Power, Sex, Suicide: Mitochondria and the Meaning of Life by Nick Lane Page B

was compatible with a simple early lifestyle as scavengers that engulfed their food whole by phagocytosis. Presumably, one fine morning, two thousand million years ago, a cousin of these simple cells engulfed a bacterium, and for some reason failed to digest it. The bacterium lived on and divided inside the archezoon. Whatever the original benefit might have been to either party the intimate association was eventually so successful that the chimeric cell gave rise to all modern eukaryotes with mitochondria—all the familiar plants, animals, and fungi.
    According to this reconstruction, the original benefit of the merger was probably related to oxygen. Presumably it was not a coincidence that the merger took place at a time when oxygen levels were rising in the air and the oceans. A great surge in atmospheric oxygen levels certainly occurred around two billion years ago, probably in the wake of a global glaciation, or ‘snowball earth’. This timing corresponds closely to that of the eukaryotic merger. Modern mitochondria make use of oxygen to burn sugars and fats in cell respiration, so it is not surprising that mitochondria should have become established at a time when oxygen levels were rising. As a form of energy-generation, oxygen respiration is much more efficient than other forms of respiration, which generate energy in the absence of oxygen (anaerobic respiration). All that said, it is unlikely that superior energy generation could have been the original advantage. There is no reason why a bacterium living inside another cell should pass on its energy to the host. Modern bacteria keep all their energy for themselves, and the last thing they do is export it benevolently to their neighbouring cells. Thus while there is a clear advantage for the ancestors of the mitochondria, which had intimate access to any of the host’s nutrients, there is no apparent advantage to the host cell itself.
    Perhaps the initial relationship was actually parasitic—a possibility first suggested by Lynn Margulis. Important work from Siv Andersson’s laboratory at the University of Uppsala in Sweden, published in
Nature
in 1998, showed thatthe genes of the parasitic bacterium
Rickettsia prowazekii
, the cause of typhus, correspond closely with those of human mitochondria, raising the possibility that the original bacterium might have been a parasite not unlike
Rickettsia
. Even if the original invading bacterium was a parasite, the unbalanced ‘partnership’ may have survived, as long as its unwelcome guest did not fatally weaken the host cell. Many infections today become less virulent over time, as parasites also benefit from keeping their host alive—they do not have to search for a new home every time their host dies. Diseases like syphilis have become much less virulent over the centuries, and there are hints that a similar attenuation is already underway with AIDS. Interestingly, such attenuation over generations also takes place in amoebae such as proteus. In this case, the infecting bacteria initially often kill the host amoebae, but eventually become necessary for their survival. The nuclei of infected amoebae become incompatible with the original amoebae, and ultimately lethal to them, effectively forcing the origin of a new species.
    In the case of the eukaryotic cell, the host is good at ‘eating’ and through its predatory lifestyle provides its guest with a continuous supply of food. We are told that there is no such thing as a free lunch, but the parasite might simply burn up the metabolic waste-products of the host without weakening it much at all, which is not far short of a free lunch. Over time the host learned to tap into the energy-generating capacity of its guest, by inserting membrane channels, or ‘taps’. The relationship reversed. The guest had been the parasite of the host, but now it became the slave, its energy drained off to serve the host.
    This scenario is only one of several possibilities, and