The Blind Watchmaker (30 page)

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Authors: Richard Dawkins

Tags: #Science, #Life Sciences, #Evolution, #General

BOOK: The Blind Watchmaker
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The reason for this is interesting, and worth a digression because it provides a good genetic analogy. When you tell a computer to delete a file, it appears to obey you. But it doesn’t actually wipe out the text of that file. It simply wipes out all
pointers
to that file. It is as though a librarian, ordered to destroy
Lady Chatterley’s Lover
, simply tore up the card from the card index, leaving the book itself on the shelf. For the computer, this is a perfectly economical way to do things, because the space formerly occupied by the ‘deleted’ file is automatically available for new files, as soon as the pointers to the old file have been removed. It would be a waste of time actually to go to the trouble of filling the space itself with blanks. The old file won’t itself be finally lost until all its space happens to be used for storing new files.

But this re-using of space occurs piecemeal. New files aren’t exactly the same size as old ones. When the computer is trying to save a new file to a disc, it looks for the first available fragment of space, writes as much of the new file as will fit, then looks for another available fragment of space, writes a bit more, and so on until all the file is written
somewhere on
the disc. The human has the illusion that the file is a single, orderly array, only because the computer is careful to keep records ‘pointing’ to the addresses of all the fragments dotted around. These ‘pointers’ are like the ‘continued on page 94’ pointers used by the
New York Times
. The reason many copies of any one fragment of text are found on a disc is that if, like all my chapters, the text has been edited and re-edited many dozens of times, each edit will result in a new saving to the disc of (almost) the same text. The saving may ostensibly be a saving of the same file. But as we have seen, the text will in fact be repeatedly scattered around the available ‘gaps’ on the disc. Hence multiple copies of a given fragment of text can be found all around the surface of the disc, the more so if the disc is old and much used.

Now the DNA operating system of a species is very very old indeed, and there is evidence that it, seen in the long term, does something a bit like the computer with its disc files. Part of the evidence comes from the fascinating phenomenon of ‘introns’ and ‘exons’. Within the last decade, it has been discovered that any ‘single’ gene, in the sense of a single continuously read passage of DNA text, is not all stored in one place. If you actually read the code letters as they occur along the chromosome (i.e. if you do the equivalent of breaking out of the discipline of the ‘operating system’) you find fragments of ‘sense’, called exons, separated by portions of ‘nonsense’ called introns. Any one ‘gene’ in the functional sense, is in fact split up into a sequence of fragments (exons) separated by meaningless introns. It is as if each exon ended with a pointer saying ‘continued on page 94’. A complete gene is then made up of a whole series of exons, which are actually strung together only when they are eventually read by the ‘official’ operating system that translates them into proteins.

Further evidence comes from the fact that the chromosomes are littered with old genetic text that is no longer used, but which still makes recognizable sense. To a computer programmer, the pattern of distribution of these ‘genetic fossil’ fragments is uncannily reminiscent of the pattern of text on the surface of an old disc that has been much used for editing text. In some animals, a high proportion of the total number of genes is in fact never read. These genes are either complete nonsense, or they are outdated ‘fossil genes’.

Just occasionally, textual fossils come into their own again, as I experienced when writing this book. A computer error (or, to be fair, it may have been human error) caused me accidentally to ‘erase’ the disc containing Chapter 3. Of course the text itself hadn’t literally all been erased. All that had been definitely erased were the
pointers to
where each ‘exon’ began and ended. The ‘official’ operating system could read nothing, but ‘unofficially’ I could play genetic engineer and examine all the text on the disc. What I saw was a bewildering jigsaw puzzle of textual fragments, some of them recent, others ancient ‘fossils’. By piecing together the jigsaw fragments, I was able to recreate the chapter. But I mostly didn’t know which fragments were recent and which were fossil. It didn’t matter for, apart from minor details that necessitated some new editing, they were the same. At least some of the ‘fossils’, or outdated ‘introns’, had come into their own again. They rescued me from my predicament, and saved me the trouble of rewriting the entire chapter.

