Mitochondria—A billion years of cohabitation
An engulfment of a small bacterium by a larger archaeon more than a billion years ago resulted not in death, but in one of the most successful partnerships on earth. As you sit there, each of your cells (apart from your red blood cells) contains hundreds or thousands of the descendants of that bacterium, still earning their keep as part of that endosymbiotic deal struck in some ancient pool. However, a billion years of intimacy has blurred the distinction between these partners and shaped them irrevocably. The host cell provides protection and food to the mitochondrion, and supplies all but a handful of the hundreds of proteins needed to run its affairs (this handful are encoded by a tiny rudimentary mitochondrial genome, a mere vestige of its bacterial forebear). The deal cuts both ways, though, and as a quid pro quo the cell delegates a number of rather grubby tasks to these tiny organelles. The most obvious of these is that the mitochondria make most of the cell’s energy currency, in the form of ATP. But they also help store and regulate calcium, synthesize and degrade specific chemicals, and take part in the cell’s decision to commit suicide. Like many factories, mitochondria are dangerous places with unpleasant chemicals, and handling the cell’s dirty work takes its toll on the organelles, threatening their integrity and that of their pared down genomes. This makes the quality control of mitochondria in the face of such damage a crucial issue in evolution, disease, and aging. A recent study in PLOS Biology by Nick Lane and colleagues [1] suggests that the need to pass on high-quality mitochondria to our offspring has determined how organisms choose which cells will contribute to the next generation. Plants can generate gametes from many parts of their bodies, even relatively late in development, producing flowers from recently grown stems. However, humans—and many other animals—have elected to set aside (“sequester”) a distinct “germline” at an early stage of development, keeping it safe for when it’s needed (Fig 1). Why the difference in strategy? These authors use a mathematical model to argue that a major determinant of this decision —to sequester or not—is down to selection for mitochondrial quality. Each time a cell divides, mutations arise and mitochondria are partitioned between the daughter cells (and the tissues they form), generating a population with variable fitness on which selection can act. Plants and primitive animals, which have low mutation rates, can afford selection to occur over many rounds of somatic cell division en route to gamete formation. The evolution of metabolically expensive lifestyles like predation (and its corollary—evasion) in the Cambrian explosion, however, entailed substantially increased mitochondrial mutation rates. The authors show that this shifts the balance, favouring the early set-aside of the cells from which breeding occurs (the germline), and thereby limiting the number of rounds of cell division incurred. In addition, where transmission of mitochondria is a job entrusted wholly to the mother (as in humans), this has further intriguing consequences. Here the opportunity for selection on mitochondrial quality is further reduced by the large number of mitochondria in each egg; this is addressed by a profligate process in which a huge excess of oocytes is produced through