Genome: The Autobiography of a Species in 23 Chapters. Matt Ridley

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СКАЧАТЬ that it will one day be testable. The fossil record will tell us only a little about behaviour; the bones are too dry and random to speak. But the genetic record will tell us more. Natural selection is the process by which genes change their sequences. In the process of changing, though, those genes laid down a record of our four-billion year biography as a biological lineage. They are, if we only know how to read them, a more valuable source of information on our past than the manuscripts of the Venerable Bede. In other words, a record of our past is etched into our genes.

      Some two per cent of the genome tells the story of our different ecological and social evolution from that of chimpanzees, and theirs from us. When the genome of a typical human being has been fully transcribed into our computers, when the same has been done for the average chimpanzee, when the active genes have been extracted from the noise, and when the differences come to be listed, we will have an extraordinary glimpse of the pressures of the Pleistocene era on two different species derived from a common stock. The genes that will be the same will be the genes for basic biochemistry and body planning. Probably the only differences will be in genes for regulating growth and hormonal development. Somehow in their digital language, these genes will tell the foot of a human foetus to grow into a flat object with a heel and a big toe, whereas the same genes in a chimpanzee tell the foot of a chimp foetus to grow into a more curved object with less of a heel and longer, more prehensile toes.

      It is mind-boggling even to try to imagine how that can be done – science still has only the vaguest clues about how growth and form are generated by genes – but that genes are responsible is not in doubt. The differences between human beings and chimpanzees are genetic differences and virtually nothing else. Even those who would stress the cultural side of the human condition and deny or doubt the importance of genetic differences between human individuals or races, accept that the differences between us and other species are primarily genetic. Suppose the nucleus of a chimpanzee cell were injected into an enucleated human egg and that egg were implanted into a human womb, and the resulting baby, if it survived to term, were reared in a human family. What would it look like? You do not even need to do the (highly unethical) experiment to know the answer: a chimpanzee. Although it started with human cytoplasm, used a human placenta and had a human upbringing, it would not look even partly human.

      Photography provides a helpful analogy. Imagine you take a photograph of a chimpanzee. To develop it you must put it in a bath of developer for the requisite time, but no matter how hard you try, you cannot develop a picture of a human being on the negative by changing the formula of the developer. The genes are the negative; the womb is the developer. Just as a photograph needs to be immersed in a bath of developer before the picture will appear, so the recipe for a chimpanzee, written in digital form in the genes of its egg, needs the correct milieu to become an adult – the nutrients, the fluids, the food and the care – but it already has the information to make a chimpanzee.

      The same is not quite true of behaviour. The typical chimpanzee’s hardware can be put together in the womb of a foreign species, but its software would be a little awry. A baby chimpanzee would be as socially confused if reared by human beings as Tarzan would be if reared by chimps. Tarzan, for instance, would not learn to speak, and a human-reared chimp would not learn precisely how to appease dominant animals and intimidate subordinates, to make tree nests or to fish for termites. In the case of behaviour, genes are not sufficient, at least in apes.

      But they are necessary. If it is mind-boggling to imagine how small differences in linear digital instructions can direct the two per cent difference between a human body and a chimpanzee body, how much more mind-boggling is it to imagine that a few changes in the same instructions can alter the behaviour of a chimpanzee so precisely. I wrote glibly of the mating system of different apes – the promiscuous chimpanzee, the harem-polygamous gorilla and the long-pair-bond human being. In doing so I assumed, even more glibly, that every species behaves in a characteristic way, which, further, assumes that it is somehow at least partly genetically constrained or influenced. How can a bunch of genes, each one a string of quaternary code, make an animal polygamous or monogamous? Answer: I do not have the foggiest idea, but that it can do so I have no doubt. Genes are recipes for both anatomy and behaviour.

       CHROMOSOME 3 History

      We’ve discovered the secret of life.

       Francis Crick, 28 February 1953

      Though he was only forty-five in 1902, Archibald Garrod was already a pillar of the British medical establishment. He was the son of a knighted professor, the famous Sir Alfred Baring Garrod, whose treatise on that most quintessential of upper-class afflictions, gout, was reckoned a triumph of medical research. His own career was effortlessly distinguished and in due course the inevitable knighthood (for medical work in Malta during the First World War) would be followed by one of the most glittering prizes of all: the Regius professorship of medicine at Oxford in succession to the great Sir William Osler.

      You can just picture him, can you not? The sort of crusty and ceremonious Edwardian who stood in the way of scientific progress, stiff in collar, stiff in lip and stiff in mind. You would be wrong. In that year, 1902, Archibald Garrod risked a conjecture that would reveal him to be a man far ahead of his time and somebody who had all but unknowingly put his finger on the answer to the greatest biological mystery of all time: what is a gene? Indeed, so brilliant was his understanding of the gene that he would be long dead before anybody got the point of what he was saying: that a gene was a recipe for a single chemical. What is more, he thought he had found one.

      In his work at St Bartholomew’s Hospital and Great Ormond Street in London, Garrod had come across a number of patients with a rare and not very serious disease, known as alkaptonuria. Among other more uncomfortable symptoms such as arthritis, their urine and the ear wax turned reddish or inky black on exposure to the air, depending on what they had been eating. In 1901, the parents of one of these patients, a little boy, had a fifth child who also had the affliction. That set Garrod to thinking about whether the problem ran in families. He noticed that the two children’s parents were first cousins. So he went back and re-examined the other cases: three of the four families were first-cousin marriages, and of the seventeen alkaptonuria cases he saw, eight were second cousins of each other. But the affliction was not simply passed on from parent to child. Most sufferers had normal children, but the disease could reappear later in their descendants. Luckily, Garrod was abreast of the latest biological thinking. His friend William Bateson was one of those who was excited by the rediscovery just two years before of the experiments of Gregor Mendel, and was writing tomes to popularise and defend the new creed of Mendelism, so Garrod knew he was dealing with a Mendelian recessive – a character that could be carried by one generation but would only be expressed if inherited from both parents. He even used Mendel’s botanical terminology, calling such people ‘chemical sports’.

      This gave Garrod an idea. Perhaps, he thought, the reason that the disease only appeared in those with a double inheritance was because something was missing. Being well versed not only in genetics but also in chemistry, he knew that the black urine and ear wax was caused by a build-up of a substance called homogentisate. Homogentisate might be a normal product of the body’s chemistry set, but one that was in most people then broken down and disposed of. The reason for the build-up, Garrod supposed, was because the catalyst that was meant to be breaking down the homogentisate was not working. That catalyst, he thought, must be an enzyme made of protein, and must be the sole product of an inherited factor (or gene, as we would now say). In the afflicted people, the gene produced a defective enzyme; in the carriers this did not matter because the gene inherited from the other parent could compensate.

      Thus was born Garrod’s bold hypothesis of the ‘inborn errors of metabolism’, with its far-reaching assumption that genes were there to produce chemical catalysts, one gene to each highly specialised catalyst. Perhaps that was what genes were: devices for making СКАЧАТЬ