There is evidence that, in living species too, ‘fossil genes’ occasionally come into their own again, and are re-used after lying dormant for a million years or so. To go into detail would carry us too far from the main pathway of this chapter, for you will remember that we are already out on a digression. The main point was that the total genetic capacity of a species may increase due to gene duplication. Reusing of old ‘fossil’ copies of existing genes is one way in which this can happen. There are other, more immediate, ways in which genes may be copied to widely distributed parts of the chromosomes, like files being duplicated to different parts of a disc, or different discs.

Humans have eight separate genes called globin genes (used for making haemoglobin, among other things), on various different chromosomes. It seems certain that all eight have been copied, ultimately from a single ancestral globin gene. About 1,100 million years ago, the ancestral globin gene duplicated, forming two genes. We can date this event because of independent evidence about how fast globins habitually evolve (see Chapters 5 and 11). Of the two genes produced by this original duplication, one became the ancestor of all the genes that make haemoglobin in vertebrates. The other became the ancestor of all the genes that make myoglobins, a related family of proteins that work in muscles. Various subsequent duplications have given rise to the so-called alpha, beta, gamma, delta, epsilon and zeta globins. The fascinating thing is that we can construct a complete family tree of all the globin genes, and even put dates on all the divergence points (delta and beta globin parted company, for example, about 40 million years ago, epsilon and gamma globins 100 million years ago). Yet the eight globins, descendants as they are of these remote branchings in distant ancestors, are still all present inside every one of us. They diverged to different parts of an ancestor’s chromosomes, and we have each inherited them on our different chromosomes. Molecules are sharing the same body with their remote molecular cousins. It is certain that a great deal of such duplication has gone on, all over the chromosomes, and throughout geological time. This is an important respect in which real life is more complicated than the biomorphs of Chapter 3. They all had only nine genes. They evolved by changes in those nine genes, never by increasing the number of genes to ten. Even in real animals, such duplications are rare enough not to invalidate my general statement that all members of a species share the same DNA ‘addressing’ system.

Duplication within the species isn’t the only means by which the number of cooperating genes has increased in evolution. An even rarer, but still possibly very important occurrence, is the occasional incorporation of a gene from another species, even an extremely remote species. There are, for example, haemoglobins in the roots of plants of the pea family. They don’t occur in any other plant families, and it seems almost certain that they somehow got into the pea family by cross-infection from animals, viruses perhaps acting as intermediaries.

An especially important event along these lines, according to the increasingly favoured theory of the American biologist Lynn Margulis, took place at the origin of the so-called eukaryotic cell. Eukaryotic cells include all cells except those of bacteria. The living world is divided, fundamentally, into bacteria versus the rest. We are part of the rest, and are collectively called the eukaryotes. We differ from bacteria mainly in that our cells have discrete little mini-cells inside them. These include the nucleus, which houses the chromosomes; the tiny bomb-shaped objects called mitochondria (which we briefly met in Figure 1), filled with intricately folded membranes; and, in the (eukaryotic) cells of plants, chloroplasts. Mitochondria and chloroplasts have their own DNA, which replicates and propagates itself entirely independently of the main DNA in the chromosomes of the nucleus. All the mitochondria in you are descended from the small population of mitochondria that travelled from your mother in her egg. Sperms are too small to contain mitochondria, so mitochondria travel exclusively down the female line, and male bodies are dead ends as far as mitochondrial reproduction is concerned. Incidentally, this means that we can use mitochondria to trace our ancestry, strictly down the female line.

Margulis’s theory is that mitochondria and chloroplasts, and a few other structures inside cells, are each descended from bacteria. The eukaryotic cell was formed, perhaps 2 billion years ago, when several kinds of bacteria joined forces because of the benefits that each could obtain from the others. Over the aeons they have become so thoroughly integrated into the cooperative unit that became the eukaryotic cell, that it has become almost impossible to detect the fact, if indeed it is a fact, that they were once separate bacteria.

