ade3, adenosine 3
Gene model reviewed during 5.49
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.55
4.7, 1.7 (northern blot)
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\Gart using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signalsView Dmel\Gart 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: Gart ade3
Renamed from 'ade3' to 'Gart' (in FB2018_01) to reflect usage in the literature and provide nomenclature consistent with the clear vertebrate ortholog (and replace existing nomenclature suggesting incorrect relationships to yeast orthologs).
Encodes the three enzymes in the purine biosynthetic pathway, glycineamide ribotide synthetase (GARS), aminoimidazole ribotide synthetase (AIRS) and GART.
Purine nucleoside auxotroph supplementable with adenine, adenosine and inosine. Recovery of ade3 progeny from crosses between ade31 and ade31/SM5 is about 1% when raised on minimal medium. Less than 3% of the normal activity purine de novo synthetic pathway enzyme, glycineamide ribotide transformylase (GART). Mutants, if viable, have a brownish eye colour and wing and bristle defects.
Nucleotide excision repair of (6-4)photoproducts has been assayed in the ade3 locus of Kc (embryonic) cell line, after exposure to UV light. The ade3 locus is transcriptionally active in Kc cells, but the repair rate is the same as for the transcriptionally inactive white gene, as well as for the transcriptionally active N gene. Repair rate is enhanced with prior exposure to photoreactivating light. No strand specificity of repair is observed.
Removal of UV-induced pyrimidine dimers is measured in genes ade3, N and w in two diploid immortalised cell lines (Kc and SL2) to investigate whether preferential repair forms part of DNA excision repair. Data supports the idea that preferential repair is not restricted to transcriptionally active sequences.
The organization of the ade3 protein in Drosophila has multiple domains with GAR transformylase at the carboxyl terminus preceded by an extensive repeat.