The coordinated expression of the nuclear and the mitochondrial genome (mtDNA) control mitochondrial function. Mitochondria use complex signaling pathways – retrograde signaling - to communicate with the nucleus about stress and damage and guarantee cellular homeostasis. Persistent mitochondrial dysfunction induced by environmental stressors or mtDNA mutations leads to aberrant retrograde signaling that significantly impacts the progression of a vast repertoire of human disorders by imposing energy constriction, fostering tissue inflammation, and promoting degeneration.

In the lab, we perform foundational research to better understand aberrant mitochondrial signaling by defining its mechanistic aspects, triggering events, and propagation within cells and tissues. We use a wide gamut of genetic models, ranging from acute stress induced by mtDNA damage, inducible models of mtDNA deletions, and CRISPR reconstituted disease models. As a team, we will explore the functional consequences of aberrant mitochondrial stress through targeted experiments and exploratory next-generation -omics approaches.