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The physiological control of gene action in the eyeless and eyegone mutants of Drosophila melanogaster

Published online by Cambridge University Press:  14 April 2009

David M. Hunt
Affiliation:
M.R.C. Experimental Genetics Unit, Department of Animal Genetics, University College London, Wolfson House, 4 Stephenson Way, London, NW 1 2HE
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The effect of dietary supplements of individual l-amino acids on the expression of the eyegone and eyelessK mutants of Drosophila melanogaster are compared. In both mutants, eye size is reduced by excess levels of tryptophan, phenylalanine and methionine, and in each case the effects are independent of metabolic competition for pyridoxal phosphate. A dietary interaction involving methionine and UNA can be demonstrated in the eyK strain, but the mechanism of action of this amino acid is obscure. Tryptophan metabolism is examined in detail. Although both tryptamine and serotonin have significant effects, the action of tryptophan on eye development is largely independent of its metabolic products. Conversely, the effect of dietary supplements of certain catecholamines is consistent with the action of phenylalanine. The action of certain metabolic inhibitors provides additional support for the suggestion that the catecholamines have an important effect on morphogenesis in the eye imaginai disks. Eye development is also affected by increasing concentrations of γ-amino-butyric acid, and this, taken together with the effect of the catecholamines and indolalkylamines, suggests that physiological control of the action of the mutant genes on eye development involves a group of compounds characteristically associated with nervous tissue. Eye development in the eyK strain may be influenced by the availability of acetyl CoA, which would be expected to affect acetylcholine biosynthesis. Possible mechanisms of action of the effective dietary treatments are discussed, together with a tentative hypothesis regarding the mode of action of the mutant genes on eye development.

