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Physiological genetics of melanotic tumours in Drosophila melanogaster VII. The relationship of dietary sterols to tumour penetrance

Published online by Cambridge University Press:  14 April 2009

Jonathan Cooke  and
J. H. Sang
Jonathan Cooke
Affiliation:
School of Biology, Sussex University, Brighton, England
J. H. Sang
Affiliation:
School of Biology, Sussex University, Brighton, England

Summary

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A strain of Drosophila, homozygous for the variably penetrant gene tu bw, which causes the formation of abnormal masses of melanizing haemocytes (melanotic tumours), has been reared on defined axenic diets containing various sterols, both singly and in pairs. Both optimal and deficient nutritional levels of sterol have been employed, as well as certain sterols inadequate by themselves to support development. The effect of these diets upon probability of tumour formation has been studied in relation to their nutritional adequacy, as defined by the growth-rate, survival, and in one case, adult body-weight.

The results demonstrate a rather complex pattern of interaction between dietary sterols in determining the variables of the phenotype produced, under circumstances suggesting that all the sterols investigated have entered the developing larvae. There is only a partial overall correlation, and occasionally an inverse relationship, between tumour suppressant and growth-promoting properties of particular sterols. Within single molecules, structural sterol features tend to exert their characteristic effects additively upon the phenotype, except for an inadequacy in utilization of molecules containing the Δ7 double bond, which dominates at low concentrations. With pairs of dietary sterols, however, non-additive or ‘saving’ effects are sometimes seen.

It is suggested that the tu bw allele allows the resolution of several discrete developmental functions for sterols and/or their immediate metabolic products in Drosophila, which cannot synthesize its own sterol. However, the molecular nature of these functions is little understood.

Type
Research Article
Information
Genetics Research , Volume 20 , Issue 3 , December 1972 , pp. 317 - 329
Copyright
Copyright © Cambridge University Press 1972

References

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