Physiological genetics of melanotic tumours in Drosophila melanogaster: VIII. The role of choline in the expression of the tumour gene tu bw and of its suppressor, su-tu

SUMMARYThe melanotic tumour gene tu bw of Drosophila melanogaster has a specific suppressor su-tu. The genotypes tu bw; +su-tu and tu bw; su-tu show opposite responses, as measured by tumour penetrance, to increasing choline levels in the defined axenic medium. The three major metabolic functions of choline have been examined using additions to the axenic medium to determine which biochemical pathway(s) are different in the two genotypes. It is concluded that the opposite strain responses are due to changes in the pattern of phospholipid synthesis, and that the gene product of the su-tu gene probably functions in this area of metabolism.

The genetics of some second chromosome melanotic tumour mutants of Drosophila melanogaster

SummaryThe genetic relationships of the available second chromosome melanotic tumour mutants in Drosophila melanogaster have been investigated. Complementation tests demonstrate the existence of new alleles of the tu bw locus and show that tu-W and tu-g are alleles. The data suggest that there is a minimum of three major gene loci on the second chromosome involved in tumorigenesis. A number of modifier genes were found which affect the penetrance of the major tumour genes analysed. These and the problems they cause in mapping the low penetrant tumour genes are discussed. It has not been possible to map tu-48a, tu- W and tu-g accurately, due largely to the presence of modifier genes. It appears that the genetic basis for melanotic tumour formation is complex.

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

SUMMARYThe 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.