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Cholera Bacteria Kill Each Other With Spears To Steal DNA

The Highlander film series is about a race of immortal warriors who try to behead each other with swords, so they can steal the powers of their fallen rivals.

This is basically the same story but instead of badly accented Scotsmen with katanas, we have diarrhoea-causing bacteria with syringes. And the stolen powers, rather than moving into victors via weird blue lightning, shuffle across as DNA.

The protagonist of this story is Vibrio cholerae. It’s a comma-shaped bacterium with a whip-like tail. We know it best as the cause of cholera—a disease that spreads through contaminated water, and that makes people lose water through both ends. But V.cholerae is only an unfortunate passer-by in drinking supplies and human guts. Its true home is the ocean. There, it hitchhikes on small crustaceans by latching itself to the chitin in their shells.

Chitin changes V.cholerae in important ways. In its presence, the bacteria start making enzymes that can absorb DNA from the environment, including that left behind by other dead and decaying microbes. The bacteria can then integrate the scavenged genes into their own genomes. This new material might allow them to resist antibiotics or infect their hosts more effectively. In other words, the microbes can adapt to new challenges more quickly by sucking up the genetic flotsam left by other bacteria that already had the right adaptations.

This process is called “natural competence for transformation”. It basically means “stealing the powers of your peers”.

But V.cholerae isn’t just a scavenger, waiting to suck up any DNA that happens to floats past. Instead, Sandrine Borgeaud from the Swiss Federal Institute of Technology in Lausanne has shown that it actively kills its neighbours to release their genes, which it can then absorb. It’s a predator. Worse, it’s a cannibal.

Borgeaud initially focused on TfoX—a master gene that is activated in the presence of chitin, and allows V.cholerae to absorb external DNA. To find out how the master dishes out its order, she identified a list of genes that are controlled by TfoX—and found something surprising.

TfoX switches on three clusters of genes that collectively build a fearsome weapon, which bacteria use to stab their competitors. It’s called a “Type Six Secretion System (T6SS)” and consists of 13 separate components. There’s a sheath that contracts to violently ram a tube straight through the outer membrane of another cell. The tube then dispenses proteins that kill and rupture the target.

Type Six Secretion System. It’s a truly dull name for something that’s a cross between a spear-gun and a syringe.

Borgeaud’s team found that V.cholerae can use this weapon to kill other bacteria, including the gut microbe E.coli and even other strains of V.cholerae. They behave like predators that prey upon their own kind. But they don’t kill for nothing. When their prey cells burst open, they release DNA, and the predators can absorb this DNA and whatever adaptive genes it might contain.

Borgeaud confirmed that this happens by unleashing predatory strains of V.cholerae, wielding T6SS spears, upon harmless prey strains. The predators could resist the antibiotic rifampicin, and the prey could resist a different antibiotic—kanamycin. After mixing the two groups of bacteria, Borgeaud exposed them to both antibiotics. By right, every cell should have succumbed to one or either drug. But instead, some of the predators survived and grew because they had absorbed kanamycin-resistance genes from their prey.

The team even developed a way of watching these kills. These time-lapse shots depict one such massacre in progress. The predatory bacteria are dressed in red, and their prey are wearing green. Any time you see a red and a green cell next to each other, the green one is in trouble. As the minutes tick by, the green cells start contracting from commas into full stops, until they eventually burst and die.

Predatory Vibrio cholerae (red) killing prey cells (green). Credit: Borgreaud et al, 2014.
Predatory Vibrio cholerae (red) killing prey cells (green). Credit: Borgreaud et al, 2014.

If you look closely, you can even see the predators feasting on their remains. Borgeaud painted the predators by attaching a glowing red molecule to a protein called ComEA, which they use to smuggle DNA into themselves. ComEA is normally spread throughout its host cell, but it gathers at specific points when its services are required. And you can see that happening in the images above. Focus on the cell with the yellow arrow, and notice how its red glow concentrates into two sharp dots. That’s ComEA gathering. That’s the predator sucking up the remains of its prey.

This discovery is the latest in a long line of research that dates back to the 1920s, when scientists first noticed that harmless strains of bacteria could suddenly start causing disease after mingling with the pulped remains of infectious strains. Something in the extracts was changing these microbes. In 1943, a “quiet revolutionary” named Oswald Avery showed that this transformative material was DNA, which the non-infectious strains had absorbed and integrated into their own genomes.

Matthew Cobb, a zoologist and science historian, describes Avery’s result as “one of the most important discoveries in the history of science” because it suggested, against conventional wisdom, that DNA (and not proteins) was the stuff of genes. He set the groundwork for later discoveries that would cement DNA’s status as the all-important molecule of life—including this new one, which paints DNA as a resource that bacteria will kill for.

Reference: Borgeaud, Metzger, Scrignari & Blokesch. 2014. The type VI secretion system of Vibrio cholerae fosters horizontal gene transfer. http://dx.doi.org/10.1126/science.1260064

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Raiding the Oldest Arsenal

Life on this planet has existed for at least 3.5 billion years. For most of that time, it was microscopic. Bacteria and other microbes had the world to themselves, but since they still had to compete, they evolved a wide arsenal of weapons for scuppering and killing their rivals. Humans have spent the last century plundering these arsenals. The vast majority of our antibiotics come from chemicals that microbes use on each other.

But you don’t need Alexander Fleming, the scientific method, or a pharmaceutical industry to exploit a microbe’s antimicrobial weapons. All you need is time and a little luck.

Seemay Chou and Matthew Daugherty from the University of Washington School of Medicine have found that one group of antibiotic genes have repeatedly jumped from bacteria into eukaryotes—the catch-all term for complex life forms, including animals, plants, fungi, and more. The genes made these crossings on at least six separate occasions, and they are now part of their hosts’ immune systems.

In an instant, these hosts acquired what scientists take decades of research to develop: a new tool for controlling microbes and protecting against infections.

kclkdpayub7roood8nmlChou and Daugherty made their discovery by accident. They were studying the tae genes, which make proteins that can digest a bacterium’s outer wall, causing it to leak and rupture. These are weapons built by bacteria, for use against bacteria. So why, when Chou and Daugherty searched for these genes, did they find them all over the tree of life? Why were these bacterial genes also in ticks, mites and scorpions? In limpets, water fleas, sea slugs, oysters, and sea anemones? In the lancelet, a close relative of back-boned animals like us? In weird single-celled pond creatures like Naegleria and Oxytricha?

The genes certainly hadn’t come from contaminating bacteria, since they were riddled with junk sequences that are only ever found in eukaryotic DNA. They were genuine parts of their hosts, so the team called them dae genes, with the ‘d’ standing for domesticated. They then compared the dae genes with their bacterial tae counterparts to reconstruct their origins.

