Role of Mitochondrial Droplet-Like Structures in Regulating Aging
Unexpected setbacks in scientific research can sometimes lead to valuable discoveries that shape career paths. Marina Feric, Robert and Peggy Schlegel Early Career Professor of Biochemistry and Molecular Biology and Assistant Professor of Chemistry at Penn State University, experienced such a turning point during her postdoctoral work at the National Cancer Institute.
Feric’s research focuses on understanding how cells organize themselves, driven by a broader goal of uncovering mechanisms behind aging and improving human health span. She highlights the paradox of aging, echoing ideas from George C. Williams—how complex organisms successfully develop from a single cell but struggle to maintain themselves over time.
Her work centers on biomolecular condensates, membrane-less cellular structures formed through phase separation. Unlike traditional membrane-bound organelles, these condensates—similar to droplets forming in oil-water mixtures allow specific biomolecules to cluster and perform specialized functions efficiently.
During her postdoctoral research, Feric investigated these condensates within mitochondria, organelles closely linked to aging. Mitochondria contain their own DNA (mtDNA), organized into droplet-like structures called nucleoids. While imaging these structures, she observed an unexpected phenomenon: nucleoids merged into larger droplets under stress conditions, resembling those seen in premature aging diseases.
This observation was traced back to a technical artifact—fluorescent labeling triggered the production of reactive oxygen species, inducing mitochondrial stress. Rather than being a setback, this “happy accident” provided a controlled model to study how these droplet-like structures change during aging.
Feric’s lab now explores how mitochondrial condensates form, regulate gene expression, and contribute to age-related dysfunction. By integrating biophysics, biochemistry, cell biology, and advanced imaging, her team aims to uncover how disruptions in these structures influence aging and to identify potential pathways to extend health span.
