UTHSC Physiology and Barshop Institute
Dr. Shane Rea did his Post Doctoral from McGill University of Colorado.
The goal of the research in the Rea laboratory is to understand the causes of human aging at a molecular genetic level and to use this information to slow the aging process. Dr. Reaâ€™s research group utilizes the nematode Caenorhabditis elegans and focuses specifically on the Mit mutants, which (paradoxically) have disruptions in their mitochondrial electron transport chain yet are long-lived. This model is short-lived (~20 days), self-fertilizing, genetically powerful, easily and cheaply cultivated, and provides excellent molecular and bioinformatic resources. Twenty-five percent of worm genes have human orthologues. Pathways already known to influence aging in C. elegans act similarly in humans (e.g., insulin/IGF-1 like receptor). Mitochondria function similarly in almost all eucaryotes. Life extension in the Mit mutants is restricted to a specific window of mitochondrial dysfunction. The Mit mutants provide a new model for several human mitochondrial-associated diseases. Nuclear DNA damage, cell-cycle checkpoint functions, alternate metabolic pathways, and ROS signalling appear to be central players in lifespan regulation of the Mit mutants. The Rea laboratory also explores the connection between functionally impaired mitochondria, nuclear checkpoint proteins and life extension in the Mit mutants. This research team performs metabolic fingerprinting of the Mit mutants as well as the biochemical and biophysical characterization of the mitochondria from long-lived and short-lived mitochondrial mutants. This group also investigates compensatory biochemical mechanisms that act to offset partial mitochondrial inhibition. They strive to translate their work into higher eucaryotes and to ameliorate human mitochondrial-associated diseases.