myosin III, DRONINAC, Nina C
Gene model reviewed during 5.47
5, 4 (northern blot)
1501, 1135 (aa); 174, 132 (kD observed)
Interacts with rtp.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\ninaC using the Feature Mapper tool.
A polyclonal antibody recognizes both the 132 and 174 kD ninaC proteins in head, but not body, extracts.
GBrowse - Visual display of RNA-Seq signalsView Dmel\ninaC in GBrowse 2
Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete
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.
Light-dependent translocation of Arr2 protein into the rhabdomere requires ninaC protein (the ninaC p132 isoform is the primary isoform needed). The interaction between the Arr2 and ninaC proteins is phosphoinositide (PI) dependent and ninaC protein binds PIs directly.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
Mutation rate at microsatellite loci in 119 lines maintained for approximately 250 generations is estimated to be 6.3x10-6, at least one order of magnitude lower than the mutation rate in mammals.
Using whole-cell recording and measurements of the pupil mechanisms the p174 protein of ninaC is suggested to be required for normal termination of the transduction cascade.
Both Ca2+-dependent binding sites in the ninaC calmodulin binding domain are required for normal calmodulin distribution in vivo and for phototransduction. The electrophysiological phenotype resulting from mutation of the binding sites indicates the p174-calmodulin interaction has a role in the termination of the photoresponse.
The calcium content of light and dark raised flies demonstrates that calcium accumulation is a secondary effect, rather than primary effect, in the degeneration process.
Two different phylogenetic methods used to analyse all available myosin head sequences: there are at least three equally divergent classes of myosin, demonstrating that the current classification into two classes needs to be reexamined.
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.
Mutations affect eye morphology.
Basic physiological and rhodopsin-depleted phenotypes like those of ninaB or ninaD mutants, except that amplitude of prolonged depolarizing afterpotential and rhodopsin levels are not so severely depressed and these phenotypes cannot be rescued by vitamin A (or other retinoid) feeding.
ninaC is required for maintenance of the rhabdomeres during light and for normal phototransduction.
ninaC gene product is a regulatory protein that modulates the activity of other proteins important in phototransduction by phosphorylation.
Decreased rhodopsin content is due to reduction in diameter of the rhabdomeres; the microvilli are shorter than normal and have reduced cytoskeletal electron-dense regions.