Laura BurrackFaculty

One aspect of biology that fascinates me is how organisms balance genome stability with adaptation and evolution. If the balance tips toward genome stability, the genetic diversity necessary for evolution will not arise. However, excess genome instability can be lethal and defects in genome stability are associated with human diseases and the development of antimicrobial resistance in pathogens. The focus of my research is to understand the role of flexibility in chromosome segregation mechanisms and to determine the phenotypic consequences of this flexibility in the evolution of microorganisms under stress and in the development of increased fitness as a model for cancer cells. Microorganisms are particularly useful to study genome stability due to their large population size and the ease in which different conditions and genetic phenotypes can be tested. The kinetochore is a large complex of proteins assembled at centromere DNA to allow attachment of the DNA to spindle microtubules and chromosome segregation during mitosis. In most eukaryotes, including humans, centromere regions are maintained epigenetically rather than being defined by a specific sequence and centromeres exhibit flexibility in size and position.

In my research, I use the yeast Candida albicans as a model system to explore the mechanisms and consequences of centromere and kinetochore flexibility using a combination of microbiology, molecular biology, genetics, biochemistry, and cell biology techniques. Using C. albicans, we will look at how altered chromosome segregation mechanisms influence the ability of the organism to evolve antimicrobial drug resistance. Additionally, we will use the C. albicans model to increase our understanding of whether altered chromosome segregation mechanisms are a driver of genomic instability as seen in cancer cells.

For more information and links to publications, see: http://lauraburrack.weebly.com/.

Courses Taught