PhDOxidative phosphorylation couples ATP synthesis to respiratory electron
transport. This coupling occurs in mitochondria, which carry DNA. Respiratory
electron transport in the presence of molecular oxygen generates mutagenic reactive
oxygen species (ROS) at a frequency that is itself increased by mutation. Damage to
mitochondrial DNA (mtDNA) therefore accumulates within the lifespan of
individual organisms. Syngamy requires motility of one gamete, and this motility
requires ATP. It has been proposed that that oxidative phosphorylation is absent in
the special case of quiescent, template mitochondria, and that these remain
sequestered in oocytes and female germ lines. Oocyte mtDNA is thus protected from
damage. Here I present evidence that female gametes, which are immotile, repress
mitochondrial DNA transcription, mitochondrial membrane potential (!!m), and
ROS production. In contrast, somatic cells and male gametes are seen actively to
transcribe mitochondrial genes for respiratory electron carriers, and to produce ROS.
I find that this functional division of labour between sperm and egg is widely
distributed within the animal kingdom, and characterised by contrasting
mitochondrial size and morphology. If quiescent oocyte mitochondria alone retain
the capacity for an indefinite number of accurate replications of mtDNA, then
"female" can be defined as that sex which transmits genetic template mitochondria.
Template mitochondria then give rise to mitochondria that perform oxidative
phosphorylation in somatic cells and in male gametes of each new generation.
Template mitochondria also persist within the female germ line, to populate the
oocytes of daughters. Thus mitochondria are maternally inherited
