If mitochondria need a core of genes to control the speed of respiration, might this explain why bacteria can't evolve into eukaryotes by natural selection alone? I believe so, although I should emphasize that this is my own speculation (which I have expanded on elsewhere: see Further Reading). Bacteria are about the same size as mitochondria, so clearly a single set of genes can control respiration over a certain area of energetic membranes. Presumably the same is true of bacteria that evolved extensive internal membrane systems, such as
Nitrosomonas and Nitrosococcus. They get by with a single gene set, so presumably that must be enough too. But let's expand our bacterium; let's double the area of internal membranes. Now, perhaps, we're beginning to lose control over some parts of the membrane. If you don't think so, double the area again. And again. We could double the internal membrane area of Nitrosomonas six or seven times before we're level with the eukaryotes. I doubt we could maintain control over the speed of respiration now. How might we regain control?
One way would be to copy a subset of genes and delegate it to regulate the extra membranes—but how could we choose the right genes? There is no way I can think of that does not involve some kind of foresight (an awareness of which genes to choose), and evolution has none. The only way such delegation might work would be to replicate the entire genome, and then whittle away at one of the two genomes until all the superfluous genes were gone (as actually happened in the mitochondria). But how would we know which genome should lose its genes? Both must be active for genetic control to work. In the meantime, however, we have a bacterium with two active genomes, each under a heavy selective pressure to throw away any excess genes. Either of the two genomes might be expected to lose some genes—but then the two dissimilar genomes would compete with each other, potentially leading to the destruction of the cell (more on this in Part 6), and certainly not stabilizing it in the selective battle against other cells.
Such competition between genomes might be stopped if it was possible to demark the sphere of influence of each genome. The eukaryotes solved the sphere-of-influence problem by sealing off the mitochondrial genomes within a double membrane. This is not possible in bacteria, however. If the spare set of genes were sealed off, there would be no way of getting food supplies in and ATP out. In particular, ATP exporters do not exist among bacteria—exporting energy in the form of ATP to their competitors in the outside world would be a suicidal behavioural trait for bacteria. The ATP exporters, along with the family of 150 mitochondrial transport proteins to which they belong, are a eukaryotic invention. We know this because the gene sequences of the ATP exporters are clearly related in plants, animals, and fungi, but there are no similar bacterial genes. This implies that the ATP exporters evolved in the last common ancestor of all the eukaryotes, before the divergence of the major groups, but after the formation of the chimeric ancestral eukaryotic cell.
The eukaryotes had time to evolve such niceties because the relationship between the two partners of the chimera was stable over evolutionary time. The two partners lived in harmony together, and didn't need anything else—there was ample time and stability for evolutionary change to take place. This stability was only possible because there were other advantages to the association between the collaborating partners. If the hydrogen hypothesis is correct, the initial advantage was the mutual chemical dependency of two radically different cells, which lasted for long enough for the ATP exporters to evolve. In the case of bacteria evolving simply by natural selection, however, there is no corresponding stability. Simply duplicating a gene set and sealing it off within a membrane could in itself provide no advantages in the interim. Far from it: maintaining extra genes and membranes without any payback is energy sapping, and would no doubt be swiftly dumped by natural selection. Whichever way we look at it, selection pressure is always likely to jettison the burdensome additional genes needed for respiratory control over a wide area of membranes in bacteria. The most stable state is always a small cell that respires across the outer cell membrane. Such a cell will almost invariably be favoured by selection in place of any larger, inefficient, free-radical-generating competitors.
So we can now finally appreciate the full set of barriers to large size and complexity in bacteria. Bacteria replicate as quickly as they can, and are limited at least partly by the speed at which they can generate ATP. They generate ATP by pumping protons across their external membrane. They can't grow larger because their energetic efficiency tails away as their size increases. This fact in itself makes the predatory eukaryotic lifestyle unlikely, because phagocytosis requires a combination of large size with abundant energy that is precluded by respiration across the outer membrane. Some bacteria developed complex internal membrane systems. However, the area of these is several orders of magnitude less than that of the mitochondrial membranes in a single eukaryotic cell, because without gene outposts bacteria can't control the speed of respiration over a wider area. Given the strong selection pressures for fast reproduction and efficient energy generation, any of the possible transition states en route to establishing such genetic outposts would likely have been selected against whenever they arose. Only endosymbiosis was stable enough to provide the long-term conditions necessary for respiratory control on a wider scale.
Would things have happened differently somewhere else in an infinite universe? Anything is possible, but it seems to me unlikely. Natural selection is probabilistic: similar selection pressures are most likely to generate similar outcomes anywhere in the universe. This explains why natural selection so often converges on similar solutions, such as eyes and wings. Despite 4000 million years of evolution, we know of no single example of bacteria that succeeded in becoming eukaryotes by natural selection alone, or for that matter, of any mitochondria that lost all of their genes and still functioned as mitochondria. I doubt whether such events would happen any more often anywhere else either.
What of a eukaryotic-style chimera? We saw in Part 1 that the eukaryotic cell evolved here on earth just once, by way of what seems to have been a deeply improbable chain of circumstances. Perhaps a similar concatenation would be repeated elsewhere, but I see nothing in the laws of physics to suggest that the rise of complexity was inevitable. Physics is stymied by history. At best, the evolution of multicellular complexity seems to have been improbable; and without a kernel of complexity, intelligence is unthinkable. Yet once the loop that had kept bacteria simple was broken, the birth of that first large, complex cell, the first eukaryote, marked the beginning of a road that led, almost inexorably, to the spectacular feats of bioengineering that we see all around us today, including ourselves. This path was just as dependent on mitochondria as the origin of the eukaryotic cell itself, for the existence of mitochondria made the evolution of large size and greater complexity not just possible, but probable.
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