ABSTRACT
Mitochondria are cellular organelles, which uniquely contain their own genetic system in a circular DNA. Biogenesis of mitochondria and activation of mitochondrial functions require a full coordination between the nuclear and the mitochondrial genomes-a process that is integrated by the action of nuclear chromatin factors (Poyton and McEwen 1996). A major function of mitochondria is to maintain the bioenergetic cellular state through oxidative phosphorylation (OXPHOS) sustained by catabolic pathways (Hate 1985; Wallace et al. 2010). Other important cellular processes such as apoptosis also depend on mitochondrial components interacting with cytoplasmic factors leading to cell death (Oberst et al. 2008). Genetic or signaling dysregulation of mitochondria cause a broad myriad of pathologies affecting systemic and tissue-specic functions (Wallace 2005; DiMauro and Hirano 2009). Hence, the inability of mitochondria to adequately respond to nutrient and environmental signals is a whole signature of metabolic instability linked to age-associated diseases, including the metabolic syndrome, neurodegeneration, or cancer. Here, we will discuss nuclear chromatin regulatory components, which impinge on mitochondrial bioenergetic function and maintain a “healthy” cellular and tissue state with implications for organismal survival and longevity.
