Cis-regulatory divergence at the Insulin Receptor locus contributes to evolution of a reproductive morphology between two Drosophila species. Delbert A. Green¹, Cassandra G. Exatavour². 1) Molecular and Cellular Biology, Harvard University, Cambridge, MA; 2) Organismic and Evolutionary Biology, Harvard University, Cambridge, MA.

   An open question in evolutionary genetics and evolutionary developmental biology is the precise genetic architecture of morphological change between species. We extend the list of such closely examined traits to Drosophila ovariole number, a reproductive morphology with direct impact on fitness. Previously we determined that differences in terminal filament (TF) number, and hence ovariole number, between D. melanogaster (Oregon R strain) and D. sechellia (Robertson strain) are due to differences in somatic gonad cell precursor establishment and also subsequent cell proliferation rate. Here, we analyze the genetic and molecular basis for ovariole number difference between these two species. Interspecific genetic analysis indicates that the Drosophila Insulin receptor (InR) promoter contains sequence that controls ovariole number difference between these species. A putative null coding mutation in D. melanogaster InR can complement the D. sechellia InR locus in hybrids. This suggests a model in which InR expression level, versus differential activity from species-specific receptors, is responsible for the difference. Consistent with this hypothesis, InR is more highly expressed in whole female larvae of D. melanogaster than of D. sechellia. Additionally, we find that ovariole number in both species is hypersensitive to poor larval nutrition compared to body size. However, D. melanogaster shows a significantly greater reduction in both traits than does D. sechellia. Taken together, these results indicate that in Drosophila, one mechanism of controlling reproductive capacity is through modulating nutritional sensitivity. We propose that this is achieved through species-specific regulation of InR expression via cis-regulatory sequence evolution at the InR promoter.