Type
Research Article
Copyright
Copyright © Cambridge University Press 1971

References

REFERENCES

Arking, R. (1969). Phenogenetics of the eyeless-dominant mutant of Drosophila melanogaster. I. Development of the lethal larvae. Journal of Experimental Zoology, 171, 285296.CrossRefGoogle ScholarPubMed
Becking, G. C. & Johnson, W. L. (1967). The inhibition of tryptophan pyrrolase by allo-purinol, an inhibitor of xanthine oxidase. Canadian Journal of Biochemistry 45, 16671672.CrossRefGoogle Scholar
Bradford, H. F. (1968). Carbohydrate and energy metabolism. In Applied Neurochemistry (ed. Davison, A. N. and Dobbing, J.), pp. 222250. Oxford: Blackwell Scientific Publications.Google Scholar
Burnet, B. & Sang, J. H. (1968). Physiological genetics of melanotic tumors in Drosophila melanogaster. V. Amino acid metabolism and tumor formation in the tubw; st-su strain. Genetics 59, 211235.CrossRefGoogle Scholar
Fugio, Y. (1962). Studies on development of eye-antennal discs of Drosophila melanogaster in tissue culture. II. Effects of substances secreted from cephalic complexes upon eye-antennal discs of eye-mutant strains. Japanese Journal of Genetics 37, 110117.Google Scholar
Goldstein, M., Anagnoste, B., Tauber, E. & McKereghan, M. R. (1964). Inhibition of dopamine-β-hydroxylase by disulfiram. Life Sciences 3, 763767.CrossRefGoogle ScholarPubMed
Goldstein, M. & Contrera, J. F. (1962). The activation and inhibition of phenylalanine-β-hydroxylase. Experientia 18, 334.CrossRefGoogle Scholar
Hunt, D. M. (1969). Gene-environment interactions of the eye-gone mutant in Drosophila melanogasler and a comparison with eyeless. Genetical Research 13, 313320.CrossRefGoogle Scholar
Hunt, D. M. (1970). Lethal interactions of the eye-gone and eyeless mutants in Drosophila melanogaster. Genetical Research 15, 2934.CrossRefGoogle ScholarPubMed
Hunt, D. M. & Burnet, B. (1969). Gene-environment interactions of the eyeless mutant in Drosophila melanogaster. Genetical Research 13, 251265.CrossRefGoogle ScholarPubMed
Jacobs, M. E. (1968 a). β-Alanine use by ebony and normal Drosophila melanogaster with notes on glucose, uracil, dopa, and dopamine. Biochemical Genetics 1, 267275.CrossRefGoogle ScholarPubMed
Jacobs, M. E. (1968 b). Effects of beta-alanine on glucose and fructose catabolism in Drosophila melanogaster with notes on beta-aminoisobutyric and gamma-aminobutvric acids. Journal of Insect Physiology 14, 12591264.CrossRefGoogle ScholarPubMed
Koe, B. K. & Weissman, A. (1966). p–Chlorophenylalanine: a specific depletor of brain serotonin. Journal of Pharmacology and Experimental Therapeutics 154, 499516.Google ScholarPubMed
Marzluf, G. A. (1969). The use of specific metabolic inhibitors to study morphological mutants of Drosophila. Journal of Insect Physiology 15, 12911300.CrossRefGoogle Scholar
Neame, K. D. (1968). Transport, metabolism and pharmacology of amino acids in brain. In Applied Neurochemistry (ed. Davison, A. N. and Dobbing, J.), pp. 119177. Oxford: Blackwell Scientific Publications.Google Scholar
Park, D. H. & Gubler, C. J. (1969). Studies on the physiological functions of thiamine. V. Effects of thiamine deprivation and thiamine antagonists on blood pyruvate and lactate levels and activity of lactate dehydrogenase and its isozymes in blood and tissues. Biochimica biophysica Acta 177, 537543.Google ScholarPubMed
Ray, P. D., Foster, D. O. & Lardy, H. A. (1966). Paths of carbon in gluconeogenesis and lipogenesis. IV. Inhibition by L-tryptophan of hepatic gluconeogenesis at the level of phos-phoenolpyruvate formation. Journal of Biological Chemistry 241, 39043908.CrossRefGoogle Scholar
Sang, J. H. (1956). The quantitative nutritional requirements of Drosophila melanogaster. Journal of Experimental Biology 33, 4572.CrossRefGoogle Scholar
Sang, J. H. (1969). Biochemical basis of hereditary melanotic tumors in Drosophila. National Cancer Institute Monographs 31, 291301.Google ScholarPubMed
Sang, J. H. & Burnet, B. (1963). Environmental modification of the eyeless phenotype in Drosophila melanogaster. Genetics 48, 16831699.CrossRefGoogle ScholarPubMed
De Schaepdryver, A., Preziosi, P. & Scapagnini, U. (1969). Brain monoamuies and adreno-cortical activation. British Journal of Pharmacology 35, 460467.CrossRefGoogle Scholar
Schneider, I. (1964). Differentiation of larval Drosophila eye-antennal discs in vitro. Journal of Experimental Zoology 156, 91104.CrossRefGoogle ScholarPubMed
Sourkes, T. L. & D'Lorio, A. (1963). Inhibitors of catechol amine metabolism. In Metabolic Inhibitors, vol.II (ed. Hochster, R. M. and Quastel, J. H.), pp. 7998. New York: Academic Press.CrossRefGoogle Scholar
Springe, H., Parker, C. M., Jameson, D. & Josephs, J. A. (1969). Experimental alteration of tryptophan metabolism by methionine: neuropharmacologic implications. International Journal of Neuropharmacology 8, 615626.CrossRefGoogle Scholar
Taylor, R. J. Jr., Stubbs, C. S. Jr. & Ellenbogen, L. (1969). Tyrosine hydroxylase inhibition in vitro and in vivo by chelating agents. Biochemical Pharmacology 18, 587594.CrossRefGoogle ScholarPubMed
Woolf, B. (1951). Calculation of X 2 for a 2 × 2 table. Nature 168, 1087.CrossRefGoogle Scholar