the single cones of wild fish. Our results reveal unprecedented developmental defects associated with diminished
cone opsin expression and suggest that visual
opsin genes are involved in regulatory processes that precede photoreceptor differentiation.