Gene model reviewed during 5.43
Gene model reviewed during 5.47
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\Dhod using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signalsView Dmel\Dhod 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.
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.
A novel class of Dhod RNA of approximately 1.6kb is relatively abundant in adult males. Expression of a male specific promoter is limited to spermatogenic cells. This RNA is subject to a translational delay system operative during spermatogenesis.
Structural organisation, embryonic transcript and protein product of Dhod are characterised.
The location of the Dhod gene within 85A has been determined by mapping two rearrangement mutations. A cDNA clone has been isolated and the developmental expression of the Dhod transcript has been studied.
Dhod was involved in a complementation analysis of the 85A region.
Likely to be the structural gene for dehydroorotate dehydrogenase, which catalyzes the fourth enzymatic step of de novo pyrimidine biosynthesis (DHOdehase). Homozygotes for null alleles display less than 3% normal levels of enzyme activity; heterozygotes have half-normal levels; flies with three normal alleles show increased levels. Enzyme appears to be monomeric; no interallelic complementation among null alleles. Enzyme activity located in outer surface of inner mitochondrial membrane in other species; also mitochondrial in Drosophila. Homozygotes for null alleles exhibit wing truncation, irregular lengths and distribution of hairs on wing margin, deformed posterior legs and female sterility, as seen in r and r-l. Viability normal. Phenotype suppressed, but enzyme level not restored, by su(r). Null mutants suppress eye mottling characteristic of r-l in doubly mutant genotypes.