Welcome to the Poyton Research Page

One of the major challenges of modern biology is understanding the aging process in humans and other species. Aging is certain to be driven by multi-factorial processes. A major one of these involves the way cells and tissues sense oxygen and use it to produce energy and generate free radicals (both reactive oxygen species and reactive nitrogen species)--important intra- and extra- cellular signaling molecules. Oxygen utilization, oxygen sensing, energy production, and free radical production are dependent on mitochondria and the signaling pathways between nuclear and mitochondrial genomes. It is now well documented that an increase in defective mitochondrial DNA (mtDNA) accompanies aging in several species. This defective mtDNA profoundly affects both mitochondrial respiratory function and the cross talk that occurs between the mitochondrion and the nucleus. This cross talk involves signaling pathways that connect either mitochondrial respiration or the mitochondrial genome (independently of its respiratory function) to the expression of specific nuclear genes. These signaling pathways make use of mitochondrially-generated free radicals (peroxynitrite and nitric oxide). During the past few years mitochondria-nuclear crosstalk has taken on increased importance in models for oxygen sensing, disease, and aging in many organisms.

Current questions of interest include:

(1) How do cells sense oxygen concentration and adjust gene expression to the specific oxygen concentrations present in different tissues?

(2) What oxygen concentrations are optimal for stem cell function in regenerative medicine?

(3) How does mitochondrial function and dysfunction contribute to aging and degenerative disease?

(4) How do free radicals function in disease and the aging process? Do they have both positive and negative effects?