Power, Sex, Suicide: Mitochondria and the Meaning of Life Read Online Free PDF Page B

work by blocking protein assembly in bacteria, and also block protein synthesis in the mitochondria, but not from the nuclear genes in eukaryotes.
    Taken together, these parallels might sound compelling, but in fact there are possible alternative interpretations, and it was these that underpinned the long dispute. In essence, the bacterial properties of mitochondria could be explained if the speed of evolution was slower in the mitochondria than in the nucleus. If so, then the mitochondria would have more in common with bacteria simply because they had not evolved as fast, and so as far. They would retain more atavistic traits. Because the mitochondrial genes are not recombined by sex, this position was sustainable, if somewhat unsatisfying. It couldonly be refuted when the actual rate of evolution was known, which in turn required the direct sequencing of mitochondrial genes, and the comparison of sequences. Only after Fred Sanger’s group in Cambridge had sequenced the human mitochondrial genome in 1981 did it transpire that the evolution rate of mitochondrial genes was
faster
than that of the nuclear genes. Their atavistic properties could only be explained by a direct relationship; and this relationship was ultimately shown to be with a very specific group of bacteria, the α-proteobacteria.
    Even the visionary Margulis was not correct about everything, luckily for the rest of us. Aligning herself with the earlier advocates of symbiosis, Margulis had argued that it would one day prove possible to grow mitochondria in culture—it was only a matter of finding the right growth factors. Today, we know that this is not possible. The reason was also made clear by the detailed sequence of the mitochondrial genome: the mitochondrial genes only encode a handful of proteins (13 to be exact), along with all the genetic machinery needed to make them. The great majority of mitochondrial proteins (some 800) are encoded by the genes in the nucleus, of which there are 30 000 to 40 000 in total. The apparent independence of mitochondria is therefore truly apparent, and not genuine. Their reliance on two genomes, the mitochondrial and the nuclear, is evident even at the level of a few proteins that are composed of multiple subunits, some of which are encoded by the mitochondrial genes, and others by the nuclear genes. Because they rely on both genomes, mitochondria can only be cultured within their host cells, and are correctly designated ‘organelles’, rather than symbionts. Nonetheless, the word ‘organelle’ gives no hint of their extraordinary past, and affords no insight into their profound influence on evolution.
    There is another sense in which many biologists today still disagree with Lynn Margulis, and that relates to the evolutionary power of symbiosis in general. For Margulis, the eukaryotic cell is the product of multiple symbiotic mergers, in which the component cells have been subsumed into the greater whole to varying degrees. Her theory has been dubbed the ‘serial endosymbiosis theory’, meaning that eukaryotic cells were formed by a succession of such mergers between cells, giving rise to a community of cells living within one another. Besides chloroplasts and mitochondria, Margulis cites the cell skeleton with its organizing centre, the centriole, as the contribution of another type of bacteria, the
Spirochaetes
. In fact, according to Margulis the whole organic world is an elaboration of collaborative bacteria—the microcosm. The idea goes back to Darwin himself, who wrote in a celebrated passage: ‘Each living being is a microcosm—a little universe formed of self-propagating organisms inconceivably minute and numerous as the stars in the heavens.’
    The idea of a microcosm is beautiful and inspiring, but raises a number of difficulties. Cooperation is not an alternative to competition. A collaborationbetween different bacteria to form new cells and organisms merely raises the bar for competition, which is