Let’s take just one example. This family tree shows that the dae2 genes of ticks and mites (dark green box) are most closely related to tae2 in Burkholderia bacteria (red arrow). The next closest relatives are more dae2 genes in water fleas (light green).

Dae2 family tree. Credit: Chou et al, 2014, Nature.
Dae2 family tree. Credit: Chou et al, 2014, Nature.

If these genes were just passing down from parent to offspring, there is no way you’d get a pattern like this. Instead, the tick and water flea genes would be on neighbouring branches, while the bacterial genes would all sit on some very distant part of the family tree. The only explanation for the actual pattern is that tae2 genes have jumped into animals at least twice, once in the common ancestor of all ticks and mites and again in the common ancestor of water fleas.

Among bacteria, these kinds of “horizontal gene transfers” are very common. Among eukaryotes, they are relatively rare. Scientists have documented many examples, but the transferred genes are often just useless flotsam. In rare cases, they can plug into their new hosts in valuable ways, allowing a beetle pest to destroy coffee plants or allowing caterpillars to resist poisonous meals.

The dae genes belong to this elite club. Chou and Daugherty found that the genes are switched on in deer ticks, lancelets, and Naegleria amoebas, and they all still make proteins that can sunder bacterial walls. Even though they left bacteria hundreds of millions of years ago, they still carry out their ancient destructive roles.

The team reasoned that the hosts must be using these genes as part of their immune systems, and they confirmed this idea by focusing on the deer tick. This parasite makes Dae2 proteins in its salivary glands and guts—the organs most likely to encounter fresh microbes from a victim’s blood.

The protein is very specific. It degrades the walls of certain bacteria, including the cause of Lyme disease—Borellia burgdoferi. When the team switched off the dae2 gene, ticks were no longer able to control this particular microbe. If they fed on infected mice, they ended up with 10,000 times more B.burgdoferi in their bodies. This borrowed gene matters to them—and to us too! Lyme disease affects hundreds of thousands of people every year, and the tick that spreads it relies on a bacterial gene to control the microbe that causes it.

In hindsight, we should probably have expected something like this. Chou says that the tae genes are “prime candidates for horizontal gene transfer”. They make small, potent proteins that don’t require a supporting cast to work. And they are universally useful, since every living thing has to contend with bacteria. It’s no coincidence that a different group recently found another antibiotic gene that has hopped all over the tree of life. The war between bacteria, which had raged for billions of years, has created a reservoir of genetic weapons that latecomers can exploit.

Reference: Chou, Daugherty, Peterson, Biboy, Yang, Jutras, Fritz-Laylin, Ferrin, Harding, Jacobs-Wagner, Yang, Vollmer, Malik & Mougous. 2014. Transferred interbacterial antagonism genes augment eukaryotic innate immune function. http://dx.doi.org/10.1038/nature13965

Find out more about horizontal gene transfers here

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How An Antibiotic Gene Jumped All Over The Tree of Life

Every living thing on the planet has to contend with bacteria. To many viruses, they are prey. To other bacteria, they are competitors. To animals and plants, they can be the cause of devastating diseases or beneficial partners that provide everything from nutrition to immunity to light. They have been around for some 3 billion years, and they are everywhere. So, it makes sense that a gene which allows its owners to deal with bacteria might find a home throughout the entire tree of life.

That’s what Jason Metcalf and colleagues from Vanderbilt University have now discovered. They tracked a gene called GH25-muramidase, which makes an enzyme that can break apart a bacterium’s outer wall. It’s common in bacteria, which use it to remodel themselves and reproduce by dividing in two. But Metcalf showed that it has also jumped from bacteria into every other major branch of life. It’s in animals, plants, fungi, archaea, and even some viruses.

There are many similarly universal genes, which were present in the last common ancestor of all living things, and were passed down from parent to offspring. But GH25-muramidase is different. It arose in bacteria and then jumped horizontally into other kingdoms. “It has been co-opted by different domains of life to be used as an antibacterial weapon,” says Seth Bordenstein, who led the study.

I’ve written about these horizontal gene transfers a lot (here’s the latest piece from just last week). But this example stands out for its promiscuity. Genes hop between bacteria all the time, carrying traits like antibiotic resistance with them. There are also several examples of genes jumping from bacteria to animals, from bacteria to archaea, from animals to animals, and every other combination you can think of. But there are very few examples of genes that have moved everywhere. There are clearly highways of gene traffic that connect every branch of the tree of life, but very few genes have taken the complete roadtrip.

Why? Horizontal gene transfers aren’t always a good thing; maybe they often aren’t. The genes could be harmful in the wrong host, or might disrupt important genes. So even if jumps happen, they might get quickly purged by natural selection. If that’s the case, only genes with universal appeal would have universal presence.

That’s what Bordenstein’s team found. They initially studied a virus that attacks Wolbachia—a extremely cool and successful bacterium that infects around two-thirds of insect species. They found that the virus kills Wolbachia using GH25-muramidase, and then searched for this gene in the sequenced genomes of other species. To their surprise, they found it all over the place: in many different bacteria; the plant-sucking pea aphid; the ancient spikemosses (a group of plants); fungi that infect rice; and Aciduliprofundum boonei, an archaeon that lives in hot, belching, deep-sea vents. (Archaea are one of the three great domains of life.)

Metcalf compared GH25-muramidase in all of these species to reconstruct its evolutionary history. And he found that the family tree of the different versions didn’t look anything like the family tree of their owners—a clear sign of horizontal jumps from one group to another. Also, the aphid is the only insect that has this gene, and the spikemosses are the only plants that do. This also suggests that they got it horizontally from some bacterium, rather than vertically from their ancestors.

In fact, the archaea, fungi, spikemosses, and viruses all inherited their copies of GH25-muramidase from different groups of bacteria. In each case, the donor and recipient are neighbours. The archaeon got its copy from one of the Firmicutes, a group that often colonises deep-sea vents. The spikemoss got its copy from Actinobacteria, which lord over soil communities. And both the aphid and the Wolbachia viruses seem to have picked up their copies from Proteobacteria, which are often found in the bodies of insects.

But the team was especially interested in the archaeon, A.boonei. Archaea build their cell walls using different molecules than bacteria, so they are immune to GH25-muramidase. Instead, the team showed that A.boonei can use its borrowed gene as a weapon against its bacterial neighbours. Its version can kill many different bacteria, especially those that live in the same deep-sea vents. And when the team grew A.boonei alongside with one of those vent bacteria, it churned out large amounts of GH25-muramidase and outnumbered its competitor. A.boonei won out, even though it is the slower grower of the two microbes.

“They cast the story in terms of competition,” says Bill Martin from Heinrich-Heine University in Dusseldorf. But since Aciduliprofundum eats other things, “maybe it is not so much carving out a competitor-free niche as helping itself to a bite of bacterium for lunch.”

