Around 8 to 10 per cent of your DNA comes from viral ancestors. These sequences are the remains of prehistoric viruses that inserted their DNA into the genes of our ancestors, hundreds of millions of years ago. Some of them became permanent residents, and were passed down from parent to child. These endogenous retroviruses, or ERVs, are a legacy of epidemics past.
We understand how ERVs got into our DNA in the first place. But why have they been such successful invaders, to the point where they fill around a tenth of our genome? Gkikas Magiorkinis from the University of Oxford has an answer. By comparing the ERVs of 38 mammals, from humans to dolphins, he has found that the critical step in these invasions was the moment when the viruses hung up their coats.
Writers often compare the human genome to a collection of recipes for making a person. Each gene contains the instructions for building a protein, and our thousands of proteins work together to build and maintain our bodies.
But if the genome is a recipe book, it’s one that was written without a good editor. It is riddled with typos, unnecessary repetitions and meaningless drivel. A miniscule proportion actually codes for proteins. The rest looks like a scrapyard. It contains the remnants of dead genes that are no longer used and have degenerated into nonsense. It contains jumping genes that hop around the genome under their own power, sometimes leaving copies of themselves behind. And it contains the remains of these jumping genes, which have lost their hopping ability and stayed in place.
These “non-coding sequences” are often called junk DNA, and for good reason. It seems that they’re largely useless… but not entirely so. Ever since these non-coding sequences were first discussed, scientists have suspected that some of them play fruitful roles in the body. Many examples have since come to light, and Francois Cartault and his colleagues have found the latest one. He has shown that one piece of supposed “junk” might explain why some people from a tiny French island die from a bizarre brain disease.
For fans of a velvety latte or a jolting espresso, meet your greatest enemy: the coffee berry borer beetle. This tiny pest, just a few millimetres long, can ruin entire coffee harvests. It affects more than 20 million farming families, and causes losses to the tune of half a billion US dollars every year- losses that are set to increase as the world warms.
But the beetle isn’t acting alone. It has a secret weapon, stolen from an unwitting accomplice.
Ricardo Acuña has found that the beetle’s ancestors pilfered a gene from bacteria, most likely the ones that live in its gut. This gene, now on permanent loan, allows the insect to digest the complex carbohydrates found in coffee berries. It may well have been the key to the beetle’s global success.
A bout of Salmonella food poisoning isn’t a pretty affair. Your digestive tract churns, you can’t keep your food down, and you feel exhausted. But you aren’t the only one affected. Your gut contains trillions of bacteria, which outnumber your own cells by ten to one. They are your partners in life, and they are also transformed by the presence of the invading Salmonella.
Minority members of this intestinal community start to bloom, greatly increasing in number as the guts around them become inflamed. And these gut bacteria start to trade genes with Salmonella.
These swaps are a regular part of bacterial life. In their version of sex, two cells become united by a physical bridge, through which they shunt rings of DNA called plasmids. These rings can act like mobile weapons packages. Some give otherwise harmless bacteria the ability to cause disease. Others confer resistance to antibiotics. It’s a network of shady arms trading, and in your inflamed bowels, it happens at an unprecedented level.
There is a vast, unseen marketplace that connects us all. The traders are the trillions of bacteria that live on or within our bodies; the commodities they exchange are genes. This flow of genes around our bodies allows bacteria to rapidly evolve new skills, including the abilities to resist antibiotics, cause disease, or break down environmental chemicals. In the past, scientists have caught glimpses of individual deals, but now the full size of the marketplace is becoming clear.
The human body is home to 100 trillion microbes, whose cells outnumber ours by ten to one, and whose genes outnumber ours by a hundred to one. These genes are not only more numerous than ours, but they operate under different rules. While we can only pass down our DNA to our children, bacteria and other microbes can swap genes between one another. For example, the gut bacteria of Japanese people have a gene that helps them to digest seaweed. They borrowed it from an oceanic species that hitched its way into Japanese bowels, aboard uncooked pieces of sushi.
This was an isolated example, but such ‘horizontal gene transfers’ are fairly commonplace. When Chris Smillie and Mark Smith from MIT looked at the genomes of over 2,200 species of bacteria, they found 10,000 genes that had been recently swapped. These genes were more than 99 percent identical, even though they came from bacteria that were distantly related*. Standing out like beacons of similarity amid seas of difference, they must have been transferred from one species to another, rather than inherited from mother cell to daughter.
