Reference Report
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| Citation | Rawls, J.M. (2006). Analysis of pyrimidine catabolism in Drosophila melanogaster using epistatic interactions with mutations of pyrimidine biosynthesis and beta-alanine metabolism. Genetics 172(3): 1665--1674. (Export to RIS) | ||
| FlyBase ID | FBrf0192211 | ||
| Publication Type | Research paper | ||
| PubMed ID | 16361227 | ||
| PubMed Abstract | The biochemical pathway for pyrimidine catabolism links the pathways for pyrimidine biosynthesis and salvage with beta-alanine metabolism, providing an array of epistatic interactions with which to analyze mutations of these pathways. Loss-of-function mutations have been identified and characterized for each of the enzymes for pyrimidine catabolism: dihydropyrimidine dehydrogenase (DPD), su(r) mutants; dihydropyrimidinase (DHP), CRMP mutants; beta-alanine synthase (betaAS), pyd3 mutants. For all three genes, mutants are viable and fertile and manifest no obvious phenotypes, aside from a variety of epistatic interactions. Mutations of all three genes disrupt suppression by the rudimentary gain-of-function mutation (r(Su(b))) of the dark cuticle phenotype of black mutants in which beta-alanine pools are diminished; these results confirm that pyrimidines are the major source of beta-alanine in cuticle pigmentation. The truncated wing phenotype of rudimentary mutants is suppressed completely by su(r) mutations and partially by CRMP mutations; however, no suppression is exhibited by pyd3 mutations. Similarly, su(r) mutants are hypersensitive to dietary 5-fluorouracil, CRMP mutants are less sensitive, and pyd3 mutants exhibit wild-type sensitivity. These results are discussed in the context of similar consequences of 5-fluoropyrimidine toxicity and pyrimidine catabolism mutations in humans. | ||
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| Secondary IDs | FBrf0190764 | ||
| Language of Publication | English | ||
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Parent Publication
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| Publication Type | Journal | ||
| Abbreviation | Genetics | ||
| Title | Genetics | ||
| Publication Year | 1916- | ||
| ISBN/ISSN | 0016-6731 | ||
Data from Reference
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Aberrations (1)
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Alleles (20)
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Constructs (4)
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Genes (7)
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Insertions (3)
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Natural transposons (1)
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