Gene model reviewed during 5.45
Annotated transcripts do not represent all supported alternative splices within 5' UTR.
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.51
Gene model reviewed during 6.23
661 (aa); 95 (kD observed)
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\rdgC using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signalsView Dmel\rdgC 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.
Source for merge of: rdgC CG13814
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
The calmodulin/rdgC interaction is required to potentiate dephosphorylation of rhodopsin in vivo and for rapid termination of the photoresponse.
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.
In disrupted photoreceptor cells metarhodopsin is not stabilised until arrestin is present. In intact photoreceptor cels significant metarhodopsin stabilisation occurs even in the absence of bound arrestin.
Phototransduction, a phospholipase C-mediated, calcium-regulated G protein-coupled pathway, is studied for genetic dissection of G protein-coupled receptor (GPCR) function and regulation.
ninaE mutants act as dominant rhodopsin mutants by suppressing the production of the wild type ninaE rhodopsin. As a consequence of the lowered rhodopsin content the mutations suppress the rapid retinal degeneration associated with rdgC and norpA mutations.
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.