Gene model reviewed during 5.50
None of the polypeptides share 100% sequence identity.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\ninaD using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signalsView Dmel\ninaD in GBrowse 2
Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see GBrowse for alignment of the cDNAs and ESTs to the gene model.
For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.
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.
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).