Cells depleted of mitochondrial DNA (ρ 0) yield insight into physiological mechanisms

A resurgence of interest in mitochondrial physiology has recently developed as a result of new experimental data demonstrating that mitochondria function as important participants in a diverse collection of novel intracellular signaling pathways. Cells depleted of mitochondrial DNA, or ρ 0 cells, lack critical respiratory chain catalytic subunits that are encoded in the mitochondrial genome. Although ρ 0 cells contain petit mitochondria, they cannot support normal oxidative phosphorylation and must survive and replicate using ATP derived solely from glycolysis. Without a functional electron transport chain, ρ 0 cells cannot normally regulate redox potential and their mitochondria appear to be incapable of generating reactive oxygen species. Emerging evidence suggests that these signals are important components in a number of mitochondria-initiated signaling pathways. The present article focuses on how ρ 0 cells have contributed to an understanding of the role that mitochondria play in distinct physiological pathways involved with apoptosis, glucose-induced insulin secretion, and oxygen sensing.