Hostname: page-component-586b7cd67f-t7czq Total loading time: 0 Render date: 2024-11-23T00:59:48.641Z Has data issue: false hasContentIssue false
  • English
  • Français

The effects of nutritional deficiencies on the maroon-like maternal effect in Drosophila

Published online by Cambridge University Press:  14 April 2009

A. Chovnick  and
J. H. Sang
A. Chovnick
Affiliation:
Biological Sciences, University of Connecticut, Storrs, Connecticut, U.S.A.
J. H. Sang
Affiliation:
School of Biological Sciences, University of Sussex, Brighton, England
Rights & Permissions [Opens in a new window]

Extract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

1. The maroon-like maternal effect, present when ma-l flies are bred from non-mutant mothers, is not found among the late emergents from normal cultures. The hypothesis that this is due to a deficiency of some nutrient(s) in old cultures is tested by growing larvae on defined, germ-free media with the nutrients reduced one at a time.

2. Omission of lecithin (but not reduction of casein, sucrose, RNA or cholesterol) decreases the percentage of maternally affected emergents, in proportion to the lowering of the lecithin supply. This is not a consequence of choline deficiency but of the shortage of fatty acids. Oleic, palmitic and linoleic acids can substitute for lecithin, when adequate choline is provided.

3. Pantothenic acid, nicotinic acid, thiamine and biotin deficiencies (but not reduced pyridoxine, riboflavine or folic acid) also lower the proportion of maternally affected flies. There is an interaction between pantothenic acid and lecithin, but not between lecithin and the other effective vitamin deficiencies.

4. Addition of the excretory product hypoxanthine to the complete diet significantly lowers the proportion of maternally affected emergents, but equivalent amounts of uric acid, or of guanylic acid, do not. It is argued that the quantitive relationships make it improbable that accumulation of excretory products play any great part in the disappearance of the maternal effect, whereas it is more likely that nutritional deficiencies do.

5. ma-l larvae grown on low lecithin have the same complement of xanthine dehydrogenase as those reared on normal lecithin. The lecithin effect is therefore assumed to operate by affecting the pattern of pteridine synthesis. Phenylalanine, which would also be expected to alter this pattern, modifies the maternal effect similarly.

Type
Research Article
Information
Genetics Research , Volume 11 , Issue 1 , February 1968 , pp. 51 - 61
Copyright
Copyright © Cambridge University Press 1968

References

REFERENCES

Brenner-Holzach, O. & Leuthardt, F. (1961). Untersuchung über die Biosynthese der Pterine bie Drosophila melanogaster. Helv. chim. acta 44, 1480–1495.CrossRefGoogle Scholar
Chovnick, A. (1966). Genetic organisation in higher organisms. Proc. S. Soc. B 164, 198–208.Google ScholarPubMed
Courtright, J. B. (1967). Polygenic control of aldehyde oxidase in Drosophila. Genetics 57, 25–39.CrossRefGoogle ScholarPubMed
Forrest, H. S., Hanly, E. W. & Lagowski, J. M. (1961). Biochemical differences between the mutants rosy 2 and maroon-like of Drosophila melanogaster. Genetics 46, 1455–1463.CrossRefGoogle ScholarPubMed
Glassman, E. (1965). Genetic regulation of xanthine dehydrogenase in Drosophila melanogaster. Fedn Proc. 24, 1243–1251.Google ScholarPubMed
Glassman, E. & Keller, E. C. (1965). The maternal effect of ma-l +: the effect of hypoxanthine; the effect of lxd. Drosoph. Inf. Serv. 40, 92.Google Scholar
Glassman, E. & McLean, J. (1962). Maternal effect of ma-l + on xanthine dehydrogenase of Drosophila melanogaster. II. Xanthine dehydrogenase activity during development. Proc. natn. Acad. Sci. U.S.A. 48, 1712–1718.CrossRefGoogle ScholarPubMed
Glassman, E. & Mitchell, H. K. (1959). Mutants in Drosophila melanogaster deficient in xanthine dehydrogenase. Genetics 44, 153–162.CrossRefGoogle ScholarPubMed
Gordon, C. & Sang, J. H. (1941). The relation between nutrition and exhibition of the gene antennaless (Drosophila melanogaster). Proc. B. Soc. B 130, 151–184.Google Scholar
Hubby, J. L. & Forrest, H. S. (1960). Studies on the mutant maroon-like in Drosophila melanogaster. Genetics 45, 211–224.CrossRefGoogle ScholarPubMed
Kaufman, S. (1963). The structure of the phenylalanine-hydroxylation cofactor. Proc. natn. Acad. Sci. U.S.A. 50, 1085–1093.CrossRefGoogle ScholarPubMed
Keith, A. D. (1967). Fatty acid metabolism in Drosophila melanogaster: interactions between dietary fatty acids and de novo synthesis. Comp. Biochem. Physiol. 21, 587–600.CrossRefGoogle ScholarPubMed
Keller, E. C. & Glassman, E. (1965). Phenocopies of the ma-l and ry mutants of Drosophila melanogaster. Inhibition in vivo of xanthine dehydrogenase by 4-hydroxypyrazole (3, 4-d) pyrimidine. Nature, Lond. 208, 202–203.CrossRefGoogle Scholar
Kidder, G. W. & Dewey, V. C. (1963). Relationship between pyrimidine and lipid biosynthesis and unconjugated pteridine. Biochem. Biophys. Res. Comm. 12, 280–283.CrossRefGoogle ScholarPubMed
Sang, J. H. (1965). The quantitative nutritional requirements of Drosophila melanogaster. J. exp. Biol. 33, 45–72.CrossRefGoogle Scholar
Sang, J. H. & Burnet, B. (1963). Environmental modification of the eyeless phenotype in Drosophila melanogaster. Genetics 48, 1683–1699.CrossRefGoogle ScholarPubMed
Sang, J. H., McDonald, J. & Gordon, C. (1949). The ecological determinants of population growth in a Drosophila culture. VI. The total population count. Physiol. Zool. 22, 223–235.CrossRefGoogle Scholar