Published online by Cambridge University Press: 14 April 2009
The mutant phenotype Abnormal abdomen is under the control of a major gene, A53g located distally on the X chromosome. The phenotypic abnormalities are a result of the developmental interaction between this major gene and a modifier system associated with the residual genotype. The primary developmental effect of this mutant genotype is an interference with adult histoblast differentiation resulting in a raggedness or loss of tergite material due to the changes in the formation of the adult abdominal hypoderm. A secondary effect is an interference with middorsal fusion of the histoblasts.
The developmental effect of the genotype is influenced by a number of factors which include crowding, humidity, temperature, and the age of the culture. The mutant phenotype is due to an interaction of the major gene and the modifier system in association with these environmental factors. Gene action in relation to the final phenotype is postulated to be a two-step affair. The first is an increase in protein synthesis under the influence of the modifier system; and the second is the reaction of the histoblast, under the influence of the major gene, to this increase in protein synthesis during its differentiation into adult hypoderm. The function of the environment in this sequence of developmental reactions is postulated to be in its control of the utilization of the increased protein associated with the action of the enhancer genes. This hypothesis is discussed in terms of (1) the production and utilization of gene products and of (2) the regulation of development in terms of this production and utilization in a balanced developmental system.