In addition to its central role in cellular stress signaling, the tumor suppressor p53 modulates mitochondrial
respiration through its nuclear transcription factor activity and localizes to mitochondria, where it enhances
apoptosis and suppresses mitochondrial DNA (mtDNA) mutagenesis. Here we demonstrate a new conserved
role for p53 in mtDNA copy number maintenance and mitochondrial reactive oxygen species (ROS)
homeostasis. In mammals, mtDNA is present at thousands of copies per cell and is essential for normal
development and cell function.