Gene model reviewed during 5.45
There is only one protein coding transcript and one polypeptide associated with this gene
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\ninaA using the Feature Mapper tool.
Eye-enriched transcripts determined by ratio of expression level in wild-type heads. versus expression level in so heads.
GBrowse - Visual display of RNA-Seq signalsView Dmel\ninaA 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.
Source for identity of: ninaA CG3966
In a sample of 79 genes with multiple introns, 33 showed significant heterogeneity in G+C content among introns of the same gene and significant positive correspondence between the intron and the third codon position G+C content within genes. These results are consistent with selection adding against preferred codons at the start of genes.
700,000 mutagenised flies were screened for visible deep pseudopupil ninaA phenotype, and 70 new alleles were isolated and characterised. Deep pseudopupil phenotype was scored on a 1-5 scale where 1= null ninaA phenotype and 5= weakest detectable ninaA phenotype. The rate of base changes suggests that mutagenic saturation of ninaA is being approached and that the majority of amino acid changes that remain unrecovered as mutations may be of no phenotypic consequence.
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.
Strong blue light leads to anomalously small degree of photoreceptor inactivation, and the prolonged depolarizing afterpotential PDA (seen after such treatment of wild-type photoreceptor cells) degrades rapidly following blue-light exposure reaching baseline levels within a few seconds.
Mutations in ninaA severely inhibit opsin transport from the ER, leading to dramatic accumulations of ER cisternae in the photoreceptor cells.
ninaA gene product is required for the synthesis of rhodopsin in a subset of photoreceptor cell types.
Only the six outer photoreceptors (R1-R6) in each eye facet are aberrant physiologically.Rhodopsin levels are much lower than normal in these outer cells; altered gene dosage of ninaA+ does not effect changes in rhodopsin levels; ninaA's mutant phenotypes are not suppressed by feeding on retinoid (e.g. vitamin A-enriched) media.