The team acknowledge this possibility. And either way, the gene clearly allows the archaeon to do something to bacteria. That’s a first. Other groups have suggested that archaea might wield antibacterials, but no one had identified a specific gene before. This discovery suggests (with the usual caveats) that archaea might be a good source of new antibiotics, especially since they’re great at tolerating high temperatures and pressures.

It’s less clear how the borrowed gene benefits the other recipients. Metcalf’s team have tried to purify these other versions of GH25-muramidase but with no success. Still, based on their sequence, it certainly looks like they should also be able to target bacteria in the same way. And perhaps this explains why the gene has been so promiscuous. By imparting a universally useful trait, it proved to be a welcome immigrant into every corner of life.

And as David Baltrus from the University of Arizona points out, the team really only focused on a fragment of GH25-muramidase. “Not only has this motif been independently recruited by various [organisms], but it has been incorporated and elaborated into much larger proteins across species,” says Baltrus. In other words, different species have borrowed this basic bacterial tool and used it to fashion even more complex molecular machines.

“Horizontal gene transfer is widely recognized as a powerful force shaping evolution within bacterial populations but as more genomes are sequenced, it becomes increasingly apparent that its effects are not limited to microbes,” adds Baltrus.

Reference: Metcalf, Funkhouser-Jones, Brileya, Reysenbach & Bordenstein. 2014. Antibacterial Gene Transfer Across the Tree of Life. eLife. http://dx.doi.org/10.7554/eLife.04266


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A Flood of Borrowed Genes at the Origins of Tiny Extremists

We love origin stories. When we see successful groups of animals and plants, we wonder where they came from, and how they rose to power. How did the tetrapods—the group of four-legged animals that we belong to—start walking on land? What made the insects the most diverse group of animals on the planet? Why did flowering plants suddenly start diversifying during the Cretaceous period, filling the world with blossoms?

These enduring questions are so fundamental to biology that we sometimes forget how strongly they’re influenced by the limits of our senses. We can see the creatures they concern with our naked eyes. We can observe changes in their bodies, and we can tell that they must have gone through transformations from fins to legs, or needles into petals.

It’s much harder to make such observations when you deal with microbes. At that scale, it’s not so much physical features that set organisms apart, but genetic and biochemical ones. Groups differ more in what they do rather than what they look like. So to discover their origin stories, or even to know which origin questions to ask in the first place, you need to study their genes.

Shijulal Nelson-Sathi did this for the archaea, a group of single-celled microbes that excel at growing in extreme and inhospitable places. Volcanic springs and salty lakes—these are places where archaea thrive, although some also live in milder environments like your intestines.

Superficially, archaea look like bacteria and for the longest time, that’s what scientists thought they were. That changed in 1977, when the revolutionary scientist Carl Woese showed that archaea and bacteria were genetically distinct. Woese drew a tree of life with three great trunks or “domains”. The bacteria sat on one. The eukaryotes—the group that includes animals, plants, fungi and algae—occupied another. And the archaea were the third. Woese elevated these obscure extremists to one of life’s highest ranks. And he was right. As I’ve written before, archaea and bacteria turned out to be as different in their biochemistry as PCs and Macs are in their operating systems.

The archaea are still mysterious. No one knows, for example, how many species there are. But scientists have sequenced the complete genomes of at least 134 of them and, based on differences in their genes, classified them into 13 major groups. So, the classic origin questions raise their heads: how did these groups arise, and why?

To find answers, Nelson-Sathi developed software that took all the genes in every known archaeal genome and grouped them into some 26,000 families. At least two-thirds of these families were invented by archaea, and have no counterparts among other living things. And 85 percent of them are found in only one of the 13 major groups—an indication of just how distinct these lineages are from one another.

And then, the team found something weird.

In the Haloarchaea, a group of archaea that grow in extremely salty water, the team found 1,000 gene families that had originally come from bacteria. Some time ago, an ancestral Haloarchaean borrowed genes on a massive scale, and this loan happened at the origin of the group.

The team then looked at the other 12 lineages and found exactly the same pattern. The origin of every major archaeal group was marked by the acquisition of bacterial genes—sometimes dozens, sometimes thousands. They borrowed, then they branched out. “The implication here is that such transfers played an important role in the actual establishment of the groups themselves,” says John Archibald from Dalhousie University.

“It was a surprise for us,” says Bill Martin from Heinrich-Heine University in Dusseldorf, who led the study. “You might ask why no one else has seen this before.” It’s probably because most scientists focused on the essential “core genes” that are common to all archaea. But the core genes comprise just 1 percent of the genome. They can tell us the shape of the archaeal family tree, but they say nothing about the characteristics that define the branches. To do that, you need to look at the entire genome, which is exactly what Nelson-Sathi did.

The “horizontal gene transfers” that he found are alien to us humans, who can only pass genes from parent to child. But bacteria and archaea don’t suffer the yoke of vertical inheritance. They can pass genes to one another with great ease.

These transfers could flow in either direction but in reality, they were mostly one-way. Nelson-Sathi found that bacteria have donated gene families to archaea five times more frequently than vice versa, and none of the archaea-to-bacteria transfers correspond to the rise of major bacterial groups. Bacteria have repeatedly thrust their archaeal peers into new evolutionary directions, but the reverse isn’t true.

Why? Here’s a clue: most of the gene families that moved from bacteria to archaea are involved in metabolism. That is, they help their owners to exploit new sources of energy. Another clue: most of the recipients are methanogens—archaea that can grow on carbon dioxide and hydrogen alone. This trick allows methanogens to survive in deep-sea vents, cow guts, Greenland ice, and baking desert soils. But it’s also about as simple and specialised a lifestyle as you can get.

The methanogens are specialists that have colonised many difficult but narrow niches, and become stuck in their ways. They’re like the microbial version of pandas. “They’re rock-bottom. The only way is up,” says Martin. “And the only way they have of reaching new niches is to let bacteria do the inventing.” By borrowing bacterial genes, these specialists could carry out new chemical reactions and expand beyond their extreme niches.

“I think most of us envisaged horizontal gene transfer happening a gene at a time,” Martin adds. “You get one in here or there, and you tinker. But that doesn’t’ work very well when you’re changing your lifestyle. When you change a methanogen into something that isn’t, one gene at a time won’t help very much. Instead, it looks like the genes were coming in big chunks. We see lump acquisition, the wholesale introduction of new pathways.”

“This paper is one of the best demonstrations of the key role of horizontal gene exchange in the evolution of prokaryotes,” says Eugene Koonin from the National Center for Biotechnology Information. (Prokaryotes is a term that refers to both bacteria and archaea.) But Koonin adds that it’s now time to nail down the specifics.

Archibald agrees. The study “provides strong evidence for the existence of gene-sharing pathways in the evolutionary history of prokaryotes,” he says. But it’s a starting point. The team now need to follow up on each major archaeal group and working out how the bacterial genes changed the abilities and the lives of their recipients.

