Fast-forward to the 1980s and one of the most stunning surprises to greet scientists when they first opened up animal genomes: fly geneticists found a small group of genes called the hox genes that seemed to set out the body plan of the fly during its early development—telling it roughly where to put the head, legs, wings and so on. But then colleagues studying mice found the same hox genes, in the same order, doing the same job in Mickey's world—telling the mouse where to put its various parts. And when scientists looked in our genome, they found hox genes there too.

Hox genes, like all genes, are switched on and off in different parts of the body at different times. In this way, genes can have subtly different effects, depending on where, when and how they are switched on. The switches that control this process—stretches of DNA upstream of genes—are known as promoters.

Small changes in the promoter can have profound effects on the expression of a hox gene. For example, mice have short necks and long bodies; chickens have long necks and short bodies. If you count the vertebrae in the necks and thoraxes of mice and chickens, you will find that a mouse has seven neck and 13 thoracic vertebrae, a chicken 14 and seven, respectively. The source of this difference lies in the promoter attached to HoxC8, a hox gene that helps shape the thorax of the body. The promoter is a 200-letter paragraph of DNA, and in the two species it differs by just a handful of letters. The effect is to alter the expression of the HoxC8 gene in the development of the chicken embryo. This means the chicken makes thoracic vertebrae in a different part of the body than the mouse. In the python, HoxC8 is expressed right from the head and goes on being expressed for most of the body. So pythons are one long thorax; they have ribs all down the body.

To make grand changes in the body plan of animals, there is no need to invent new genes, just as there's no need to invent new words to write an original novel (unless your name is Joyce). All you need do is switch the same ones on and off in different patterns. Suddenly, here is a mechanism for creating large and small evolutionary changes from small genetic differences. Merely by adjusting the sequence of a promoter or adding a new one, you could alter the expression of a gene.

In one sense, this is a bit depressing. It means that until scientists know how to find gene promoters in the vast text of the genome, they will not learn how the recipe for a chimpanzee differs from that for a person. But in another sense, it is also uplifting, for it reminds us more forcefully than ever of a simple truth that is all too often forgotten: bodies are not made, they grow. The genome is not a blueprint for constructing a body. It is a recipe for baking a body. You could say the chicken embryo is marinated for a shorter time in the HoxC8 sauce than the mouse embryo is. Likewise, the development of a certain human behavior takes a certain time and occurs in a certain order, just as the cooking of a perfect soufflé requires not just the right ingredients but also the right amount of cooking and the right order of events.

How does this new view of genes alter our understanding of human nature? Take a look at four examples.

Language
Human beings differ from chimpanzees in having complex, grammatical language. But language does not spring fully formed from the brain; it must be learned from other language-speaking human beings. This capacity to learn is written into the human brain by genes that open and close a critical window during which learning takes place. One of those genes, FoxP2, has recently been discovered on human chromosome 7 by Anthony Monaco and his colleagues at the Wellcome Trust Centre for Human Genetics in Oxford. Just having the FoxP2 gene, though, is not enough. If a child is not exposed to a lot of spoken language during the critical learning period, he or she will always struggle with speech.

Love
Some species of rodents, such as the prairie vole, form long pair bonds with their mates, as human beings do. Others, such as the montane vole, have only transitory liaisons, as do chimpanzees. The difference, according to Tom Insel and Larry Young at Emory University in Atlanta, lies in the promoter upstream of the oxytocin- and vasopressin-receptor genes. The insertion of an extra chunk of DNA text, usually about 460 letters long, into the promoter makes the animal more likely to bond with its mate. The extra text does not create love, but perhaps it creates the possibility of falling in love after the right experience.

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