Laura Reed

Laura Reed

she/her/hers
she/her/hers

Professor
Chair of Advisory Committee

  • lreed1@ua.edu
  • (205) 348-1345
  • 2330 Science and Engineering Complex (SEC)
  • Website
  • Accepting Undergraduate Students

Education

  • Postdoctoral research: North Carolina State University
  • Ph.D., Ecology and Evolutionary Biology, University of Arizona, 2006

Research Interests

My research interests lie at the intersection of quantitative genetics and population genetics, where I explore the evolution of complex traits such as metabolic disease that are the result of multiple genetic effects and the environment.

A Drosophila Model for Metabolic Syndrome

Our primary research uses systems biology to correlate empirical data from across physiological levels such as RNA and metabolites, to decipher the relative contribution of natural genetic variation and environment to metabolic diseases like obesity and type-2 diabetes. Specifically, we are characterizing how variation in metabolic disease phenotypes maps to the metabolic pathway, by integrating metabolomic profiling with phenotypic, genomic, and gene expression data.

Metabolic Syndrome (MetS) is a constellation of symptoms such as obesity, elevated blood lipids, and insulin resistance that are predictive of type-2 diabetes and cardiovascular disease. MetS is a recently developed syndrome caused by our increased calorie intake and decreased exercise that exposes cryptic genetic variation: some people can eat high-fat, high-sugar diets without adverse impact while others are highly sensitive to their diet. My research explores these effects using Drosophila, which also harbor cryptic genetic variation for disease, as a model to characterize the architecture of genotype-by-environment interactions of human-like metabolic disorders. With this charismatic model organism, we gain all the advantages of a carefully dissected metabolic and genetic system with substantial metabolic similarity to humans, while also being able to sample natural variation with high throughput genomic methods. Thus, using Drosophila, we can gain insights into a genetically complex disease that affects humans.

We have identified significant genotype-by-diet interactions for weight gain and other metabolic phenotypes in Drosophila, indicating that some genetic lines are metabolically sensitive to their diet while others are not. Presently, we are analyzing whole genome expression analyses and metabolomic profiling on a common set of samples to identify genes that are changing in expression in concert with diet and genotype, and the correlated response in metabolites.

Evolutionary Genetics of Speciation

Ecological context is essential to understanding the evolution of genetic architecture. In my graduate work, I used cactophilic Drosophila, a species endemic to the desert Southwest with an interesting ecology, to clarify the ecological history the species group based on population genetics and phylogenetics (Reed et al. 2007), and to address the fundamental evolutionary puzzle of the genetic basis of speciation. We found significant within-species genetic polymorphism for between-species postzygotic isolation (Reed and Markow, 2004). We mapped the genetic architecture of hybrid male sterility as it is manifested directly in the F1 hybrids (Reed et al., 2008). By discovering that hybrid male sterility is controlled by multiple contributing loci and epistatic interactions, we found that it is a complex trait before it becomes fixed in the incipient species. These findings indicate that postzygotic isolation is likely to evolve largely by the haphazard force of drift or, perhaps, balancing selection, allowing it to languish in a polymorphic state. I am interested in returning to look at questions of local adaptation and speciation in Drosophila native to the Southeast.

Selected Publications

  • ­­­­­­­­­­­­L.K. Reed, S. Williams, M. Springston, J. Brown, K. Freeman, C.E. DesRoches, M.B. Sokolowski, G. Gibson, 2010 “Genotype-by-Diet Interactions Drive Metabolic Phenotype Variation in Drosophila melanogaster” Genetics 185: 1009–1019.
  • G.Gibson and L.K. Reed, 2008 “Cryptic genetic variation” Current Biology 18(21): R989-R990.
  • L.K. Reed, B.A. LaFlamme, T.A. Markow, 2008 “Genetic Architecture of Hybrid Male Sterility in Drosophila: Analysis of Intraspecies Variation for Interspecies Isolation.” PLoS ONE 3(8): e3076 doi:10.1371/journal.pone.0003076
  • Drosophila 12 Genomes Consortium (L.K. Reed coauthor), 2007 “Evolution of genes and genomes in the Drosophila phylogeny” Nature 450: 203-218.
  • L.K. Reed, M.E. Nyboer, & T.A. Markow, 2007 “Evolutionary relationships of Drosophila mojavensis geographic host races and their sister species Drosophila arizonae.” Molecular Ecology, 16: 1007–1022.
  • L.K. Reed & T.A. Markow, 2004 “Early Events in Speciation: Polymorphism for hybrid male sterility in Drosophila” PNAS, 101: 9009-9012.