The fitness of an individual depends heavily on the number of offspring produced by that individual. Evolutionary changes in the morphologies and processes that determine the number of offspring can therefore impact fitness, and may be subject to natural selection. We are interested in how reproductive system morphology and function impact reproductive capacity, and how evolutionary changes in gonad development and function may have contributed to changes in reproductive capacity and hence fitness. We study this problem using ovariole number in Drosophilid flies as a model.
All insect ovaries are divided into egg-producing units called ovarioles. Ovariole number is highly variable between species, but highly heritable within species. Ovariole number in some insects also displays phenotypic plasticity, and can be influenced by environmental temperature or larval nutrition. The first step in ovariole morphogenesis in Drosophila is the formation of stacks of eight to ten cells, called terminal filaments, in the anterior of the larval ovary. The number of terminal filaments that form during larval development determines adult ovariole number. This means that to understand the genetic basis of ovariole number, we need to understand the genetic control of terminal filament formation.
We have found that the critical parameter that determines terminal filament number (and hence ovariole number) is the number of terminal filament cells. Species-specific ovariole number in Drosophilids can therefore be predicted from the total number of terminal filament cells in a given species. Interestingly, we have shown that temperature-dependent plasticity in ovariole number is not achieved by altering terminal filament cell number, but instead by changes in terminal filament cell sorting during terminal filament formation.
The number of terminal filament cells depends on how many cells are allocated to the somatic gonad primordium during embryogenesis, the proliferation rate of these cells during larval development, and the morphogenetic movements undergone by these cells in late larval life. We have uncovered a novel role for the conserved Hippo pathway, which regulates growth in animals, in the proliferation of all ovarian cell types. However, in the ovary the Hippo pathway appears to operate via distinct downstream signaling pathways in different cells of the same organ. Ongoing and planned projects in this area include further elucidation of the molecular mechanisms of Hippo-mediated ovarian size control, and screens to discover additional genes involved in regulating ovariole number.