The nucleus is not enough

But this answer is not quite convincing. All species have lost almost all their mitochondrial genomes but not one species has lost them all. None has more than a hundred genes left, having started out with probably several thousand some two billion years ago, so the process has run very nearly to completion in all species. This gene loss has occurred in parallel: different species have lost their mitochondrial genes independently. As a proportion of the genes lost, all species have now lost between 95 and 99.9 per cent of their mitochondrial genes. If chance alone were the dominating factor, we might expect that at least a few species would have gone the whole hog by now, and transferred all mito-chondrial genes to the nucleus. Not one has done so. All known mitochondria have retained at least a few genes. What's more, mitochondria isolated from different species have invariably retained the same core of genes: they have independently lost the great majority of their genes but kept essentially the same handful, again implying that chance is not to blame. Interestingly, exactly the same applies to chloroplasts, which, as we have seen, are in a similar position: no chloroplast has lost all of its genes, and again, the same core of genes always figures among them. In contrast, other organelles related to mitochondria, such as hydrogenosomes and mitosomes, have almost invariably lost all their genes.

A number of reasons have been put forward to account for the fact that all known mitochondria have retained at least a few genes. Most are not terribly convincing. One idea once popular, for example, is that some proteins can't be targeted to the mitochondria because they are too large or too hydrophobic— but most of these proteins have in fact been successfully targeted to the mitochondria, either in one species or another, or by means of genetic engineering. Clearly the physical properties of proteins are not insurmountable obstacles to their parcelling and delivery to the mitochondria. Another idea is that the mitochondrial genetic systems harbour exceptions to the universal genetic code, and so mitochondrial genes are no longer strictly analogous to nuclear genes. If these genes were moved to the nucleus and read off according to the standard genetic code, the resulting protein would not be quite the same as that produced by the mitochondrial genetic system, and might not function correctly. But this can't be the full answer either, as in many species the mitochondrial genes do conform to the universal genetic code. There is no discrepancy in these cases, and therefore no reason why all the mitochondrial genes could not be transferred to the nucleus—and yet they remain stubbornly in the mitochondria. Likewise, there are no variations in the universal genetic code in chloroplast genes, and yet, like mitochondria, they always retain a core contingent of genes on site.

The answer that I believe to be correct is only now gaining credence among evolutionary biologists, despite being put forward by John Allen, then at the University of Lund in Sweden, as long ago as 1993. Allen argues that there are many good reasons why all the mitochondrial genes should have moved to the nucleus, and no clear 'technical' reasons why any should have stayed. Therefore, he says, there must be a very strong positive reason for their retention. They have not remained there by chance, but because natural selection has favoured their retention despite the manifold disadvantages. In the balance of pros and cons, the pros prevailed, at least in the case of the small number of genes that remain. But if the cons are so obvious and important, it is remarkable that we have overlooked the pros—they must be even weightier.

The reason, says Allen, is no less than the raison d'etre of mitochondria: respiration. The speed of respiration is very sensitive to changing circum-stances—whether we're awake or asleep, or doing aerobics, sitting around, writing books, or chasing a ball. These sudden shifts demand that mitochondria adapt their activity at a molecular level—a requirement that is too important, and abruptly swinging, to be controlled at a distance by the bureaucratic confederation of genes far away in the nucleus. Similar sudden shifts in requirements occur not just in animals but also in plants, fungi, and microbes, which are even more subject to the vicissitudes of the environment (such as changing oxygen levels, heat, or cold) at the molecular level. To respond effectively to these abrupt changes, Allen argues, mitochondria need to maintain a genetic outpost on site, as the redox reactions that take place in the mitochondrial membranes must be tightly regulated by genes on a local basis. Notice that I'm referring to the genes themselves here, and not to the proteins that they encode; we'll look into why the genes are important in a moment. But before we move on, let's note that the need for local genetic rapid-response units not only explains why mitochondria must retain a contingent of genes, but also, I

believe, why the bacteria could not evolve into more complex eukaryotic cells by natural selection alone.

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