The Greatest Show on Earth

  Natural selection is the differential survival of successful genes rather than alternative, less successful genes in gene pools. Natural selection doesn’t choose genes directly. Instead it chooses their proxies, individual bodies; and those individuals are chosen – obviously and automatically and without deliberative intervention – by whether they survive to reproduce copies of the very same genes. A gene’s survival is intimately bound up with the survival of the bodies that it helps to build, because it rides inside those bodies, and dies with them. Any given gene can expect to find itself, in the form of copies of itself, riding inside a large number of bodies, both simultaneously in a population of contemporaries, and successively as generation gives way to generation. Statistically, therefore, a gene that tends, on average, to have a good effect on the survival prospects of the bodies in which it finds itself will tend to increase in frequency in the gene pool. So, on average, the genes that we encounter in a gene pool will tend to be those genes that are good at building bodies. This chapter has been about the procedures by which genes build bodies.

  Haldane’s interlocutor found it implausible that natural selection could put together in, say, a billion years, a genetic recipe for building her. I find it plausible, although of course neither I nor anybody else can tell you the details of how it happened. The reason it is plausible is precisely that it is all done by local rules. In any one act of natural selection, the mutation that is selected has had – in lots of cells and in lots of individuals in parallel – a very simple effect on the shape into which a protein chain spontaneously coils up. This, in turn, through catalytic action, speeds up, say, a particular chemical reaction in all the cells in which the gene is turned on. This changes, perhaps, the rate of growth of the embryonic primordium of the jaw. And this has consequential effects on the shape of the whole face, perhaps shortening the muzzle and giving a more human and less ‘ape-like’ profile. Now, the natural selection pressures that favour or disfavour the gene can be as complicated as you like. They might involve sexual selection, perhaps aesthetic choice of a high order by would-be sexual partners. Or the change in jaw shape might have a subtle effect on the animal’s ability to crack nuts, or its ability to fight rivals. Some hugely elaborate combination of selection pressures, conflicting and compromising with one another in bewildering complexity, can bear upon the statistical success of this particular gene, as it propagates itself through the gene pool. But the gene knows nothing of this. All it is doing, within different bodies and in successive generations, is rejigging a carefully sculpted dent in a protein molecule. The rest of the story follows automatically, in branching cascades of local consequences, from which, eventually, a whole body emerges.

  Even more complicated than the selection pressures in the ecological, sexual and social environments of the animals is the phantasmagoric network of influences that go on within and among the developing cells: influences of genes on proteins, genes on genes, proteins on the expression of genes, proteins on proteins; membranes, chemical gradients, physical and chemical guide rails in embryos, hormones and other mediators of action at a distance, labelled cells seeking others with identical or complementary labels. Nobody understands the whole picture, and nobody needs to understand it in order to accept the exquisite plausibility of natural selection. Natural selection favours the survival in the gene pool of the genetic mutations responsible for making crucial changes in embryos. The whole picture emerges as a consequence of hundreds of thousands of small, local interactions, each one comprehensible in principle (although it may be too hard or too time-consuming to unravel in practice) to anyone with sufficient patience to examine it. The whole may be baffling and mysterious in practice, but there is no mystery in principle, either in embryology itself, or in the evolutionary history by which the controlling genes came to prominence in the gene pool. The complications accumulated gradually over evolutionary time: each step was only a tiny bit different from the one before, and each step was accomplished by a small, subtle change in an existing local rule. When you have a sufficient number of small entities – cells, protein molecules, membranes – each at its own level obeying local rules and influencing others – then the eventual consequence is dramatic. If genes survive or fail to survive as a consequence of their influence on such local entities and their behaviour, natural selection of successful genes – and the emergence of their successful products – will inevitably follow. Haldane’s questioner was wrong. It is not in principle difficult to make something like her.

  And, as Haldane said, it only takes nine months.

