Biologists often say that the most dangerous thing a cell can do is divide. This is because, during the complex process of replication—the unspooling of DNA, the assembling of two genomes from the halves of one—there is always the chance that the cell will make a mistake. Mutations can cost an organism its life, but they are also essential to evolution. Without them, there would be no novelty and no change; the slow-churning Darwinian search algorithm would stop. In this sense, transposons—wandering snippets of DNA that hide in genomes, copying and pasting themselves at random—are unsung heroes of natural selection. Although the information that they carry is spare, they account for fifty per cent of all mammalian genetic material. Our own DNA is a battlefield between self and other.

Each of us is the product of trillions of successful divisions, and so our cells are remarkably good at silencing transposons. (In humans, the majority of these nomadic genes are known technically as retrotransposons.) Until recently, in fact, they were thought to be dormant in most areas of the body. This turns out to be true almost everywhere but in the brain. Fifteen years ago, the neurobiologist Rusty Gage and his colleagues at the Salk Institute, in La Jolla, California, were studying neurogenesis, the development of adult brain cells from immature stem cells. When they ran a survey of all the genes being expressed in these stem cells, compared with mature neurons, they were puzzled to find that transposons were the most active. Far from being silenced, they were singing.

For some time the finding floated around the lab as a sort of curiosity. It was hard getting anyone to work on the project, Gage told me, because the results were unexpected, even a little disturbing. If transposons were tampering with the DNA of every future neuron, then they were endowing each one with a slightly different genome. Even neurons that budded from the same mother would behave differently. This phenomenon, which is known as genetic mosaicism, doesn’t happen much in other tissues. The cilia that guard our lungs are genetically identical to the blood cells that circulate in our arteries, even though one looks like a sea anemone and the other looks like a cough drop. The two appear different only because they express various genes differently, in developmentally predetermined ways. Although neurons are similarly programmed, the Salk study suggested that transposons were giving them the ability to ad-lib. Several years after the initial discovery, members of Gage’s lab sequenced hundreds of individual neurons from human cadavers and found this to be true. Cells in the same brain are, indeed, genetically distinct from one another.

Gage quickly recognized that this strange revelation might help answer a longstanding question in neuroscience: how does nature wire up a system as complex as the human brain? Consider one of biology’s favorite model organisms, the millimetre-long roundworm Caenorhabditis elegans. Its twenty thousand genes furnish it with three hundred and two neurons. Our twenty thousand genes, by contrast, furnish us with some eighty billion neurons. It’s like asking two chefs, given the same ingredients, to come up with either a few recipes or a few hundred million. The second chef would have a much easier time reaching her quota if the parsley occasionally turned into cumin, or the potatoes into eggplants. According to Gage’s theory, transposons may make such transformations possible; they may generate novelty, and therefore complexity, in a way that our genes alone cannot. If this is, indeed, why they are unsilenced during neural development, then our brains can be thought of as hosting a kind of evolution in miniature. Just as the beaks of Darwin’s finches are suited to different food sources, each neuron may develop its own specialty in the ecosystem of the brain. (Immune cells make use of transposons for similar reasons, exploiting them in order to generate a large range of antibodies to tag new intruders.)

Not only is each brain different but it cannot ever exist again. Transposon insertions in the brain are not heritable. A daughter’s cerebral ecosystem is distinct from her mother’s and even her twin sister’s. Here, another model organism again provides a useful analogy. C57BL/6, a common strain of laboratory mouse, has been inbred for generations to insure a totally uniform genome. This is done to control for individual differences. It doesn’t. Gage described a hypothetical experiment involving the animals: “Take ten of them. Put them in an open field. All the same gender, all the same age, raised by the same mother—they’re identical twins. Try to control everything you can. Put them in any behavioral paradigm. What’s going to happen?” The mice will be all over the map, he said. One might be frozen with fear while another runs frantically in circles. This explains, in part, why scientists have had such a hard time finding the genetic underpinnings of neurological diseases: there isn’t a standard genome in the brain. In fact, a number of brain disorders have been linked to elevated transposon events. It isn’t yet clear whether there is any causal connection.

What may be most interesting about transposons, from the perspective of human evolution, is what isn’t changing. In 2013, Gage and his colleagues compared transposon activity in ape and human stem cells. They determined that insertions are far more common in our nearest taxonomic cousins than in us, both in heritable ways and during neural development. As a result, two chimpanzees whose troops are separated by a few miles have more genetic diversity between them than do any two humans on Earth. A couple of the genes that silence transposon activity in humans do the same in chimps and bonobos, but we express them ten to twenty times more. When I asked Gage why this might be so, he was reluctant to speculate. He suggested, though, that the answer might lie in some event in our evolutionary history. The transposon-repressing genes that we overexpress also have antiviral properties (perhaps not surprising, given that transposons behave a little like viruses). A just-so explanation, Gage said, might be that, at some point, early humanity was reduced in population by a viral plague, and the stronger expression of these genes allowed certain people to survive and reproduce. Transposons were merely caught in the crossfire.

It is, on a Darwinian level, scary to learn that our genetic diversity as a species is so narrow. But Gage argued that this may have helped us move away from molecular evolution and toward cultural evolution. We manage viral plagues with medicine rather than hoping that our genes will catch up. We put our trust in generations’ worth of language and technology, not in our frail biology. If it is our similarities that allow us to communicate well, it is our mosaic brains that may deepen our capacity for individual invention and imagination. The strange genetic entities hitchhiking on our DNA have helped us become who we are.