NDPK, K-pn, l(3)j2A4, Kpn, abnormal wing disc
Gene model reviewed during 5.57
Gene model reviewed during 5.49
Three different translation starts have been annotated. The downstream transription/translation start is supported by RNA-seq and TSS data and is conserved in numerous insect species. The upstream transcription starts are used less frequently and are supported by RNA-seq data. The upstream translation start is conserved among Drosophila species.
Gene model reviewed during 5.56
Gene model reviewed during 6.02
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\awd using the Feature Mapper tool.
awd transcript is detected in larval wing discs. Transcript levels are highest in the posterior region of the wing pouch, but expression is detected in the anterior region of the dics by late third instar.
awd is expressed throughout development, as assesed by nucleotide diphodphate kinase enzyme assays. Highest levels of enzyme activity are detected between early embryonic and early larval stages, and lowest levels are detected during puparation.
GBrowse - Visual display of RNA-Seq signalsView Dmel\awd 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 merge of: awd l(3)j2A4
Source for merge of: awd l(3)L8700
Source for merge of: awd anon- EST:Liang-2.28
Source for merge of: awd BcDNA:RH27794
Source for merge of: awd BcDNA:GM19775
Source for merge of: awd anon-WO0172774.80 anon-WO0172774.82
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
Identification: as a modifier of a temperature sensitive paralytic mutation of shi.
There is an embryonic requirement for maternal germline awd expression, but the amount required is quite low.
The crystal structure of the awd protein has been solved at a resolution of 2.4 Angstroms. The active protein is a homohexamer.
An analysis of the biochemical properties of wild type and mutant awd proteins suggest that the mutation affects protein folding.
Homozygotes for loss-of-function alleles die in late third larval instar; wing discs variably hypoplastic; other discs appear grossly normal. Trypan blue staining reveals cell death in wing disc, either in area of presumptive wing blade, or scattered throughout disc; other discs reveal lesser amounts of cell death later in development than in wing discs. Extensive lipid vacuolization in larval ventral ganglion, brain lobes, and proventriculus. Mutant discs exhibit slow growth when transplanted into wild-type hosts; normal discs in mutant hosts grow normally. Metamorphosis of eye-antennal, wing and leg discs when transplanted into normal larvae severely restricted; few or no adult structures develop; mutant ovaries do not survive transplantation to wild-type hosts; however, transplanted awd pole cells capable of producing both awd/+ and awd/awd progeny. Epidermal clones nearly lethal and with thin, short, bent bristles and hairs when induced early; survive in reduced numbers and size when induced late.
Gain-of-function alleles first identified as Killer-of-prune, on the basis of their dominant synthetic lethality with mutant alleles of pn.
Encodes a nucleoside diphosphate kinase.