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Stacey Rodenbeck, Ph.D.

Associate Professor of Biology

Disciplines

  • Biology

Research Interests

  • I completed my Ph.D. in Cellular and Integrative Physiology while working in the lab of Dr. Michael Sturek at Indiana University School of Medicine in Indianapolis, IN. While there, I developed an intense interest in “broken” biology and the ways in which “breaking” normal biological patterns in one body system would affect other body systems. Metabolic syndrome is defined as the clustering of metabolic conditions, including central obesity, hypertension, dyslipidemia, hyperinsulinemia, and glucose intolerance. Interestingly, these metabolic conditions are also risk factors for cardiovascular complications. In particular, I am interested in teasing out the contributions of these risk factors to aberrant intracellular calcium handling in the smooth muscle cells lining the coronary arteries. These changes in calcium handling are associated with increases in atherosclerotic plaque formation, which in turn contributes to mortality due to myocardial infarction.

Rebekah Rampey, Ph.D.

Professor and Chair of the Biology Department

Disciplines

  • Biology

Research Interests

  • Auxins are a class of phytohormones that influence virtually every aspect of plant development. Plants regulate auxin levels through complex interactions among de novo synthesis, degradation, influx, efflux, and conjugate synthesis and hydrolysis. A thorough knowledge of these pathways is key to understanding the roles of auxins in plants. In a collaborative effort with Dr. Bethany Zolman, an Associate Professor of Biology at the University of Missouri in St. Louis, we are using genetic approaches to better understand the function of certain proteins involved in auxin storage and metabolism in the model plant Arabidopsis thaliana. A forward genetic screen identified a mutant defective in auxin-conjugate response, J56. We have used next-generation sequencing to compare mutant and genomic sequences and several mutations were identified in J56. Students are working to identify the causative mutation for the J56 auxin phenotype using several approaches, including isolating mutant alleles for candidate genes, using PCR to assay homozygous J56 lines for segregation of each mutation, and using quantitative PCR to measure expression levels of the candidate genes.