Of course, this is not the first indication that bacteria have dramatically changed the evolution of archaea. Martin and others have argued that the origin story of all complex life on Earth began when a bacterium and an archaeon fused together. This singular and incredibly improbable event provided the archaeal host with a source of extra energy, allowing it to become big and complex in a way that none of their kin could manage. That was the birth of the eukaryotes—the unique merger that made you and ewe and yew. You can read more about this extraordinary story in my Nautilus feature from earlier this year.

Reference: Nelson-Smith, Sousa, Roettger, Lozada-Chavez, Thiergart, Janssen, Bryant, Landan, Schonheit, Siebers, McInerney & Martin. 2014. Origins of major archaeal clades correspond to gene acquisitions from bacteria.

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With Evolutionary Rocket Fuel, Bacteria Give Peas a Chance

Imagine that I could implant all the world’s medical knowledge into your head. You blink, and you instantly know every bit of anatomy, every surgical procedure, and every diagnostic criterion for every disease. You land a job in a hospital. And you suck. Despite your newfound skills, you still have no idea how hospitals work, how to talk to patients, or how to cooperate with your fellow doctors. Ill-suited and out-of-place, you quit.

The lesson behind this little vignette is that it takes social skills, as well as technical savvy, to succeed in a new job. And that’s a guideline that bacteria duly follow.

If you look at the roots of legumes, like peas or beans, you’ll find small swollen nodules. Each one contains billions of bacteria that live nowhere else. They earn their keep by ‘fixing’ nitrogen. That is, they convert it into ammonia, which can then be used to make amino acids, DNA and other essential molecules. The plants depend on this process, and the bacteria depend on the plants. It’s a classic case of symbiosis.

These root bacteria are called rhizobia. They come from at least 13 different lineages, which are typically full of species that digest dead plants or infect living ones. But from these groups of undertakers and disease-makers, several members have repeatedly and independently evolved into plant partners. They did it by picking up large packages of genes from other microbes that had already colonised roots. These “horizontal gene transfers” are everyday events for bacteria, allowing them to instantly pick up new skills without having to evolve them from scratch.

In this case, the packages contain genes for colonising plant roots, creating nodules to live in, and fixing nitrogen—everything an unassuming soil bacterium would theoretically need to become a plant collaborator.

Scientists know this happened in the wild because they can trace the history of the same symbiosis genes as they jump form one bacterial group to another. But this process is hard to duplicate in the lab. Bacteria that receive the packages don’t immediately become productive partners. They still need to adapt to their hosts. They’re like the hypothetical person from the start of this piece—armed with all the right know-how, but incapable of fitting in.

Philippe Remigi and colleagues from the Laboratory of Plant-Microorganism Interactions in France have discovered how the microbes seal the deal. Their symbiosis packages also contain genes that trigger a temporary flurry of new mutations in a recipient’s genome. These genes are adaption accelerants—a kind of evolutionary rocket fuel that microbes can pass to one another. They allow bacteria, now suddenly armed with the tools for symbiosis, to quickly adapt to life with a plant.

Bacteria often pick up simple skills by trading genes, such as resistance to antibiotics or the ability to cause infections. Here, they’re picking up evolvability.

The team, led by Catherine Masson-Boivin, began this line of research began in 2010. They transferred a cluster of symbiosis genes from a bacterium that lives on the touch-me-not plant into Ralstonia solanacearum, a soil microbe that causes a wilting disease. Ralstonia didn’t become a symbiont straight away, but quickly evolved into one when placed on touch-me-nots. Some strains picked up mutations that disabled their virulence genes. They stopped causing disease, and started forming nodules and fixing nitrogen instead. Over 400 generations—no time at all for a bacterium—they became dramatically better partners.

When the team sequenced the genomes of these newly minted symbionts, they found an astonishing number of mutations—more than would usually have appeared in that amount of time. The cause of these mutations lay within the symbiosis cluster itself. It contained three genes called ImuABC, which the team hadn’t noticed before. Two of these create enzymes that copy DNA, but in a very sloppy way. They make errors as they work, introducing mutations into the genomes that they create. The team found that the ImuABC cluster increases Ralstonia’s mutation rate by 15 times. And strains with this cluster transformed into root symbionts much faster than those without it.

ImuABC is only activated under stressful competitions, and an unfamiliar environment like a plant root certainly counts. When Ralstonia first landed on the touch-me-nots, ImuABC sprang into action, triggering a temporary burst of new mutations. Some of these knocked out disease-causing genes, allowing Ralstonia to colonise the plants in more beneficial ways. The other symbiosis genes equipped Ralstonia with the technical skills it needed in its new job, but ImuABC gave it the social skills it needed to get on with its new partner.

ImuABC is widespread among bacteria, but root symbionts are far more likely to have it on a plasmid—a free-floating ring of DNA that can be easily transferred from one cell to another. In some of these microbes, ImuABC has started to degenerate. It’s possible that after facilitating the early handshakes of the plant-microbe relationship, these genes were no longer needed, and are gradually being lost.

Time and again, microbes have formed alliances with plants, animals, and other organisms (I’m writing a book about this, coming out in 2016). They hide squid with light, they supplement the diets of bed bugs, and they fix nitrogen for beans. These symbioses underlie the evolutionary success of entire groups of organisms, from the grazing herds in Africa’s savannahs to animal communities in the abyssal oceans, to the aphids currently wrecking my garden.

But their earliest stages of these alliances are often mysterious. How does a random environmental bacterium, or one that causes disease, set up a lasting and productive partnership with a host? How does symbiosis itself evolve? Studies like this provide a clue. They show that bacteria can pick up traits that allow them to evolve more quickly into fitting partners—to shoot past that difficult getting-to-know-you phase, and go straight into a peaceful co-existence.

Reference: Remigi, Capela, Clerissi, Tasse, Torchet, Bouchez, Batut, Cruveiller, Rocha & Masson-Boivin. 2014. Transient Hypermutagenesis Accelerates the Evolution of Legume Endosymbionts following Horizontal Gene Transfer. PLoS Biol 12(9): e1001942. http://dx.doi.org/10.1371/journal.pbio.1001942

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Genetic Gift May Have Turned Ferns Into Masters of Shadow

Even in their quietest and stillest moments, forests are places of fierce competition. Sunlight is the one of the most precious commodities here, and plants jostle, circumvent, and kill each other for prime positions beneath the incoming rays. Ferns are masters of this game; they excel at growing in the shade. Fay-Wei Li from Duke University thinks that their success depends on a single moment that happened around 180 million years ago, when an ancient fern stole a gene from another plant.

