Mitochondria are essential organelles found in every eukaryotic cell, required to convert food into usable energy. The mitochondrial oxidative phosphorylation (OXPHOS), which produces the majority of cellular energy in the form of ATP, is controlled by two distinct genomes: the nuclear and the mitochondrial genome (mtDNA). Mutations in mitochondrial genes encoded by either genome could cause mitochondrial disorders; have emerged as a key factor in a myriad of “common” diseases, including Parkinson’s and Alzheimer’s Disease, Type 2 Diabetes; and are strongly correlated to the aging process. Despite all this, it is surprising that our understanding of the mechanisms governing the mitochondrial gene expression, its reliance on the complex nature of dual genome control and associated pathologies remain superficial, with therapeutic interventions largely unexplored.
Remarkably, mitochondria seem to be central signaling hubs in the cell and within a last few years, multiple mitochondria-centric signaling mechanisms have been proposed, including release of reactive oxygen species and the scaffolding of signaling complexes on the outer mitochondrial membrane. It has also been shown that mitochondrial dysfunction causes induction of stress responses, bolstering the idea that mitochondria communicate their fitness to the rest of the cell.

We aim to further understand these largely unknown mechanisms that play a central role in determining the extent of tissue specific defect arising from the respiratory deficiency. The primary focus of our research is in deciphering the precise signaling cascade of the pathogenic mechanisms leading to mitochondrial diseases and aging, with the ultimate goal of identifying new therapeutic targets and strategies. We are working on two different model systems: transgenic mice and roundworm, Caenorhabditis elegans.