  * I have been warned that ‘All things bright and beautiful’ will not necessarily strike my readers as nostalgically as it does me. It is an Anglican hymn for children written by Mrs C. F. Alexander in 1848, comfortably extolling the beauties of nature (and, in one verse, the political status quo) with the refrain, ‘The Lord God made them all’. It is the subject of a splendid parody written by Eric Idle and sung by the Monty Python team:

  All things dull and ugly

  All creatures short and squat

  All things rude and nasty

  The Lord God made the lot.

  Each little snake that poisons

  Each little wasp that stings

  He made their brutish venom

  He made their horrid wings.

  All things sick and cancerous

  All evil great and small,

  All things foul and dangerous

  The Lord God made them all.

  Each nasty little hornet

  Each beastly little squid

  Who made the spiky urchin?

  Who made the sharks? He did!

  All things scabbed and ulcerous

  All pox both great and small

  Putrid, foul and gangrenous

  The Lord God made them all.

  * Note for professionals at the interface between biologists and computer scientists: Charles Simonyi, who speaks with the authority of a distinguished software designer, put it as follows, after reading an early draft of this chapter: ‘. . . the recipe (of the eye, brain, blood, etc.) is much much simpler than the blueprint for the same (in terms of bits or base-pairs) so evolution would be literally impossible (in less than 10^100 years) especially because small variations in the blueprint would be unlikely to have any positive effect, whereas a variation in the recipe would.’ Alluding to my own ‘computer biomorphs’ and ‘arthromorphs’ (see Chapter 2), Dr Simonyi goes on: ‘The artificial creatures that you [programmed for The Blind Watchmaker and Climbing Mount Improbable] are all described by recipes, not by blueprint – a blueprint would be just a jumble of vectors of black lines – can you imagine trying to play evolution on them by varying the endpoints of the black lines one at a time or even two at a time?’ As you’d expect from one described by Bill Gates, no less, as ‘one of the great programmers of all time’, this is exactly right for the computer biomorphs, and it is surely right for living things too.

  * There is a risk that ‘epigenesis’ will be confused with ‘epigenetics’, a modish buzz-word now enjoying its fifteen minutes of fame in the biological community. Whatever ‘epigenetics’ might mean (and its enthusiasts cannot seem to agree even with themselves, let alone with each other), all I intend to say about it here is that it is not the same thing as epigenesis.

  * My medieval historian colleague Dr Christopher Tyerman confirms that this was indeed a myth that was invented in Victorian times for idealistic reasons, but that there was never a scintilla of truth in it.

  * Invaginate: ‘fold inwards to form a hollow’, ‘turn or double back within itself’ (Shorter Oxford English Dictionary).

  * The craze died out, but I reintroduced it to the same school in the 1950s, whereupon it spread just like a second epidemic of the same disease.

  * I am sorry I am at a loss to explain why the notochord gets an ‘h’, like a musical or mathematical chord, while the spinal cord doesn’t, like a bit of string. I have always found it mysterious, and have e
ven wondered whether it might represent some long-forgotten but fossilized mistake. Admittedly, the Oxford English Dictionary lists ‘chord’ as an alternative spelling for the string kind of cord, but the difference does seem queer given that the spinal cord and the notochord run the length of the embryonic body, one above the other.

  * And that’s a fascinating story in its own right, by the way. It has gripped my imagination ever since the great Cambridge physiologist Joseph Needham (a polymath who became even better known as the leading expert on the history of Chinese science) came to my school to demonstrate it, at the invitation of his nephew who happened to be our student teacher at the time: a boon of nepotism for which I remain grateful. Under Dr Needham’s guidance, we peered at muscle fibres down our microscopes and watched them shorten, as if by magic, when we gave them a drop of ATP, adenosine triphosphate, the universal energy currency of the body.

