In many animal species, including humans, adult males and females have different body sizes. However, despite the commonality of this phenomenon, scientists have a very poor understanding of the mechanisms that cause males and females to grow to different sizes. Previous research, using the fruit fly Drosophila melanogaster as a model organism, suggest that the difference in body size between sexes is due to differences in how males and females respond to nutrition during their growth. In almost all animals, high levels of nutrition during growth increase adult body size. Preliminary data show that while males and females are the same size when reared on a poor-quality diet, females are better able to respond to a high-quality diet than males, and grow to a larger size. Consequently, females are more nutritionally-sensitive than males. The goal of this study is to discover the developmental and physiological mechanisms that make females more nutritionally-sensitive than males with respect to their growth and final body size. This research contributes to a growing understanding of how and why females and males respond differently to environmental stimuli, a phenomenon that has wide-ranging and important implications for many aspects of biology, including human biology. The grant will also support broader impact activities designed to bring together academic, medical, and educational workers from across the UIC campus and wider Chicago-land area, to discuss the scientific, medical, and societal impacts of biological differences between females and males.
Research by the Shingleton Laboratory and others indicate that sexual-size dimorphism (SSD) in Drosophila melanogaster is at least partially regulated by the insulin/IGF-signaling pathway, a regulator of body size with respect to nutrition in almost all animals; that is, nutritional plasticity. These data, as well as several adaptive hypotheses on the evolution of SSD, suggest a relationship between SSD and sex-specific plasticity (SSP), the phenomenon whereby body size in one sex is more environmentally variable than in the other sex. Preliminary data from the Shingleton Laboratory support such a relationship by showing a strong genetic correlation between SSD and SSP among isogenic Drosophila lineages. The goal of this project is therefore to use Drosophila melanogaster as a model organism to test the hypothesis that the developmental genetic mechanisms that regulate sexual SSD also regulate SSP, and that these mechanisms either target or lie within the insulin-signaling pathway. The hypothesis will be tested by: (1) using a genome-wide association study to determine whether the same loci are associated with genetic variation in SSD and SSP; (2) characterizing at the level of gene expression/activity how females and males differentially respond to changes in developmental nutrition, and; (3) functionally testing the role that genes (identified in [1] and [2]) play in regulating SSD and SSP.
This award reflects NSF's statutory mission and has been deemed worthy of support through evaluation using the Foundation's intellectual merit and broader impacts review criteria.
