Emily Beck


Dr. Emily Beck
  • Assistant Professor
  • MOLECULAR BIOSCIENCES
  • Ecology and Evolutionary Biology
  • Computational Biology
  • KU Medical Center's Alzheimer's Disease Research Center

Contact Info

5060 Haworth Hall

Biography

Dr. Beck received her PhD in Genetics from the University of Iowa in 2015. During this time she studied mitochondrial and nuclear genomic interactions and the impact of these interactions on speciation.  She then conducted an NIH-NRSA funded postdoctoral fellowship at the University of Oregon under Dr. William A. Cresko on "Systems genetics analysis of natural variation in threespine stickleback host immunity and microbiota"  where she worked in the Microbial Ecology and Theory of Animals (META) Center for Systems Biology. She then transitioned to an independent position in the School of Computer and Data Science at the University of Oregon as an Assistant Research Professor of Data Science. In 2024 she moved her research program to the University of Kansas Department of Molecular Biosciences.

Research

The Beck Laboratory is interested in understanding genetic and physiological interactions of mitochondria. Mitochondrial dysfunction is common and can present as a breakdown of any of the processes regulated by mitochondria leading to prevalent diseases including Parkinson’s Disease, Alzheimer’s disease, cancer, diabetes, and hyperactive brain disorders. As a community, we have struggled to understand mito-nuclear dynamics and their impacts on organismal health. This is in part because genomic variation – in both the nuclear and mitogenomes – can impact severity of mitochondrial dysfunction. What is needed are studies focused on the role of genetic variation in mito-nuclear dynamics. Accounting for mitogenomic variation has been a major challenge because we are limited in our ability to edit the mitogenome and most animal models are limited in their mitogenomic variation. The Beck Lab focuses on using evolutionary mutant models (EMMs) or animals with evolved adaptations that mimic something disease-causing in humans. We are looking for animals with genetic or physiological modifications to their mitochondria that humans lack. We aim to learn what these animals are doing right that humans are doing wrong to identify gene therapy targets for mitochondrial disease.