The Dhod locus of Drosophila: mutations and interrelationships with other loci controlling de novo pyrimidine biosynthesis.
Mutations at the Dhod locus have been isolated following ethylmethanesulfonate mutagenesis. These mutants express those phenotypes common to other mutations of the de novo pyrimidine pathway: specific wing and leg defects and female sterility. Dihydroorotate dehydrogenase activity is severely reduced in all Dhod mutants, whereas levels of the other pathway enzymes are largely unaffected. The twelve Dhod mutations described here comprise a single complementation group. All of these mutations are nonlethal and the collection includes apparent amorphic as well as hypomorphic alleles. These results are discussed relative to the properties of the complex loci that encode the other steps of de novo pyrimidine biosynthesis.
D000818:Animals; D003433:Crosses, Genetic; D004080:Dihydroorotase / Q000235:genetics; D004081:Dihydroorotate Oxidase / Q000235:genetics*; D004330:Drosophila / Q000201:enzymology / Q000235:genetics*; D005260:Female; D006579:Heterozygote; D006720:Homozygote; D008297:Male; D009154:Mutation; D009962:Orotate Phosphoribosyltransferase / Q000235:genetics; D009964:Orotidine-5'-Phosphate Decarboxylase / Q000235:genetics; D010088:Oxidoreductases / Q000235:genetics*; D010641:Phenotype; D011743:Pyrimidines / Q000096:biosynthesis*
D011743:Pyrimidines; D010088:Oxidoreductases; D004081:Dihydroorotate Oxidase; D009962:Orotate Phosphoribosyltransferase; D004080:Dihydroorotase; D009964:Orotidine-5'-Phosphate Decarboxylase