A genome-wide association approach to characterize natural genetic variation in the plastic response of mated lifespan and age-specific fecundity to diet in Drosophila melanogaster. Mary F. Durham¹, Michael M. Magwire², Jeff Leips¹. 1) Dept Biological Sci, Univ Maryland, Baltimore County, Baltimore, MD; 2) Department of Genetics, N.C. State University, Raleigh, NC.

   Nearly every organism experiences a wide array of variation in environmental conditions for which no single phenotype or genotype is universally advantageous. One method of maximizing individual fitness in these varying environments is to utilize phenotypic plasticity: the ability of a single genotype to produce one or more distinct, repeatable phenotypes in response to a change in a single environmental variable. Although the occurrence of phenotypic plasticity has been well demonstrated, the genetic mechanisms that drive plastic responses are poorly understood. There are two main hypotheses on the genetic mechanisms underlying phenotypic plasticity, allelic sensitivity and gene regulation. Allelic sensitivity posits that the effects of alleles on phenotypes are sensitive to the environment and so produce different phenotypes in different environments. In this case, alleles influencing plasticity will co-localize with the trait genes. The gene regulation hypothesis suggests that independent regulatory genetic components modulate the response of other genes that directly influence the focal phenotypes in varying environments, thus these plasticity genes are independent of the trait genes. Modification of the dietary regiment has been shown to result in phenotypic plasticity of lifespan and fecundity in a wide variety of organisms. We have completed a genome-wide association study on lifespan and fecundity of mated females under two different dietary regimes using the Drosophila melanogaster Genetic Reference Panel to identify naturally occurring candidate genes involved in the plastic response of lifespan and fecundity to changes in dietary protein content. We found evidence to support both the allelic sensitivity hypothesis and the gene regulation hypothesis of phenotypic plasticity.