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Background
Originally from Boulder, Colorado, I moved to Washington, DC, to attend Georgetown University
as a major in biology and government. My initial college experiences took me in the direction
of politics with a congressional internship and political fieldwork for an environmental non-profit.
While maintaining political and policy interests, I soon became fascinated by evolutionary genetics.
With Matthew Hamilton at Georgetown, I studied breeding population structure in Chesapeake Bay
striped bass in order to understand how fisheries management might better reflect the genetics of
this species.
Research
My dissertation research has focused microbial evolutionary genetics. Specifically, I investigate
the role of epistasis and pleiotropy in shaping the evolution of microbial phenotypes. This research,
thus far, has predominantly centered around three major projects.
In the budding yeast, Saccharomyces cerevisiae, my colleagues and I identified the genetic
basis of hundreds of gene expression differences in the progeny of a natural vineyard isolate. We
show that a single frameshift mutation causes hundreds of these gene expression differences. We
hypothesize that this mutation's recessivity may allow it to persist at low frequencies in natural
populations.
While investigating the evolutionary genetics of antibiotic resistance in bacteria, I pursued a
project that examines the interaction between transcription level and gene sequence. I show that
over expression of a gene encoding an antibiotic resistance enzyme in E. coli only increases
cellular resistance levels when the appropriate gene sequence is expressed. Key catalytic mutations
must be present in the gene sequence in order for increases in transcription to increase resistance.
Finally, I am investigating the role of epistasis and pleiotropy among naturally occurring mutations
at a drug resistance locus in Plasmodium falciparum. Using the resistance levels conferred
by various combinations of the resistance associate mutations, my colleagues and I demonstrate a trade
off between growth rate and drug resistance. Also, we show that different drug environments create
different mutational trajectories and different evolutionary outcomes.
Publications
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Brown, K. M., C. R. Landry, D. L. Hartl, and D. Cavalieri. 2008. Cascading
transcriptional effects of a naturally occurring frameshift mutation in Saccharomyces cerevisiae.
Mol. Ecol. 17: 2985-2997.
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Brown, K. M., G. A. Baltazar, and M. B. Hamilton. 2005. Reconciling nuclear
microsatellite and mitochondrial marker estimates of population structure: breeding population
structure of Chesapeake Bay striped bass (Morone saxatilis). Hederity 94: 606-615.
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Adams, R. I., K. M. Brown, and M. B. Hamilton. 2004. The impact of microsatellite
electromorph size homoplasy on multilocus population structure estimates in a tropical tree
(Corythophora alta) and an anadromous fish (Morone saxatilis) Mol. Ecol.
13: 2579-2588.
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Brown, K. M., G. A. Baltazar, B. M. Weinstein, and M. B. Hamilton. 2003.
Isolation and characterization of nuclear microsatellite loci in the anadromous marine fish
Morone saxatilis. Mol. Ecol. Notes 3: 414-416.
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Hobbies
Growing up at the foot of the Rocky Mountains, I connect with the outdoors. In the summer, I
make opportunities to backpack, hike and bike. I have also recently taken up fly-fishing. In
the winter, I like to ski. Because, in New England, winters are long and the powder isn't
exactly knee deep, I keep busy racquet sports and my French horn.
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