Based on these results, it is likely that the phenotypes we observed in genetically mosaic F0 animals (Figs 1 and 2) are due to a combination of loss-of-function frameshifting and gain-of-function frame-conserving mutations, modeling equivalent effects of loss-of-function and gain-of-function rhodopsin mutations responsible for recessive and dominant forms of the human disorder retinitis pigmentosa. This evidence concerns the gene RHO and retinitis pigmentosa.