Ferns are sometimes portrayed as relics of an earlier phase of plant evolution, which were outcompeted by flowering plants and relegated to the bottoms of forests. But that’s not the case. Ferns may be an ancient group (they first arose 360 million years ago), but the vast majority of living members arose much later, during the Cretaceous period. By that time, flowering plants were already dominating the world. Ferns weren’t plucky holdouts consigned to some scrapheap of existence; they diversified in the shadows of other plants.

These lineages had a tool that almost all other plants (and indeed, other ferns) lack—a light sensor called neochrome. Most plants move towards sources of light using molecules that are sensitive to blue light, although some use red-light sensors instead. But neochrome is incredibly sensitive to both blue and red. That gives ferns an advantage because blue light is largely filtered out by the upper layers of a forest, while red light penetrates more deeply. Using neochrome, ferns could ‘see’ better in a shady, flower-filled world.

But where did neochrome come from? Li decided to find out. “I love ferns and I want to know why there are so many of them,” he says. “Neochrome seemed to be a great starting point to me, so I just decided to figure out its evolutionary history.”

That was easier said than done. When Li started, there weren’t a lot of complete plant genomes on record, so he didn’t have a lot of data to work with… and what he had made no sense. “I remember walking into my advisor’s office one day and telling her my PhD is doomed because I couldn’t figure this out,” he says. Salvation came from the One Thousand Plant Project—a massive initiative to study how plants, from algae to flowers, use their genes. Suddenly, Li had data galore. He wrote a programme to analyse it, “and one night, my Macbook terminal told me that it found a neochrome-like sequence in hornworts.”

Hornworts are usually found in greasy, blue-green mats, growing in damp or humid places. They’re even older than ferns, and were among the first plants to colonise the land.

It’s possible that the common ancestor of hornworts and ferns already had neochrome, and many of its descendants—including all trees and flowers—then lost this molecule. Alternatively, both hornworts and ferns could have invented neochrome independently. But Li’s analysis showed that both of these scenarios are extremely unlikely.

The fern and hornwort versions of neochrome are clearly related and shared a common ancestor. By comparing these modern versions and working backwards, Li calculated that they diverged from each other around 179 million years ago. By contrast, the ferns and hornworts themselves split off at least 400 million years ago.

This pattern, which doesn’t apply to any other fern gene, strongly suggests that the ferns acquired the gene for neochrome directly from hornworts. After that, the gene seems to have repeatedly hopped between different fern lineages.

These “horizontal gene transfers” are everyday events for bacteria, which seem to trade DNA with the same ease that we exchange emails. They’re much rarer in plants and animals, and many reported examples have been met with scepticism. But Li’s study has certainly won over Jeffrey Palmer from Indiana University. “I’ve read their paper closely, and I think their evidence is very strong and convincing,” he says.

Palmer is more measured about the idea that gaining neochrome allowed ferns to diversify in the shadow of flowers—it’s a plausible idea, but not one that’s been proven yet. If it was, “it would be the most significant horizontal transfer yet discovered in plants,” he says. Most transferred genes, including some that Palmer has discovered, don’t do very much. But neochrome “had the potential to really shake up fern physiology in a big way, and be really adaptive.”

Li is now looking for other horizontally transferred fern genes, to see if neochrome is exceptional or just part of a general pattern. And he’s also studying neochrome in hornworts to see what the gene does in its original owners.

Reference: Li, Villarreal, Kelly, Rothfels, Melkonian, Frangedakis, Ruhsam, Sigel, Der, Pittermann, Burge, Pokorny, Larsson, Chen, Weststrand, Thomas, Carpenter, Zhang, Tian, Chen, Yan, Zhu, Sun, Wang, Stevenson, Crandall-Stotler, Shaw, Deyholos, Soltis, Graham, Windham, Langdale, Wong, Mathews & Pryer. 2014. Horizontal transfer of an adaptive chimeric photoreceptor from bryophytes to ferns. PNAS http://dx.doi.org/10.1073/pnas.1319929111

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Solar-Powered Slugs Are Not Solar-Powered

Good science is about resisting the pull of easy conclusions. It’s about testing stories that seem like they should be right to see if they actually are right.

This is no easy task. Consider the case of the “solar-powered” slugs.

There are four species of green sea slugs that supposedly can photosynthesise, just like plants. That is, they can make their own food by harnessing the power of sunlight. This skill is almost unheard of for an animal, but the slugs pull it off through an act of thievery. They steal chloroplasts—the little solar panels where photosynthesis takes place—from the algae that they eat, and store them in their bodies for several months.

The chloroplasts give them their beautiful green colour, and apparently allow them photosynthesise. You can keep them in a lab for several months without any food, and they’ll survive as long as you shine a lamp upon them.

It seemed obvious that the chloroplasts were responsible. Photosynthesis means sugar, sugar means food, food means survival. The chloroplasts provided the slugs with internal nourishment, just as they do in plants. Many scientists and journalists (including myself) started describing the slugs as “leaves that crawl” or “solar-powered” animals.

At first, Sven Gould from Heinrich-Heine University in Dusseldorf was part of this bandwagon. But the more he looked into the story, the more he realised that something wasn’t right.

He started reading papers that go back 40 years, and realised that when the slugs are starved, they grow smaller and paler with time, even when they’re exposed to light. Weirder still, some starved slugs survived just fine in the dark, while others that were kept in the light would die. Why?

To find out, graduate student Gregor Christa worked with two green sea slugs—Elysia timida from the Mediterranean and Plakobranchus ocellatus from the Philippines. He showed that when exposed to light, they convert carbon dioxide in the air into sugars—the essence of photosynthesis.

Next, Christa stopped the starving slugs from photosynthesising, either by keeping them in the dark for three months or by using chemicals. To everyone’s surprise, they survived just as well as animals that were kept in the light, and they lost just as much weight. “It was a very easy experiment,” says Gould. “You put them in the dark, take them out after four weeks and they’re all happy. That was quite a shock.”

The team concluded that the green slugs are not solar-powered. Even though they effectively have solar cells in their bodies, they don’t need to photosynthesise to survive.

“We know that we were hitting a wasp’s nest,” says Gould. “It’s like covering a beautiful piece of sushi in wasabi—it becomes hard to digest and swallow.”

Elysia timida. Credit: Parent Gery
Elysia timida. Credit: Parent Gery

He thinks that the chloroplasts are acting as food reserves—less like a plant’s leaf and more like a camel’s hump. They are loaded with fats, proteins and nucleic acids like DNA. The slugs could subsist on them when they run out of algae to graze upon. That would explain why they can endure a bout of starvation in the dark, and also why they shrink and get paler over time. “It’s pure speculation and a working hypothesis,” says Gould.

“The notion of the slugs storing chloroplasts as some sort of a food hoard seems a bit gratuitous,” says Sidney Pierce from the University of South Florida. “The plastids are only in a relatively few cells and would not seem to be much of an energy source on their own.” He adds that what is true for the species that Gould studied may not apply to all green slugs. “If their results are correct, they are very likely just species differences and the authors may be over-generalizing.”

