ISSN:
1617-4623
Keywords:
Pyrimidines
;
β-Alanine
;
Cuticle
;
rudimentary
;
black
Source:
Springer Online Journal Archives 1860-2000
Topics:
Biology
Notes:
Abstract A deficiency in the production of β-alanine causes the black (b) phenotype of Drosophila melanogaster. This phenotype is normalized by a semi-dominant mutant gene Su(b) shown previously to be located adjacent to or within the rudimentary (r) locus. The r gene codes for three enzyme activities involved in de novo pyrimidine biosynthesis. Pyrimidines are known to give rise to β-alanine. However, until recently it has been unclear whether de novo pyrimidine biosynthesis is directly coupled to β-alanine synthesis during the tanning process. In this report we show that flies carrying Su(b) can exhibit an additional phenotype, resistance to toxic pyrimidine analogs (5-fluorouracil, 6-azathymine and 6-azauracil). Our interpretation of this observation is that the pyrimidine pool is elevated in the mutant flies. However, enzyme assays indicate that r enzyme activities are not increased in Su(b) flies. Genetic mapping of the Su(b) gene now places the mutation within the r gene, possibly in the carbamyl phosphate synthetase (CPSase) domain. The kinetics of CPSase activity in crude extracts has been studied in the presence of uridine triphosphate (UTP). While CPSase from wild-type flies was strongly inhibited by the end-product, UTP, CPSase from Su(b) was inhibited to a lesser extent. We propose that diminished end-product inhibition of de novo pyrimidine biosynthesis in Su(b) flies increases available pyrimidine and consequently the β-alanine pool. Normalization of the black phenotype results.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00284686
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