Emily A Beck

The Beck Laboratory is interested in understanding genetic and physiological interactions of mitochondria. Mitochondria are responsible for the regulation of a wide range of essential cellular processes including energy production, lipid biosynthesis, calcium homeostasis, the cell cycle, cell death, and immunity. Mitochondria help regulate these processes in part using their own genomes (mitogenomes). The mitogenome is small - encoding only 13 proteins – but the mito-proteome is very large including upwards of 2,000 proteins, meaning function relies heavily on homeostasis between mito- and nuclear-encoded elements. However, the mito- and nuclear genomes are largely inherited independently and the mitogenome evolves approximately 5-10 times faster than the nuclear genome creating many opportunities for divergent evolution and incompatibility leading to dysfunction. 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.

Current projects in the lab focus on threespine stickleback fish – with extreme levels of nucleotide level variation across mitochondrial haplotypes and Antarctic icefish – with mitogenomic structural modifications and a suite of morphological adaptations allowing them to survive in extreme environments. We are also a highly collaborative group interested in applying comparative genomic approaches to identify new EMMs for mitochondrial disease and have nothing against model organisms working with others to leverage zebrafish personality lines exhibiting hyperactive brain disorders to understand mitochondrial and microbiome interactions in the regulation of brain-gut health.