for the body. The body is an emergent phenomenon consequent upon the competitive survival of DNA sequences, and a means by which the genome perpetuates itself. And though the natural selection that results in evolutionary change is very far from random, the mutations themselves are random. It is a process of blind trial and error.
Red Queen races
Even in the heart of genetics labs there is a long tradition of resistance to the idea that mutation is purely random and comes with no intentionality, even if selection is not random. Theories of directed mutation come and go, and many highly reputable scientists embrace them, though the evidence remains elusive. The molecular biologist Gabby Dover, in his book Dear Mr Darwin, tried to explain the implausible fact that some centipedes have 173 body segments without relying exclusively on natural selection. His argument was basically that it was unlikely that a randomly generated 346-legged centipede survived and bred at the expense of one with slightly fewer legs. He thinks some other explanation is needed for how the centipede got its segments. He finds such an explanation in ‘molecular drive’, an idea that remains frustratingly vague in Dover’s book, but has a strong top–down tinge. In the years since Dover put forward the notion, molecular drive has sunk with little trace, following so many other theories of directed mutation into oblivion. And no wonder: if mutation is directed, then there would have to be a director, and we’re back to the problem of how the director came into existence: who directed the director? Whence came this knowledge of the future that endowed a gene with the capacity to plan a sensible mutation?
In medicine, an understanding of evolution at the genomic level is both the problem and the solution. Bacterial resistance to antibiotics, and chemotherapeutic drug resistance within tumours, are both pure Darwinian evolutionary processes: the emergence of survival mechanisms through selection. The use of antibiotics selects for rare mutations in genes in bacteria that enable them to resist the drugs. The emergence of antibiotic resistance is an evolutionary process, and it can only be combated by an evolutionary process. It is no good expecting somebody to invent the perfect antibiotic, and find some way of using it that does not elicit resistance. We are in an arms race with germs, whether we like it or not. The mantra should always be the Red Queen’s (from Lewis Carroll’s Through the Looking-Glass): ‘Now, here, you see, it takes all the running you can do, to keep in the same place. If you want to get somewhere else, you must run at least twice as fast as that!’ The search for the next antibiotic must begin long before the last one is ineffective.
That, after all, is how the immune system works. It does not just produce the best antibodies it can find; it sets out to experiment and evolve in real time. Human beings cannot expect to rely upon evolving resistance to parasites quickly enough by the selective death of susceptible people, because our generation times are too long. We have to allow evolution within our bodies within days or hours. And this the immune system is designed to achieve. It contains a system for recombining different forms of proteins to increase their diversity and rapidly multiplying whichever antibody suddenly finds itself in action. Moreover, the genome includes a set of genes whose sole aim seems to be to maintain a huge diversity of forms: the major histocompatibility complex. The job of these 240 or so MHC genes is to present antigens from invading pathogens to the immune system so as to elicit an immune response. They are the most variable genes known, with one – HLA-B – coming in about 1,600 different versions in the human population. There is some evidence that many animals go to some lengths to maintain or enhance the variability further, by, for example, seeking out mates with different MHC genes (detected by smell).
If the battle against microbes is a never-ending, evolutionary arms race, then so is the battle against cancer. A cell that turns cancerous and starts to grow into a tumour, then spreads to other parts of the body, has to evolve by genetic selection as it does so. It has to acquire mutations that encourage it to grow and divide; mutations that ignore the instructions to stop growing or commit suicide; mutations that cause blood vessels to grow into the tumour to supply it with nutrients; and mutations that enable cells to break free and migrate. Few of these mutations will be present in the first cancerous cell, but tumours usually acquire another mutation – one that massively rearranges its genome, thus experimenting on a grand scale, as if unconsciously seeking to find a way by trial and error to acquire these needed mutations.
The whole process looks horribly purposeful, and malign. The tumour is ‘trying’ to grow, ‘trying’ to get a blood supply, ‘trying’ to spread. Yet, of course, the actual explanation is emergent: there is competition for resources and space among the many cells in a tumour, and the one cell that acquires the most helpful mutations will win. It is precisely analogous to evolution in a population of creatures. These days, the cancer cells often need another mutation to thrive: one that will outwit the chemotherapy or radiotherapy to which the cancer is subjected. Somewhere in the body, one of the cancer cells happens to acquire a mutation that defeats the drug. As the rest of the cancer dies away, the descendants of this rogue cell gradually begin to multiply, and the cancer returns. Heartbreakingly, this is what happens all too often in the treatment of cancer: initial success followed by eventual failure. It’s an evolutionary arms race.
The more we understand genomics, the more it confirms evolution.
And therefore to assume there was one person gave a name
To everything, and that all learned their first words from the same,
Is stuff and nonsense. Why should one human being from among
The rest be able to designate and name things with his tongue
And others not possess the power to do likewise? …
Lucretius, De Rerum Natura, Book 5, lines 1041–5
The development of an embryo into a body is perhaps the most beautiful of all demonstrations of spontaneous order. Our understanding of how it happens grows ever less instructional. As Richard Dawkins writes in his book The Greatest Show on Earth, ‘The key point is that there is no choreographer and no leader. Order, organisation, structure – these all emerge as by-products of rules which are obeyed locally and many times over.’ There is no overall plan, just cells reacting to local effects. It is as if an entire city emerged from chaos just because people responded to local incentives in the way they set up their homes and businesses. (Oh, hang on – that is how cities emerged too.)
Look at a bird’s nest: beautifully engineered to provide protection and camouflage to a family of chicks, made to a consistent (but unique) design for each species, yet constructed by the simplest of instincts with no overall plan in mind, just a string of innate urges. I had a fine demonstration of this one year when a mistle thrush tried to build a nest on the metal fire escape outside my office. The result was a disaster, because each step of the fire escape looked identical, so the poor bird kept getting confused about which step it was building its nest on. Five different steps had partly built nests on them, the middle two being closest to completion, but neither fully built. The bird then laid two eggs in one half-nest and one in another. Clearly it was confused by the local cues provided by the fire-escape steps. Its nest-building program depended on simple rules, like ‘Put more material in corner of metal step.’ The tidy nest of a thrush emerges from the most basic of instincts.
Or look at a tree. Its trunk manages to grow in width and strength just as fast as is necessary to bear the weight of its branches, which are themselves a brilliant compromise between strength and flexibility; its leaves are a magnificent solution to the problem of capturing sunlight while absorbing carbon dioxide and losing as little water as possible: they are wafer-thin, feather-light, shaped for maximum exposure to the light, with their pores on the shady underside. The whole structure can stand for hundreds or even thousands of years without collapsing, yet can also grow continuously throughout that time – a dream that lies far beyond the capabilities of human engineers. All this is achieved without a plan, let alone a planner.