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* Department of Biology, Knox College, Galesburg, IL 61401
Department of Genetics, Monash University, Clayton, Victoria, Australia 3168
Department of Biology, University of Calgary, Alberta Canada T2N 1N4
Commonwealth Scientific and Industrial Research Organisation, Division of Entomology, Canberra, ACT, Australia 2601
When Drosophila melanogaster larvae were fed a defined fat-free, low sucrose medium, alcohol dehydrogenase (ADH) was increased to a higher activity with a moderate, nontoxic level of ethanol (2.5% vol/vol) within 5 h. Ethanol-stimulated increases in ADH activity and cross-reacting material in late third-instar larvae were paralleled by increases in the larval ADH mRNA as indicated by dot blot analysis. Northern blot observations indicated that both adult and larval ADH messages were increased by dietary ethanol. The increased levels of the ADH mRNA transcribed from the proximal and distal promoters of ethanolfed larvae argue that the induction is a consequence of elevated levels of mRNA, not a result of changes in enzyme stability or synthesis. To determine whether the induction is of nutritional significance to larvae, the rate of flux from ethanol to lipid was estimated in control larvae and larvae that were pre-fed ethanol. Flux changes occurred; the rate of incorporation of [14C]ethanol into body lipid showed a strong association with larval ADH activity. Because the induced increase in larval ADH activity did not extend into the adult stage and attempts to stimulate ADH activity by exposing adults to ethanol were unsuccessful, the modulation of ADH activity by dietary ethanol may be a mechanism by which larvae utilize environmental ethanol as a resource, especially when free sugar levels are low. In addition, ADH in larvae is postulated to perform a second, nonethanol function that expedites the conversion of sugars to lipid when habitats are low in fats, low in ethanol and high in sugars.
KEY WORDS: alcohol tolerance polymorphism metabolic flux ethanol
1 Research in Canada was supported by a Natural Sciences and Engineering Research Council of Canada International Scientific Exchange Award and an Alberta Heritage Foundation for Medical Research Visiting Scientist Award (to M.M.B. for the visit of B.W.G.) Research in Australia was supported by the Australian Research Grants Scheme (S.W.M.) and a Fulbright Senior Scholar Award to B.W.G. Research in the United States was supported by National Institutes of Health Grant No. AA06702 (B.W.G.).
Manuscript received 29 June 1987. Revision accepted 30 October 1987.
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