OOS 10-1
Connecting short-term responses with long-term solutions: Ecological genomics in Daphnia

Tuesday, August 12, 2014: 8:00 AM
304/305, Sacramento Convention Center
Michael E. Pfrender, Department of Biological Sciences, University of Notre Dame, Notre Dame, IN
Background/Question/Methods

Understanding the underlying genetic and physiological mechanisms that facilitate and constrain the responses of organisms to changing and stressful environments is a major challenge for ecological genomics.  Organisms exposed to stressors in their environment employ a variety of short-term responses including changes in gene regulation and alterations in physiology to buffer negative effects and maintain high fitness.  These responses are a form of phenotypic plasticity that increases performance.  Similarly, populations exposed to selective pressures that impact population mean fitness over long time frames adapt through alterations in gene function and regulation.  Interestingly, we have a limited understanding of the relationship between plasticity and adaptation.  Here I use examples drawn from the versatile freshwater invertebrate, Daphnia, to illustrate these responses and discuss the relationship between short-term direct responses (i.e., acclimation) and long-term responses (i.e., adaptation).  

Results/Conclusions

I show data from functional genomics experiments contrasting the transcriptional responses of high-tolerance and low-tolerance genotypes to varying environments. In these studies we find that adaptation is the result of a mixture of the enhancement and suppression of plastic responses.  Interestingly, the multivariate directionality of acclimation and adaptation are often not aligned.  I will discuss future avenues of investigation that are now possible in this rapidly expanding nontraditional model system.  I will suggest that we need to 1) understand the network relationships of genes, 2) understand the role of genetic background (i.e., epistatic interactions) on gene regulation and the response to selection, and 3) take a population genomic view of the origin and maintenance of variation that contributes to GxE interactions.