It seems that, once the eukaryotic cell had been invented, a whole new range of designs became possible. Most interestingly from our point of view, cells could manufacture large bodies comprising many billions of cells. All cells reproduce by splitting into two, both halves getting a full set of genes. As we saw in the case of the bacteria on a pin’s head, successive splittings into two can generate a very large number of cells in rather a short time. You start with one and it splits into two. Then each of the two splits, making four. Each of the four splits, making eight. The numbers go up by successive doublings, from 8 to 16, 32, 64, 128, 256, 512, 1,024, 2,048, 4,096, 8,192. After only 20 doublings, which doesn’t take very long, we are up in the millions. After only 40 doublings the number of cells is more than a trillion. In the case of bacteria, the enormous numbers of cells produced by successive doublings go their separate ways. The same is true of many eukaryotic cells, for instance protozoa such as amoebas. A major step in evolution was taken when cells that had been produced by successive splittings stuck together instead of going off independently. Higher-order structure could now emerge, just as it did, on an incomparably smaller scale, in the two-way branching computer biomorphs.

Now, for the first time, large body size became a possibility. A human body is a truly colossal population of cells, all descended from one ancestor, the fertilized egg; and all therefore cousins, children, grandchildren, uncles,
etc.
of other cells in the body. The 10 trillion cells that make up each one of us are the product of a few dozens of generations of cell doublings. These cells are classified into about 210 (according to taste) different kinds, all built by the same set of genes but with different members of the set of genes turned on in different kinds of cells. This, as we have seen, is why liver cells are different from brain cells, and bone cells are different from muscle cells.

Genes working through the organs and behaviour patterns of many-celled bodies can achieve methods of ensuring their own propagation that are not available to single cells working on their own. Many-celled bodies make it possible for genes to manipulate the world, using tools built on a scale that is orders of magnitude larger than the scale of single cells. They achieve these largescale indirect manipulations via their more direct effects on the miniature scale of cells. For instance, they change the shape of the cell membrane. The cells then interact with one another in huge populations to produce largescale group effects such as an arm or a leg or (more indirectly) a beaver’s dam. Most of the properties of an organism that we are equipped to see with our naked eyes are so-called ‘emergent properties’. Even the computer biomorphs, with their nine genes, had emergent properties. In real animals they are produced at the wholebody level by interactions between cells. An organism works as an entire unit, and its genes can be said to have effects on the whole organism, even though each copy of any one gene exerts its immediate effects only within its own cell.

We have seen that a very important part of a gene’s environment is the other genes that it is likely to meet in successive bodies as the generations go by. These are the genes that are permuted and combined within the species. Indeed, a sexually reproducing species can be thought of as a device that permutes a discrete set of mutually accustomed genes in different combinations. Species, according to this view, are continually shuffling collections of genes that meet each other within the species, but never meet genes of other species. But there is a sense in which the genes of different species, even if they don’t meet at close quarters inside cells, nevertheless constitute an important part of each others’ environment. The relationship is often hostile rather than cooperative, but this can be treated as just a reversal of sign. This is where we come to the second major theme of this chapter, ‘arms races’. There are arms races between predators and prey, parasites and hosts, even - though the point is a more subtle one and I shan’t discuss it further - between males and females within one species.

Arms races are run in evolutionary time, rather than on the timescale of individual lifetimes. They consist of the improvement in one lineage’s (say prey animals’) equipment to survive, as a direct consequence of improvement in another (say predators’) lineage’s evolving equipment. There are arms races wherever individuals have enemies with their own capacity for evolutionary improvement. I regard arms races as of the utmost importance because it is largely arms races that have injected such ‘progressiveness’ as there is in evolution. For, contrary to earlier prejudices, there is nothing inherently progressive about evolution. We can see this if we consider what would have happened if the only problems animals had had to face had been those posed by the weather and other aspects of the nonliving environment.

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