Gould admits that other slugs like E.chlorotica—the species that the Americans have focused on—may depend on photosynthesis more strongly… but he doubts it. In winter, E.chlorotica digs itself into the mud and survives for months. “If it’s in the mud, how does it get enough light?” asks Gould. “We need to check this. Maybe we’ll be surprised and they really do die, but I doubt it.”

And there’s yet another mystery about the slugs: how do they photosynthesise at all? Chloroplasts need between 1,000 and 3,500 proteins to carry out photosynthesis. They can make between 60 and 200 because they have their own tiny genomes but for the rest, they depend on the DNA within the nucleus of their host cell. When the slugs steal the chloroplasts from their algae, they leave the nucleus behind. On their own, the chloroplasts simply shouldn’t work.

“That’s the biggest riddle,” says Gould. “Every time we give talks, plant scientists cannot believe that there are chloroplasts that perform for months and months without nuclear genes. That is not possible.”

To explain this paradox, some scientists have suggested that the slugs have also stolen genes from the algae, patching their own genomes to make themselves photosynthesis-compatible. In 2008, Mary Rumpho found evidence of one such photosynthesis gene—pbsO—in the genome of the green slug Elysia chlorotica.

But now, it seems that this result was a false alarm. In 2011, the German team found no evidence that E.timida and P.ocellatus are activating PbsO, or any other algal nuclear genes. Shortly after, Rumpho’s team showed that the same applies to E.chlorotica.

So, the stolen chloroplasts can clearly carry out photosynthesis, but we don’t know how it happens and, in at least two species, we don’t know what it’s for. “It’s an utterly complex and bizarre system,” says Gould. “It’s very difficult to digest.”

“A lot of work that’s been done on the slugs has focused on too many things at once,” he says. “[People have] confused the plastid longevity with slug survival, or gene transfer with plastid longevity. We need to tackle one tiny question after the other.”

PS: One more question: The four green slug species are relatives, but they’ve all evolved their chloroplast-hoarding ways independently. Other sea slugs have a similar trick—they eat jellyfish, steal their stinging cells, and shunt them into their own extremities. During their early evolution, these slugs seem to have gained the ability to pilfer cellular components from their food, and different lineages do it in different ways. Why? No one knows.

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Snug as a Bug in a Bug in a Bug

The citrus mealybug looks like a walking dandruff flake, or perhaps a woodlouse that’s been rolled in flour. It’s also the insect version of a Russian nesting doll. If you look inside its cells, you’ll find a bacterium called Tremblaya princeps. And if you look inside Tremblaya, you’ll find yet another bacterium called Moranella endobia.

The two bacteria aren’t just passing hitchhikers. They’re symbionts— constant fixtures of the mealybug’s cells, and necessary for its survival. The trio cooperates to manufacture essential nutrients, such as amino acids. This involves a chain of chemical reactions, and it takes enzymes from all three partners to complete every step. Imagine a single production line with machines from three different manufacturers. Raw ingredients enter; amino acids come out.

As if this wasn’t complicated enough, some of these machines are built using genetic instructions that are loaned from three other groups of bacteria. These microbes probably lived inside the mealybug’s ancestors and transferred some genes into the insect’s genome. So, six different branches on the tree of life have come together to allow this three-way partnership to make the nutrients they need! “It’s almost too fantastic,” says John McCutcheon from the University of Montana, who has studied this hierarchy.

“This is really the kind of finding that would have blown away Charles Darwin or early geneticists,” says Nancy Moran from Yale University, who studies insect symbionts.


The mealybug’s hitchhikers were first seen under the microscope in the 1950s, but only Moranella was recognised as a bacterium. Tremblaya was thought to be a special package created by the insect. It was Carol von Dohlen from Utah State University who recognised this middle partner for what it was, and described the bug-in-a-bug-in-a-bug arrangement.

In 2011, von Dohlen and McCutcheon sequenced the genomes of Tremblaya and Moranella and found that the latter was almost four times bigger, even though it sits inside the former. In fact, Tremblaya has the smallest genome of any known bacterium. Many species shrink their genomes through extreme organisation—packing their genes into ever-tighter spaces. But Tremblaya’s genome, though tiny, was also flabby. It had many wasted spaces and dead genes.

It’s also missing crucial genes, including an entire group that’s essential for building proteins. These genes are a few billion years old, and were present in the last common ancestor of all living things. They’re as indispensable for life as genes can get. There should be 20 of them. Some symbionts have lost a few. Tremblaya doesn’t have any. How does it survive?

McCutcheon suspected that Moranella probably takes up the slack. His team, led by Czech graduate student Filip Husnik, have now confirmed as much. They looked at the oat mealybug, whose cells also contain Tremblaya but not Moranella. The genome of the oat Tremblaya is also very small, but it’s still bigger and more tightly organised than that of the citrus Tremblaya. It also gives the oat mealybug all the enzymes that the citrus mealybug gets from both its partners combined.

So, at some point in the history, the mealybugs became colonised by Tremblaya and the two struck up a lasting partnership. Tremblaya lost many of the genes for a free-living existence, and its genome shrank considerably. Later, Moranella entered their alliance. By relying on the genes of this new partner, Tremblaya could lose even more of its own genes and become superlatively small.

Mealybug cells, showing Tremblaya (red), Moranella (green) and mealybug nuclei (blue). Credit: Ryuichi Koga, National Institute of Advanced Industrial Science and Technology, Japan
Mealybug cells, showing Tremblaya (red), Moranella (green) and mealybug nuclei (blue). Credit: Ryuichi Koga, National Institute of Advanced Industrial Science and Technology, Japan

No, wait, six-in-one

In some cases, symbionts have relocated their genes to the genomes of their hosts, so the missing Tremblaya genes may have ended up in the mealybug’s DNA. Indeed, the team found that the bug’s genome contains at least 22 genes of bacterial origin. But in a surprising twist, none of these came from Tremblaya or Moranella!

Instead, they hailed from three separate lineages of bacteria. All three groups contain members that regularly colonise the cells of insects, but none of them are found in the mealybug today. Maybe they colonised the insect’s ancestors, donated their genes, and have since disappeared. “These genes are like the ghosts of symbionts-past,” explains Molly Hunter from the University of Arizona. There are many examples of bacteria donating their genes to animals but “this degree is impressive, especially since its from so many different sources,” Hunter adds.

These borrowed genes aren’t sitting idly by. They are also involved in making amino acids, plugging holes in the production line that neither Tremblaya nor Moranella can fill. The citrus mealybug is effectively a mash-up of six different species, three of which aren’t even there!

So, what do you call these things?

