The Vital Question: Why Is Life the Way It Is? by Nick Lane

Author:Nick Lane
Language: eng
Format: epub
Tags: Non-Fiction
ISBN: 9781847658807
Publisher: Profile Books
Published: 2015-04-23T07:00:00+00:00

Mitochondria – key to complexity

It’s not obvious why mitochondria always retain a handful of genes. Hundreds of genes encoding mitochondrial proteins were transferred to the nucleus early in eukaryotic evolution. Their protein products are now made externally in the cytosol, before being imported into the mitochondria. Yet a small group of genes, encoding respiratory proteins, invariably remained in the mitochondria. Why? The standard textbook Molecular Biology of the Cell states: ‘We cannot think of compelling reasons why the proteins made in the mitochondria and chloroplasts should be made there, rather than in the cytosol.’ That same sentence appears in the 2008, 2002, 1992 and 1983 editions; one is entitled to wonder how much the authors did actually think about the question.

From the standpoint of eukaryotic origins, it seems to me there are two possible types of answer – trivial, or necessary. When I say ‘trivial’ I don’t mean that in a trivial sense – I mean that there is no unmodifiable biophysical reason for the mitochondrial genes to remain where they are. The fact that they have not moved is not because they can’t move, but because for historical reasons they simply have not. Trivial answers explain why genes stayed in the mitochondria: they could have moved to the nucleus, but the balance of chance and selective forces meant that some of them remained where they had always been. Possible reasons include the size and hydrophobicity of mitochondrial proteins, or minor alterations in the genetic code. In principle, the ‘trivial’ hypothesis argues, all the remaining mitochondrial genes could be transferred to the nucleus, albeit requiring a little genetic engineering to modify their sequence as necessary, and the cell would work perfectly well. There are some researchers actively working on transferring mitochondrial genes to the nucleus, on the basis that such a transfer could prevent ageing (more on that in Chapter 7). This is a problem beset with challenges, not a trivial undertaking in the colloquial use of the term; but it is trivial in the sense that these researchers believe there is no need for genes to remain in the mitochondria. They think that there are real benefits to transferring them to the nucleus. Good luck to them.

I disagree with their reasoning. The ‘necessary’ hypothesis argues that mitochondria have retained genes because they need genes – without them, mitochondria could not exist at all. The cause is unmodifiable: it is not possible to transfer these genes to the nucleus even in principle. Why not? The answer, in my view, comes from John Allen, a biochemist and long-standing colleague. I believe his answer not because he is a friend; quite the reverse. We became friends in part because I believe his answer. Allen has a fertile mind and has put forward a number of original hypotheses, which he has spent decades testing and some of which we have been arguing about for years. In this particular case, he has good evidence supporting the argument that mitochondria (and chloroplasts, for similar reasons) have retained genes because they are needed to control chemiosmotic coupling.

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