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Background
I grew up in the small town of Ketchikan, located in the rainforest of Southeast Alaska.
I went to college at the University of Chicago, where I received a B.A. in the Biological Sciences in June
of 2002. There, I studied the evolution of thermotolerance in Drosophila with Dr.
Martin Feder.
Research interests
My work focuses on rates of evolution, exploring sequence change, gene structure evolution and gene
expression divergence. Although this is a popular topic in the evolutionary genetics literature, most
studies of evolutionary rates do not employ null models and instead rely on comparisons between genes.
I've sought to provide a framework for the study of evolutionary rates. Simple models of molecular evolution
predict that both sequences and quantitative traits should evolve in accordance with a "molecular evolutionary
clock," wherein divergence is proportional to time. Through study of deviations from the null model of a
molecular clock, insight can be gained into the forces shaping evolution of genotype and phenotype.
With regard to sequence evolution, the molecular clock hypothesis further predicts that the accumulation of
sequence change should follow a Poisson process in which nucleotide or amino acid substitutions occur as rare
independent events. Generally, substitution patterns that show greater variance than the Poisson expectation
are said to be "overdispersed." Comparing the genomes of closely related species of yeast, Drosophila and
mammals, I find that sequence change is clock-like, but overdispersed. Additionally, I find that the extent of
overdispersion varies significantly between yeast, Drosophila and mammals, showing a strong negative correlation
with the effective population sizes of these organisms. These results are consistent with theoretical predictions
of evolution over nearly neutral networks.
On the other hand, I find that gene expression divergence across seven species of Drosophila does not
follow a molecular clock, instead saturating quickly across the Drosophila phylogeny. This is consistent
with the action of stabilizing selection holding expression divergence in check. These results, taken together,
suggest that sequences and their biological outcomes evolve in fundamentally different fashions, owing to the
complex mapping between genotype and phenotype.
Publications
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Bedford, T., and D. L. Hartl. 2008. Optimization of gene expression by
natural selection. In prep.
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Rogers, R. L., T. Bedford, and D. L. Hartl. 2008. Formation and longevity
of chimeric and duplicate genes in Drosophila melanogaster. Genetics. In review.
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Bedford, T., I. Wapinski, and D. L. Hartl. 2008. Overdispersion of the
molecular clock varies between yeast, Drosophila and mammals. Genetics 179:977-984.
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Bedford, T., and D. L. Hartl. 2008. Overdispersion of the molecular clock: temporal
variation of gene-specific substitution rates in Drosophila. Mol. Biol. Evol. Advance access.
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Volkman, S. K., E. Lozovsky, A. E. Barry, T. Bedford, L. Bethke, A. Myrick,
K. P. Day, D. L. Hartl, D. F. Wirth, and S. A. Sawyer. 2007. Genomic heterogeneity in the density
of noncoding single-nucleotide and microsatellite polymorphisms in Plasmodium falciparum.
Gene 387(1-2): 1-6.
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Castillo-Davis, C. I., T. Bedford, and D. L. Hartl. 2004.
Accelerated rates of intron gain/loss and protein evolution induplicate genes
in human and mouse malaria parasites. Mol. Biol. Evol. 21: 1422-1427.
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Nielsen, K. M., J. Kasper, M. Choi, T. Bedford, K. Kristiansen, D. F. Wirth,
S. K. Volkman, E. R. Lozovsky, and D. L. Hartl. 2003. Gene conversion as a source of nucleotide
diversity in Plasmodium falciparum. Mol. Biol. Evol. 20: 726-734.
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Feder M. E., T. Bedford, D. R. Albright, and P. Michalak. 2002.
Evolvability of Hsp70 expression under artificial selection for inducible thermotolerance
in independent populations of Drosophila melanogaster. Phys. Biochem. Zool.
75(4): 325-334.
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