James D. Fry

Associate Professor

Contact Information:

University of Rochester
Department of Biology

River Campus Box 270211
Rochester, New York 14627-0211

Hutchison 318 (office)
Hutchison 314 (lab)

(585) 275-7835 (office)
(585) 275-8834 (lab)

You have reached Dr. Fry's old web page. His new one is here.

Research Overview

Elucidating the genetic basis of adaptation is one of the primary goals of evolutionary biology. I am using adaptation to dietary ethanol in Drosophila melanogaster, the common fruit fly, as a model system for studying the genetics of adaptation. Ethanol occurs naturally in the decaying fruits in which D. melanogaster breed, and natural populations in temperate regions have evolved high ethanol tolerance relative to ancestral tropical populations (and most other organisms!). By taking advantage of the many genetic resources available for D. melanogaster, my laboratory is identifying the genetic changes underlying the temperate-tropical difference (e.g., Fry et al. 2008).

Other research interests, which I pursue mainly through theory and analysis of publicly available data, include the role of ecological divergence in speciation (e.g., Fry 2009) and the maintenance of genetic variation in life-history traits (e.g., Fry 2010).


For one approach to identifying genes involved in ethanol tolerance in Drosophila, we are taking advantage of the inducibility of ethanol tolerance in larvae. As shown above, larvae hatching from eggs that developed in contact with ethanol have much higher survival on ethanol-supplemented medium than larvae hatching from eggs exposed only to water (Fry 2001). We isolated RNA from ethanol-exposed and control larvae and compared gene expression using Affymetrix GeneChip© microarrays, which contain synthetic oligonucleotides from almost all 14,000 Drosophila genes (see figure below). This procedure identified many genes upregulated by ethanol, some of which likely contribute to the increased tolerance of larvae from ethanol-treated eggs. We are investigating whether some of these ethanol-inducible genes show higher baseline (non-induced) expression in more ethanol-tolerant populations than in less tolerant populations. Such genes would be strong candidates for being involved in the genetic difference in tolerance between populations.


Selected Publications

  • Fry, J.D. 2010. The genomic location of sexually antagonistic variation: some cautionary comments. Evolution 64-5: 1510-1516. [pdf]
  • Fry, J.D. 2009. Laboratory experiments on speciation. Pages 631-656 in T. Garland and M. Rose, eds., Experimental Evolution: Methods and Applications. University of Califronia Press, Berkeley. [pdf]
  • Fry, J.D., D. Donlon and M. Saweikis. 2008. A world-wide polymorphism in Aldehyde dehydrogenase in Drosophila melanogaster: evidence for selection mediated by dietary ethanol. Evolution 62:66-75. [pdf]
  • Fry, J.D. and M. Saweikis. 2006. Aldehyde dehydrogenase is essential for both adult and larval ethanol resistance in Drosophila melanogaster. Genet. Res. 87:87-92. [pdf]
  • Phadnis, N. and J.D. Fry. 2005. Widespread correlations between dominance and homozygous effects of mutations: implications for theories of dominance. Genetics 171:385-392. [pdf]
  • Fry, J.D. 2004. On the rate and linearity of viability declines in Drosophila mutation-accumulation experiments: genomic mutation rates and synergistic epistasis revisited. Genetics 166:797-806. [pdf]
  • Fry, J.D. 2003. Detecting ecological trade-offs using selection experiments. Ecology 84:1672-1678. [pdf]
  • Fry, J.D. 2003. Multilocus models of sympatric speciation: Bush vs. Rice vs. Felsenstein. Evolution 57:1735-1746. [pdf]
  • Fry, J.D. 2001. Direct and correlated responses to selection for larval ethanol tolerance in Drosophila melanogaster. Evol. Biol. 14:296-309. [pdf]