Developmental and Genetic Mechanisms of Ovariole Number Evolution in Drosophila

Abstract

The goal of the "Quantitative Trait Gene" (QTG) program is to identify genes and mutations that underlie natural phenotypic variation. My goal with this work was to contribute an additional model to the program: ovariole number evolution in Drosophila. In this thesis I describe the progress I have made towards identifying a specific genetic change that contributed to the divergence of ovariole number between two Drosophila lineages. I identify specific developmental mechanisms relevant to establishing ovariole number in different Drosophila lineages by detailing ovarian cell-type specific specification, proliferation, and differentiation. I test specific candidates of genetic regulators of these developmental mechanisms with mutational analysis in D. melanogaster. I show that independent evolution of ovariole number has resulted from changes in distinct developmental mechanisms, each of which may have a different underlying genetic basis in Drosophila. I use the interspecies comparison of D. melanogaster versus D. sechellia to test for functional differences in insulin/insulin-like growth factor (IIS) signaling between the two species. I show that IIS activity levels and sensitivity have diverged between species, leading to both species-specific ovariole number and species-specific nutritional plasticity in ovariole number. Moreover, plastic range of ovariole number correlates with ecological niche, suggesting that the degree of nutritional plasticity may be an adaptive trait. My work and quantitative genetic analyses strongly support the hypothesis that evolution of the Drosophila insulin-like receptor (InR) gene, specifically, is at least partially responsible for the divergence in ovariole number and nutritional plasticity of ovariole number between D. melanogaster and D. sechellia. I detail ongoing experiments to test this hypothesis explicitly via cross-species transgenesis.