Hostname: page-component-848d4c4894-5nwft Total loading time: 0 Render date: 2024-05-27T04:27:47.360Z Has data issue: false hasContentIssue false
  • English
  • Français

Experimental modification of the dominance relations of a melanotic tumour gene in Drosophila melanogaster

Published online by Cambridge University Press:  14 April 2009

Ann Louise Belt  and
Barrie Burnet
Ann Louise Belt
Affiliation:
Department of Genetics, University of Sheffield, England
Barrie Burnet
Affiliation:
Department of Genetics, University of Sheffield, England

Summary

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.

The melanotic tumour gene tu-C4 in Drosophila melanogaster shows incomplete dominance, together with variable penetrance and expressivity. It is tentatively located in the region of locus 52–53 on the third chromosome. Tumour formation in mutant homozygotes involves a precocious haemocyte transformation leading to the appearance of lamellocytes at the beginning of the third larval instar. These aggregate to form tumour-like masses which subsequently melanize. The process of tumour formation is in broad outline similar to that found in other tumour strains. Melanotic tumour formation is treated as a dichotomous threshold character, assuming an underlying normal distribution of liability relative to a fixed threshold. The expression of the tumour gene can be influenced by the levels of protein, phospholipid, nucleic acid and carbohydrate in the larval food medium, and changes in dominance and penetrance induced by sub-optimal environments deficient in these nutrients are positively correlated. Reinforcement by selection of the dominance relations of tu-C4 was accompanied by correlated changes in penetrance. Conversely, selection for increased penetrance was accompanied by correlated changes in dominance. Dominance and penetrance, it is concluded, are fundamentally related aspects of tumour gene expression. Recruitment of dominance modifiers linked to the tumour gene was excluded by the mating scheme employed, and the observed changes in dominance relations in response to selection were due largely to modifiers located on the second chromosome. Changes in dominance relations produced by selection could be significantly reinforced, or reversed, by environmental factors and consequently show a substantial genotype – environment interaction effect. These facts are relevant to current theories of dominance evolution.

Type
Research Article
Information
Genetics Research , Volume 20 , Issue 1 , August 1972 , pp. 115 - 135
Copyright
Copyright © Cambridge University Press 1972

