I am part of the Bacteriology / Microbiology Doctoral Training Program. I chose to attend the University of Wisconsin-Madison because I read several papers published by a faculty member on campus, Dr. Heidi Goodrich-Blair, while I was an undergraduate student. I was impressed by the quality and methodology of the work and I wanted to work in her lab for my graduate degree to acquire a similar set of skills, both in the way I thought about and carried out my work.
I attended two institutions while I fulfilled the requirements for a B.S. degree. At the first, the University of New Hampshire, I worked for the departmental stockroom preparing media and materials for laboratory courses, and I also was mentored for two summers and one semester in the lab of a faculty member, Dr. Robert Zsigray. In Dr. Zsigray’s laboratory, I worked on a project characterizing pathogenicity factors that had been identified by transposon mutagenesis screens in Yersinia pestis. I finished my degree at Brigham Young University, where I worked in the laboratory of Dr. Byron Adams, a parasitologist who specializes in nematode taxonomy and phylogenetics.
I worked on two major projects that included an 8-week field season in Antarctica working at a Long-Term Ecological Research site, and a collaborative study between three institutions studying trait deterioration in entomopathogenic nematodes.
For the past four and a half years I have been a graduate student in the laboratory of Dr. Heidi Goodrich-Blair here at the University of Wisconsin-Madison, and have been working to characterize the products of three bacterial genes that are specificity factors for host association in a model animal-bacterial mutualism.
The goal of my research is to describe the physiology of a model animal-bacterial mutualism to provide insight into how animals and bacteria associate and interact with each other in beneficial ways. The specific focus of my research is to characterize three bacterial factors that have previously been shown to be required for the association of our model organisms, the nematode S. carpocapsae and the bacterium X. nematophila. These three factors, named nematode intestine localization (nil) factors A, B, and C, are produced by the bacteria, and disrupting these genes by mutation prevents the bacteria from associating with the nematode. Recent evidence that I have acquired suggests that the products of the nilA and nilC genes are accessory factor to NilB, a surface exposed protein that is likely to interact either directly with host proteins or surfaces, or to transport molecules produced by the host, such as nutrients or signaling molecules, to encourage bacterial persistence within the nematode. I have presented this work at three seminars and three symposia here at the University, and have presented the material at four meetings of national/international organizations. This work is currently in the stages of preparation for publication. Also, as part of this work I have mentored three undergraduate students in the laboratory.
Recipient of the Philipp and Vera Gerhardt
Research Award, 2009-2010
The award I received allowed me to attend three meetings this summer, two of which were on the UW-Madison campus and another, which was in Park City, Utah. I am very grateful for the opportunity to travel to these meetings. Over the 14 collective days of meetings that I attended, supported solely on this travel award, I heard from Nobel laureates, leaders in the field, and fellow students and future collaborators. It was a great opportunity for me to learn about many fields in a condensed setting and to see where my natural tendencies and preferences lie, as well. It was a fantastic opportunity for me to become familiar with the work that these people are doing and to meet some of them. Again, the travel award was my sole supporter for all three meetings, and I am very grateful for the generosity of the donors who provided this learning experience for me. Thank you very much.