The history of life is full of bacteria that have become permanent residents in other cells. Your own cells, and those of every animal, plant and fungus, contain small structures called mitochondria, which used to be free-living bacteria. Now, they’re organelles—compartments within larger cells that perform specialised tasks. The mitochondria, for example, are batteries that provide us with energy.

So, is Tremblaya a symbiont or has it already become more of an organelle? “The distinction is a matter of debate and definition,” says Martin Kaltenpoth from the Max Planck Institute for Chemical Ecology. Tremblaya permanently lives inside other cells, helps its host to survive, and has lost many genes. These are all ticks for the organelle column.

But there are two big differences. As free-roaming bacteria transformed into mitochondria, they shrunk by shunting many of their genes into their hosts. Tremblaya hasn’t done that. It became small by relying on Moranella. Also, organelles tend to be permanent and irreplaceable. If all your mitochondria suddenly vanished, you’d die very quickly. But Tremblaya can be replaced. In some mealybugs, a different bacterium has usurped it. “I don’t want to call it an organelle. I really don’t,” says McCutcheon.

Rather than quibbling over labels, it’s more important to him to work out the details of this partnership, and there are still many mysteries left to solve. For example, how exactly does Moranella share its enzymes with Tremblaya? After all, Moranella doesn’t make any of the transporter proteins that would normally export molecules. In 2011, the team suggested that Moranella might just burst apart, releasing its contents inside Tremblaya. “That was wild speculation. We just couldn’t figure anything else out,” says McCutcheon.

But they may have been right. Moranella’s cell wall—the layer that keeps its insides inside—is made from molecules called peptidoglycans, which the bacterium can’t make on its own. Instead, it relies on genes from the mealybug, including those that were loaned from the other bacterial groups! By switching off these genes, the bug could potentially destabilise Moranella, causing it to burst and release its contents to Tremblaya. Maybe it controls the relationship between its current symbionts using genes borrowed from its old symbionts.

Wouldn’t that destroy Tremblaya as well? No, because it has lost so many essential genes that it can’t make its own cell wall or membrane. McCutcheon suspects that it somehow gets those barriers from the mealybug. If that’s true, it would be amazing. It would mean that Tremblaya relies on the mealybug to define its own boundaries. Without its host, it would be a bunch of molecules floating away in liquid!

“This is still wild speculation but at least we can now do experiments,” says McCutcheon. He could, for example, switch off the mealybug’s peptidoglycan-making genes and see what happens to Moranella numbers.

McCutcheon’s peers are already very impressed. “John is well-known for his outstanding contributions to understanding the evolution of intracellular mutualisms in insects, and this is yet another excellent piece of work from his group,” says Kaltenpoth. “I thought this paper was a masterwork,” adds Hunter.

Reference: Husnik, Nikoh, Koga, Ross, Duncan, Fujie, Tanaka, Satoh, Bachtrog, Wilson, von Dohlen, Fukatsu & McCutcheon. 2013. Horizontal Gene Transfer from Diverse Bacteria to an Insect Genome Enables a Tripartite Nested Mealybug Symbiosis. Cell http://dx.doi.org/10.1016/j.cell.2013.05.040

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How the Lord of the Springs Survives Where Most Things Die

Yellowstone volcanic spring, by Andreas Meyer
Yellowstone volcanic spring, by Andreas Meyer

Throughout Yellowstone National Park, volcanic springs bubble up through the rock. Their sulphurous water is hot, salty, extremely acidic, and laden with toxic metals like arsenic, mercury and cadmium. But even in these inhospitable conditions, there is life. The lord of the springs is a species of algae called Galdieria sulphuraria, and it has come to dominate this hostile world through genetic theft.

It’s usually simple microbes that thrive in the world’s most hostile environments—bacteria, and a group of hardy, single-celled life-forms called archaea. But G.sulphuraria is neither of these. It’s one of the so-called red algae, which is confusing because it’s not red. There’s a green version that uses sunlight to make its own nutrients like a plant, and a yellow version that breaks down chemicals in the rocks. Both live as single cells, but they can carpet Yellowstone’s rocks in colourful, slimy films. They account for 90 percent of everything living near these springs.

G.sulphuraria is also found in hot springs around the world, including in Reykjavik (in the image above) and Sicily’s Mount Etna. To understand how it survives in these difficult environments, Gerald Schönknecht from Oklahoma State University sequenced its genome.

He found that the alga has committed no fewer than 75 independent acts of genetic thievery, and at least 5 percent of its genome comes from either bacteria or archaea.

Galdieria sulphuraria, by Gerald Schönknecht
Galdieria sulphuraria, by Gerald Schönknecht

Bacteria and archaea are well known for their ability to swap genes between one another, just as you or I might exchange business cards or email addresses. This “horizontal gene transfer” allows them to rapidly adapt to new environments by raiding the entire genetic larders of nearby species for useful traits.

But G.sulphuraria belongs to neither group. It’s a eukaryote—part of the lineage of life-forms with complex cells that includes us, other animals, plants and fungi. We tend to evolve new genes by duplicating existing ones and putting the copies towards some new use. In our trunk of the tree of life, horizontal gene transfer (HGT) is meant to be a rarity. When it’s found (and there are more and more examples of this all the time), it’s rare that anyone knows what the appropriated genes are doing. Are they actually playing useful roles in their new hosts?

In the case of G.sulphuraria, Schönknecht certainly thinks so. In fact, he thinks that these transferred genes have bestowed the alga with many of its extreme survival tricks.

Consider a group of enzymes called ATPases. Living cells use a molecule called ATP as a sort of energy currency—they build it to store energy, and cash it in to release energy. ATPases drive that second part—the breakdown of ATP. They’re utterly essential. G.sulphuraria has many famlies of them, some of which seemed to have come from archaea. Many archaea can grow at extremely hot temperatures, and Schönknecht thinks that their borrowed genes conferred the same ability to the alga.

Schönknecht also found that the alga has picked up bacterial genes that: pump sodium out of its cell and allow it to thrive in salty water; get rid of unwanted arsenic; and break down mercury.

So much for pumping stuff out—the alga’s genome is also packed with instructions for building transporters that smuggle chemicals in from the environment. Many of these transporters came for bacteria and archaea, and they allow the alga to absorb common nutrients around it, like acetate or glycerol. That’s why the yellow colonies can grow on the springs’ bare rocks, without making their own food like the green ones. They just suck it up.

Galdieria sulphuraria in Reykjavik, by Christine Oesterhelt
Galdieria sulphuraria in Reykjavik, by Christine Oesterhelt

But how did G.sulfuraria absorb so much genetic material from other microbes? “This is the million-dollar question,” says Schönknecht. Maybe viruses, parasites, or partner bacteria are involved in smuggling genes from one algal cell into another? “We can only speculate.”