Imagine trying to photocopy a pile of papers, only for one of the copied sheets to magically jump back into the queue. It gets duplicated again. When the photocopier is finished, you’re left with two sets of papers and three copies of the mysteriously mobile sheet.
The same thing happens in the cells of a fly. Every time a cell divides, it duplicates its entire genome so the two daughter cells each have a copy. But some genes aren’t content to be duplicated just once. A selfish gene called a P-element has the ability to jump around its native genome. Like the paper jumping back into the photocopier queue, the P-element lands in parts of the fly genome that haven’t been copied yet. This ability allows it to spread throughout a genome, and even around the world.
Since 1948, people have been poisoning unwanted rats and mice with warfarin, a chemical that causes lethal internal bleeding. It’s still used, but to a lesser extent, for rodents have become increasingly resistant to warfarin ever since the 1960s. This is a common theme – humans create a fatal chemical – a pesticide or an antibiotic – and our targets evolve resistance. But this story has a twist. Ying Song from Rice University, Houston, has found that some house mice picked up the gene for warfarin resistance from a different species.
Warfarin works by acting against vitamin K. This vitamin activates a number of genes that create clots in blood, but it itself has to be activated by a protein called VKORC1. Warfarin stops VKORC1 from doing its job, thereby suppressing vitamin K. The clotting process fails, and bleeds continue to bleed.
Rodents can evolve to shrug off warfarin by tweaking their vkorc1 gene, which encodes the protein of the same name. In European house mice, scientists have found at least 10 different genetic changes (mutations) in vkorc1 that change how susceptible they are to warfarin. But only six of these changes were the house mouse’s own innovations. The other four came from a close relative – the Algerian mouse, which is found throughout northern Africa, Spain, Portugal, and southern France.
The two species separated from each other between 1.5 and 3 million years ago. They rarely meet, but when they do, they can breed with one another. The two species have identifiably different versions of vkorc1. But Song found that virtually all Spanish house mice carry a copy of vkorc1 that partially or totally matches the Algerian mouse version. Even in Germany, where the two species don’t mingle, a third of house mice carried copies of vkorc1 that descended from Algerian peers.
Millions of people pick up gonorrhea every year, but the bacteria that cause the disease (Neisseria gonorrheae) have picked up something in return. They carry a little bit of human DNA within their genomes. It seems that the microbe behind the clap is partly human.
The human side of N.gonorrheae is a ‘LINE-1 (L1) sequence’ – a short piece of DNA that can copy and paste itself into new locations in the human genome. It has no obvious function beyond making more copies of itself, but it is very good at that. There are around half a million L1 sequences in the human genome and together, they make up a fifth of our DNA. And one of these sequences managed to hop into N.gonorrheae.
Invisible to the naked eye, a frenetic marketplace buzzes all around you. The customers are bacteria and they are trading in genes, swapping them between individual cells as easily as humans swap presents or phone numbers. Some of the trades allow bacteria to cope with new sources of food. Others are more like arms dealing, with cells exchanging genes that allow them to beat antibiotics, or weapons that bestow the ability to cause disease.
These swaps are pervasive. At least an eighth of the genome of E.coli, a commonly studied species, has been borrowed from other bacteria. But this leads to an interesting puzzle. Genes don’t work in a vacuum; they interact with one another in a tangled web of partnerships. Some depend on other genes to switch them on or hold them back. Some encode proteins that only work in tandem. So how does a gene that finds itself in a foreign land manage to do anything, let alone play an active role in the evolution of its new host?
In the brain of a baby, developing in her mother’s womb, a horde of DNA is on the move. They copy themselves and paste the duplicates into different parts of the genome. They are legion. They have been released from the shackles that normally bind them. And in a year’s time, the baby that they’re running amok in will develop the classic symptoms of the debilitating brain disorder known as Rett syndrome.
Children with Rett syndrome – they’re almost all girls – appear normal for about a year before their development is spectacularly derailed. The neurons in their brain fail to develop properly. They lose control of their hands. Most will never speak and at least half cannot walk on their own. Digestive problems, breathing difficulties and seizure are common. They will depend on their loved ones for the rest of their lives.
In most cases, this panoply of problems are all caused by faults in a single gene called MECP2, nestled within the X chromosome. MECP2 is a genetic gag – it silences other genes in a way that’s essential for producing healthy, mature neurons. But Alysson Muotri and Maria Carol Marchetto – a husband and wife team – have found that MECP2 also has another role. It acts like a warden, restraining a mafia of mobile genes called LINE-1 sequences or L1.