ninaB and ninaD are not required in the retina, and exclusive retinal expression of either ninaB or ninaD, or both genes simultaneously, does not support rhodopsin biogenesis. Neuron-specific expression of ninaB and ninaD allows for rhodopsin biogenesis.

Major opsin genes can be transcribed in the absence of carotenoid, or retinoid. Expression of mature opsin is extremely depressed by carotenoid deprivation. The chromophore 11-cis-3-hydroxyretinal accelerates the synthesis of opsin by inducing its maturation.

Not the same gene as the very closely linked Arr1 (which produces a 'phototransduction protein'); this was shown by sequencing coding exons of genomic DNA from ninaD², ninaD³ and ninaD⁵, all of which exhibited wild-type arrestin sequences in these ORFs (Smith et al., 1990).

Basic physiological and rhodopsin-depleted phenotypes like those of ninaB mutants (e.g. rhodopsin levels reduced in all three classes of photoreceptors); ninaD mutants can be rescued by dietary supplement of vitamin A and several other retinoids. Measurements of light-induced 'quantum bumps' (the basic 'units' of the photoreceptor potential) in ninaD² (rhodopsin content, 10^-2 X wild-type) showed these responses to be basically normal (implying that, since extensive inter-rhodopsin molecular interactions are likely to be extremely rare, such interactions are not necessary for generation and adaptation of the bumps); yet, bump amplitudes approximately 4X normal (Johnson and Pak, 1986).