References

REFERENCES

Bailey, N. T. J. (1961). Introduction to the Mathematical Theory of Genetic Linkage. OxfordUniversity Press.Google Scholar
Barigozzi, C. & Pasquale, A. Di (1956). A contribution to the genetics of the so-called melanotic tumours (pseudotumours) of Drosophila melanogaster. Rendiconti Istituto Lombardo di Scienze e Lettere 90, 484–509.Google Scholar
Burnet, B. & Sang, J. H. (1964). Physiological genetics of melanotic tumours in Drosophila melanogaster. III. Phenocritical period in relation to tumour formation in the tu bw; st su-tu strain. Genetics 49, 599–610.CrossRefGoogle Scholar
Burnet, B. & Sang, J. H. (1968). Physiological genetics of melanotic tumours in Drosophila melanogaster. V. Amino acid metabolism and tumour formation in the tu bw;st su-tu strain. Genetics 59, 211–235.CrossRefGoogle Scholar
Clarke, C. A. & Sheppard, P. M. (1960). The evolution of dominance under disruptive selection. Heredity 14, 73–87.CrossRefGoogle Scholar
Crosby, J. L. (1963). The evolution and nature of dominance. Journal of Theoretical Biology 5, 35–51.CrossRefGoogle ScholarPubMed
Falconer, D. S. (1960). Introduction to Quantitative Genetics. Edinburgh: Oliver and Boyd.Google Scholar
Fisher, R. A. (1928). The possible modification of the response of the wild type to recurrent mutations. American Naturalist 62, 115–126.CrossRefGoogle Scholar
Fisher, R. A. & Holt, S. B. (1944). The experimental modification of dominance in Danforth's short-tailed mutant mice. Annals of Eugenics 12, 102–120.CrossRefGoogle Scholar
Ford, E. B. (1940). Genetic Research in the Lepidoptera. Annals of Eugenics 10, 227–252.CrossRefGoogle Scholar
Ford, E. B. (1955). Polymorphism and taxonomy. Heredity 9, 255–264.CrossRefGoogle Scholar
Gateff, E. & Schneiderman, H. A. (1969). Neoplasms in mutant and cultured tissues of Drosophila. In: A Symposium on Neoplasms and Related Disorders of Invertebrate and Lower Vertebrate Animals (ed. Dawe, C. L. and Harshbarger, J. C.). National Cancer Institute. Monograph 31. Washington D.C.Google Scholar
Gordon, H. & Gordon, M. (1957). Maintenance of polymorphism by potentially injurious genes in eight natural populations of the Platyfish, Xiphophorus maculatus. Journal of Genetics 55, 1–44.CrossRefGoogle Scholar
Gordon, C. & Sang, J. H. (1941). The relation between nutrition and exhibition of the gene antennaless (Drosophila melanogaster). Proceedings of the Royal Society of London, Series B 120, 151–184.Google Scholar
Haldane, J. B. S. (1930). A note on Fisher's theory of the origin of dominance, and on a correlation between dominance and linkage. American Naturalist 64, 87–90.CrossRefGoogle Scholar
Harshbarger, J. C. & Taylor, R. L. (1968). Neoplasms of insects. Annual Reviews of Entomology 13, 159–190.CrossRefGoogle Scholar
King, R. C. (1970). Ovarian Development in Drosophila melanogaster. New York and London: Academic Press.Google Scholar
Lewis, E. B. (1960). TM3: Third multiple 3. Drosophila Information Service 34, 51.Google Scholar
Lindsley, D. L. & Grell, E. H. (1967). Genetic Variations of Drosophila melanogaster. Carnegie Institution, Washington, Publ. no. 627.Google Scholar
Muller, H. J. (1932). Further studies on the nature and causes of gene mutations. Proceedings of the Sixth International Congress of Genetics 1, 213–255.Google Scholar
Plunkett, C. R. (1933). A contribution to the theory of dominance. American Naturalist 67, 84–85 (Abstract).Google Scholar
Rendel, J. M. (1967). Canalisation and Gene Control. London: Logos Press and Academic Press.Google Scholar
Rizki, M. T. M. (1957 a). Alterations in the haemocyte population of Drosophila melanogaster. Journal of Morphology 100, 437–458.CrossRefGoogle Scholar
Rizki, M. T. M. (1957 b). Tumour formation in relation to metamorphosis in Drosophila melanogaster. Journal of Morphology 100, 459–472.CrossRefGoogle Scholar
Sang, J. H. (1956). The quantitative nutritional requirements of Drosophila melanogaster. Journal of Experimental Biology 33, 45–72.CrossRefGoogle Scholar
Sang, J. H. (1963). Penetrance, expressivity and thresholds. Journal of Heredity 54, 143–151.CrossRefGoogle Scholar
Sang, J. H. & Burnet, B. (1967). Physiological genetics of melanotic tumours in Drosophila melanogaster. IV. Gene environment interactions of tu-bw with different third chromosome backgrounds. Genetics 56, 743–754.CrossRefGoogle ScholarPubMed
Sang, J. H. & Mcdonald, J. M. (1954). Production of phenocopies in Drosophila using salts, particularly sodium metaborate. Journal of Genetics 52, 392–413.CrossRefGoogle Scholar
Stark, M. B. & Bridges, C. B. (1926). The linkage relations of a benign tumour of Drosophila. Genetics 11, 249–266.CrossRefGoogle Scholar
Sved, J. A. & Mayo, O. (1970). The evolution of dominance. In Mathematical Topics in Population Genetics (Kojima, K.). Berlin: Springer-Verlag.Google Scholar
Whitten, M. J. (1968). Genetical control of penetrance and evolution of dominance in Drosophila. Heredity 23, 263–278.CrossRefGoogle ScholarPubMed