  * This statement needs an important reservation. The determination of the amino-acid sequence by genes is indeed absolute. But the determination of the three-dimensional shape by the one-dimensional amino-acid sequence is not absolute, and it really matters. There are some sequences of amino acids that are capable of coiling up into two alternative 3D shapes. The proteins called prions, for example, have two stable shapes. These are discrete alternatives without stable intermediates, in the same way as a light switch is stable in the up position and in the down position but nowhere in between. Such ‘switch proteins’ can be disastrous or they can be useful. In the case of prions they are disastrous. In ‘mad cow disease’, a useful protein in the brain (it’s a normal constituent of cell membranes) happens to have an alternative form – an alternative way to fold itself in auto-origami. The alternative form is normally never seen, but if it ever arises in one molecule it triggers neighbouring molecules to follow suit: they copy it and flip to the alternative form. Like a wave of falling dominoes, or like the irresponsible spreading of a rumour, the alternative prion form spreads through the brain, with disastrous results for the cow – or the person in the case of Creutzfeldt–Jakob disease, or the sheep in the case of scrapie. But sometimes molecules with the ability to auto-origami themselves into more than one alternative shape are useful. Without leaving the metaphor of the light switch we find a beautiful example. Rhodopsin, the protein in our eyes that is responsible for our sensitivity to light, has an embedded component called retinal (not itself a protein) which flips from its main stable configuration to its alternative configuration when hit by a photon of light. It then swiftly reverts, like a light switch on a cost-cutting timer, but meanwhile the flip has registered with the brain: ‘Light detected at this pinpoint location here.’ Jacques Monod’s wonderful book, Chance and Necessity, is especially good on such bi-stable switch molecules.

  * In Caenorhabditis the original cell, called Z, has a front end which is different from its rear end, and this difference will come to represent the eventual fore-and-aft body axis – anterior (front) and posterior (rear). When the cell divides, the anterior daughter cell, which is called AB, has more front-end substance than the posterior daughter cell, which is called P1, and this difference will be bootstrapped to make more differences down the line. AB is destined to give rise to well over half the cells of the body, including most of the nervous system, and I won’t discuss it further. P1 has two children, again different from each other, called EMS (defining the ventral or belly side of the eventual worm) and P2 (defining the dorsal side). They are grandchildren of Z (remember, when I use words like ‘children’ and ‘grandchildren’, I am talking about cells within a developing embryo, not individual worms). EMS now has two children called E and MS, while P2 has two children called C and P3. E, MS, C and P3 are great-grandchildren of Z (the other great-grandchildren are descended from AB, and I am not writing them down, except to say that two of them, called ABal and ABpl, define the left side, and their cousins, ABar and Abpr, define the right side of the eventual worm). P3 has two children called D and P4, which are great-great-grandchildren of Z. MS and C also have children, but I shan’t name them here. P4 is destined to give rise to the so-called germ line. The germ line consists of cells that are not involved in building the body, but instead are going to make the reproductive cells. Obviously there is no need to remember or take note of these cell names. The point is only that, although genetically identical to each other, they differ in their chemical nature, as a cumulatively bootstrapped consequence of their history in the sequence of cell divisions within the embryo.

  † Sulston, who stayed at Cambridge after Brenner left for America, was another of the triumvirate who won the Nobel Prize for the Caenorhabditis work. Sulston went on to lead the British end of the official Human Genome Project, the American end of which was headed first by James Watson and later by Francis Collins.

  CHAPTER 9

  THE ARK OF THE CONTINENTS

  IMAGINE a world without islands.