The fact that the alga is only one cell probably helps, says Andreas Weber, who led the study. “Once a gene has been incorporated into the genome, it is passed on to the progeny with each cell division,” he says. For a many-celled creature like an animal or plant to do this, the new genes would have to make their way into sperm or eggs.

Schönknecht now expects to find evidence of horizontal transfers in other single-celled eukaryotes. Some diatoms, which are commonly found among sea plankton, have more than 300 genes that came from bacteria, but no one really knows what those genes do. That’s the big thing about Schönknecht’s study: He showed that the borrowed genes are probably helping the alga to deal with some of life’s toughest challenges.

Reference: Schonknecht, Chen, Ternes, Barbier, Shrestha, Stanke, Brautigam, Baker, Banfield, Garavito, Carr, Wilkerson, Rensing, Gagneul, Dickenson, Oesterhelt, Lercher & Weber. 2013. Gene Transfer from Bacteria and Archaea Facilitated Evolution of an Extremophilic Eukaryote. Science http://dx.doi.org/10.1126/science.1231707

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How a quarter of the cow genome came from snakes

Genomes are often described as recipe books for living things. If that’s the case, many of them badly need an editor. For example, around half of the human genome is made up of bits of DNA that have copied themselves and jumped around, creating vast tracts of repetitive sequences. The same is true for the cow genome, where one particular piece of DNA, known as BovB, has run amok. It’s there in its thousands. Around a quarter of a cow’s DNA is made of BovB sequences or their descendants.

BovB isn’t restricted to cows. If you look for it in other animals, as Ali Morton Walsh from the University of Adelaide did, you’ll find it in elephants, horses, and platypuses. It lurks among the DNA of skinks and geckos, pythons and seasnakes. It’s there in purple sea urchin, the silkworm and the zebrafish.

The obvious interpretation is that BovB was present in the ancestor of all of these animals, and stayed in their genomes as they diversified. If that’s the case, then closely related species should have more similar versions of BovB. The cow version should be very similar to that in sheep, slightly less similar to those in elephants and platypuses, and much less similar to those in snakes and lizards.

But not so. If you draw BovB’s family tree, it looks like you’ve entered a bizarre parallel universe where cows are more closely related to snakes than to elephants, and where one gecko is more closely related to horses than to other lizards.

This is because BovB isn’t neatly passed down from parent to offspring, as most pieces of animal DNA are. This jumping gene not only hops around genomes, but between them.

This type of “horizontal gene transfer” (HGT) is an everyday event for bacteria, which can quickly pick up important abilities from each other by swapping DNA. Such trades are supposedly much rarer among more complex living things, but every passing year brings new examples of HGT among animals. For example, in 2008, Cedric Feschotte (now at the University of Utah) discovered a group of sequences that have jumped between several mammals, an anole lizard, and a frog. He called them Space Invaders.

The Space Invaders belong to a group of jumping genes called DNA transposons. They jump around by cutting themselves out of their surrounding DNA, and pasting themselves in somewhere new. They’re also relatively rare—they make up just 2 to 3 percent of our genome. BovB belongs to a different class of jumping genes called retrotransposons. They move through a copy-and-paste system rather than a cut-and-paste one, so that every jump produces in a new copy of the gene. For that reason, they spread like wildfire.

BovB was first discovered in the genomes of cows and other cud-chewing mammals in the 1980s, and seemed to be a signature of that group. Then, in the 1990s, Dusan Kordis and Franc Gubensek detected an extremely similar version of BovB amid the genes of the horned viper. It looked like this piece of DNA had jumped between species. Now, with complete genomes of the cow and other animals at hand, Walsh has more fully mapped BovB’s voyage through the animal kingdom.

A family tree of BovB sequences

Early on during its travels, BovB split into two major lineages. One group has made its way between a single lizard – the Lord Howe Island gecko –and the horse, the egg-laying platypus and echidna from Australia, and African mammals like the elephant and hyrax. The other group started off in lizards and snakes, and jumped from there into ruminants like cows and sheep, and marsupials like possums and wallabies.

To make sure that their results were real, the team took care to avoid contaminating samples from one animal with the DNA of another. Several different laboratories were involved, and no single one of them was responsible for collecting or processing all the samples. And if contaminated samples were producing phantom sightings of BovB, there’s no reason why those sightings would cluster in particular groups, like lizards or marsupials.

To the team, the best explanation for these bizarre patterns is that BovB jumped between species, and it must have done so at least 9 times during its history—far more than the one or two jumps that other scientists had envisaged.

How did it manage? Walsh found a huge clue when she discovered BovB in the genomes of two tick species, both of which suck the blood of lizards and snakes. Other related ticks bite mammals too, so it’s possible that by biting their way through the animal kingdom, these bloodsuckers inoculated fresh branches of the tree of life with jumping genes.

Many scientists who work in this field have suggested that parasites, including worms, bugs, and viruses, could act as vehicles for hitchhiking genes. Indeed, in their very first paper on the BovB, Kordis and Gubensek said that ticks might be spreading the gene between animals. “It’s a scenario that remains hard to prove, but [Walsh’s] data are as close to a smoking gun as can be in the field,” says Feschotte.

A tick, by the CDC. Not quite the same species as the one that Walsh identified, but closely related.

Once it lands in a fresh genome, BovB’s ability to spread throughout its new home seems to vary greatly from one animal to another. Between 10 and 11 percent of the cow genome consists of BovB,and a further 14 to 15 percent are descendants of this jumping gene. BovB accounts for 15 percent of a sheep’s and 11 percent of an elephant’s, but horses, sea urchins and zebrafish only have a few copies each.  “Some genomes seem to have provided really favourable environments for BovB to take off, such as ruminants, but others have not, such as the horse,” says David Adelson, who led the study. “I don’t yet have a hypothesis to test to explore this.”

“BovB appears to have no function other than its own replication,” says Adelson. In one case, it seems to have been incorporated into a cow gene, but otherwise, these sequences don’t seem to do anything. Nonetheless, they’re often so common that they must have had some influence.

“The inescapable conclusion from this and a plethora of other recent studies is that horizontal DNA transfer has been a powerful engine of animal genome evolution, much like it is in bacteria,” says Feschotte. “The main difference being that while bacteria swap genes, animals swap transposons.” Adelson adds: “Despite public concern over the transfer of genetic material to create genetically modified organisms, it appears that Mother Nature has been quietly shuffling genomes for some time.”

Reference: Walsh, Kortschak, Gardner, Bertozzi & Adelson. 2012. Widespread horizontal transfer of retrotransposons. PNAS http://dx.doi.org/10.1073/pnas.1205856110

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How ‘superspreader’ viruses invaded our genes

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.


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Under three layers of junk, the secret to a fatal brain disease

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.


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Beetle pest destroys coffee plants with a gene stolen from bacteria

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.


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Infectious bacteria in your gut create black market for weapons

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.


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Our bodies are a global marketplace where bacteria trade genes

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.