Abstract
A newly described mutant gene in Drosophila melanogaster suppresses the phenotype of theblack mutationb (2–48.5), which is known to cause melanization of the cuticle through a deficiency of β-alanine. The semi-dominant suppressor,Su(b) is X-linked and maps at 1–55.5 adjacent to or within therudimentary locus (r) controlling the level of the first three enzymes in the biosynthesis of pyrimidines. The suppressor ofrudimentary, su(r), known to block the degradation of uracil to β-alanine, enhances the melanization of the cuticle in theblack mutant flies. This suppressorsu(r) is epistatic over the suppressor ofblack resulting in an enhanced melanization insu(r) Su(b); b flies.
Feeding the pyrimidine analogue 6-azathymine to wild type larvae gives rise to a partial phenocopy ofblack. Resistance against melanization by 6-azathymine is provided bySu(b). The analogue 6-azauracil normalizes the mutantblack but not the double mutantsu(r);b. It is proposed thatSu(b) is a mutation in the regulatory gene for the formation of the first three enzymes in pyrimidine biosynthesis leading to overproduction of uracil. The degradation of this extra uracil into β-alanine would then permit the normal tanning of the cuticle in flies homo-or hemizygous forblack.
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Pedersen, M.B. Characterization of an X-linked semi-dominant suppessor ofblack Su(b) (1–55.5) in Drosophila melanogaster. Carlsberg Res. Commun. 47, 391–400 (1982). https://doi.org/10.1007/BF02907777
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DOI: https://doi.org/10.1007/BF02907777