  Biologists often use the word ‘island’ to mean something other than just a piece of land surrounded by water. From the point of view of a freshwater fish, a lake is an island: an island of habitable water surrounded by inhospitable land. From the point of view of an Alpine beetle, incapable of flourishing below a certain altitude, each high peak is an island, with almost impassable valleys between. There are tiny nematode worms (related to the elegant Caenorhabditis) which live inside leaves (as many as 10,000 of them in a single badly infected leaf), diving into them through the stomata, which are the microscopic holes through which leaves take in carbon dioxide and release oxygen. To a leaf-dwelling nematode worm such as Aphelencoides, a single foxglove is an island. To a louse, a single human head or crotch might be an island. There must be lots of animals and plants that regard an oasis in a desert as an island of cool, green habitability surrounded by a hostile sea of sand. And, while we are redefining words from an animal’s point of view, since an archipelago is a chain or cluster of islands, I suppose a freshwater fish might define an archipelago as a chain or cluster of lakes, such as the lakes along the Great Rift Valley in Africa. An Alpine marmot might define a chain of mountain peaks separated by valleys as an archipelago. A leaf-mining insect might regard an avenue of trees as an archipelago. A botfly might regard a herd of cattle as a moving archipelago.

  Having redefined the word ‘island’ (the sabbath was made for man, not man for the sabbath) let me return to my opening. Imagine a world without islands.

  He had bought a large map representing the sea

  Without the least vestige of land:

  And the crew were much pleased when they found it to be

  A map they could all understand.

  We won’t go quite as far as the Bellman, but imagine if all the land were gathered together in one great continent in the middle of a featureless sea. There are no islands offshore, no lakes or mountain ranges on the land: nothing to break the monotonous sweep of smooth uniformity. In this world an animal can easily go from anywhere to anywhere else, limited only by sheer distance, untroubled by inhospitable barriers. This is not a world friendly to evolution. Life on Earth would be extremely boring if there were no islands, and I want to begin this chapter by explaining why.

  HOW NEW SPECIES ARE BORN

  Every species is a cousin of every other. Any two species are descended from an ancestral species, which split in two. For example, the common ancestor of people and budgerigars lived about 310 million years ago. The ancestral species split in two, and the two strands went their separate ways for the rest of time. I chose human and budgie to make it vivid, but that same ancestral species is shared by all mammals on one side of that early divide, and all reptiles (zoologically speaking, birds are reptiles, as we saw in Chapter 6) on the other side. In the unlikely event that a fossil of this ancestral species was ever found, it would need a name. Let’s call it Protamnio darwinii. We don’t know any details about it, and the details don’t matter at all for the argument, but we won’t go far wrong if we imagine it as a sprawling lizard-like creat
ure, scurrying about catching insects. Now, here’s the point. When Protamnio darwinii split into two sub-populations they would have looked just the same as each other, and could have happily interbred with each other; but one lot were destined to give rise to the mammals, and the other lot were destined to give rise to the birds (and dinosaurs and snakes and crocodiles). These two sub-populations of Protamnio darwinii were about to diverge from each other, over a very long time and in a very big way. But they couldn’t diverge if they kept on interbreeding with each other. The two gene pools would continually flood each other with genes. So any tendency to diverge would be nipped in the bud before it could get going, swamped by gene flow from the other population.

  What actually happened at this epic parting of the ways, nobody knows. It happened a very long time ago, and we have no idea where. But modern evolutionary theory would confidently reconstruct something like the following history. The two sub-populations of Protamnio darwinii somehow became separated from each other, most likely by a geographical barrier such as a strip of sea separating two islands, or separating an island from a mainland. It could have been a mountain range that separated two valleys, or a river separating two forests: two ‘islands’ in the general sense I defined. All that matters is that the two populations were isolated from one another for long enough so that, when time and chance eventually reunited them, they found they had diverged so much that they couldn’t interbreed any more. How long is long enough? Well, if they were subject to strong and contrasting selection pressures, it could be as little as a few centuries, or even less. For example, an island might lack a voracious predator that prowled the mainland. Or the island population might have shifted from an insectivorous to a vegetarian diet, like the Adriatic lizards of Chapter 5. Once again, we can’t know the details of how Protamnio darwinii split, and we don’t need to. The evidence from modern animals gives us every reason to think that something like the story I have just told is what happened in the past, for every one of the divergences between the ancestry of any animal and any other.