Flatfish are the closest living relatives to swordfish and marlins
At first glance, a swordfish and a flounder couldn’t seem more different. One is a fast, streamlined hunter with a pointy nose, and the other is an oddly shaped bottom-dweller with one distorted eye on the opposite side of its face. Their bodies are worlds apart, but their genes tell a different story.
Alex Little from Queen’s University, Canada, has found that billfishes, like swordfish and marlin, are some of the closest living relatives to the flatfishes, like plaice, sole, flounder and halibut. This result was completely unexpected; Little was originally trying to clarify the relationship between billfishes and their supposed closest relatives – the tunas. That connection seems to make more sense. Both tunas and billfishes are among a handful of fish that are partially warm-blooded. They can heat specific body parts, such as eyes and swimming muscles, to continuously swim after their prey at extremely fast speeds with keen eyesight.
But it turns out that these similarities are superficial. Little sequenced DNA from three species of billfishes and three tunas, focusing on three parts of their main genome and nine parts of their mitochondrial one (a small accessory genome that all animal cells have). By comparing these sequences to those of other fish, Little found that the billfishes’ closest kin are the flatfish and jacks. Indeed, if you look past the most distinctive features like the long bills and bizarre eyes, the skeletons of these groups share features that tunas lack. Indeed, billfish and tuna proved to be only distant relatives. Their ability to heat themselves must have evolved independently and indeed, their bodies product and retain heat in quite different ways.
Little’s work is testament to the power of natural selection. Even closely related species, like marlins are flounders, can end up looking vastly different if they adapt to diverse lifestyles. And distantly related species like tuna and swordfish can end up looking incredibly similar because they’ve adapted to similar challenges – pursuing fast-swimming prey. This shouldn’t come as a surprise – a few months ago, a French team found that prehistoric predatory sea reptiles were probably also warm-blooded.
Reference: Molecular Phylogenetics and Evolution: http://dx.doi.org/10.1016/j.ympev.2010.04.022; images by Luc Viatour and NAOA
Ancient death-grip scars caused by fungus-controlled ants
Forty-eight million years ago, some ants marched up to a leaf and gripped it tight in their jaws. It would be the last thing they would ever do. Their bodies had already been corrupted by a fungus that, over the next few days, fatally erupted from their heads. The fungus produced a long stalk tipped with spores, which eventually blew away, presumably to infect more ants. In time, all that was left of this grisly scene were the scars left by the ants’ death-grip. Today, David Hughes from Harvard University has found such scars in a fossilised leaf from Germany.
Today, hundreds of species of Cordyceps fungi infect a wide variety of insects, including ants. Like many parasites, they can manipulate the way their hosts behave. One species, Cordyceps unilateralis, changes the brains of its ant hosts so that they find and bite into leaves, some 25cm above the forest floor. The temperature and humidity in this zone are just right for the fungus to develop its spore capsules. In its dying act, the ant leaves a distinctive bite mark that’s always on one of the leaf’s veins on its underside. And that’s exactly what Hughes saw in his fossil leaf.
Hughes originally thought that the marks were made by an insect cutting the veins of the leaf to drain away any potential poisons, something that modern insects also do. But these marks look very different – those on the fossil leaf bear a much closer resemblance to those of Cordyceps-infected ants. This is the first fossil trace of a parasite manipulating its host, but it’s not the oldest evidence for such a relationship. In 2008, another American group found a 105-million-year-old piece of amber containing a scale insect, with two Cordyceps stalks sticking out of its head. The war between insects and their Cordyceps nemeses is an ancient one indeed.
It’s not every day that you hear about spy missions that involve a lack of sex, but clearly parasitic wasps don’t pay much attention to Hollywood clichés.
These insects merge the thriller, science-fiction and horror genres, They lay their eggs inside other animals, turning them into slaves and living larders that are destined to be eaten inside-out by the developing grubs. To find their victims, they perform feats of espionage worthy of any secret agent, tapping into their mark’s communication lines, tailing them back to their homes and infiltrating their families.
Two species of parasitoid wasp – Trichogramma brassicae and Trichogramma evanescens – are particularly skilled at chemical espionage. They’ve learned to home in on sexual chemicals used by male cabbage white butterflies. After sex, a male coats the female with anti-aphrodisiac that turns off other suitors and protects the male’s sexual investment. These chemicals are signals from one male to another that say, “Buzz off, she’s taken.”
But the wasps can sense these chemicals. They feed on the nectar of the same plants that the cabbage white visit and when they do, the wasps jump her. They are tiny, smaller even than the butterfly’s eye (see the image below), and they hitch a ride to the site where she’ll lay her eggs. There, they lay their own eggs inside those of the butterfly. Amazingly, the wasps use the same trick for different species of cabbage white butterflies, which secrete very different anti-aphrodisiacs. They can even sense when the anti-aphrodisiacs are wafting among the general scent of a freshly mated female. It’s all part of a sophisticated “espionage-and-ride” strategy.
Millions of people in Latin America have been invade by a parasite – a trypanosome called Trypanosome cruzi. They are passed on through the bite of the blood-sucking assassin bug and they cause Chagas disease, a potentially fatal illness that affects the heart and digestive system. The infections are long-lasting; it can take decades for symptoms to show and a third of infected people eventually die from the disease. But T.cruzi does much more than invade our flesh and blood; it also infiltrates our genomes.
T.cruzi is unusual in that a massive proportion of its DNA, around 15-30%, lies outside of its main genome. These accessory sequences are stored in the form of thousands of interlinked DNA rings. In the parasite, these sequences are found in the mitochrondria – small structures that provide it with energy – but they have found a way to spread much further.
According to new research from Mariana Hecht and a team of Brazilian scientists, T.cruzi has the ability to inveigle its DNA rings into the genomes of those it infects. Once inside, the parasite genes can hop around, hitchhiking from one chromosome to another and leaving genetic chaos in their wake. They can even be passed on from one generation to the next. Hitching a ride aboard sperm and eggs, they can add themselves to the genomes of children, who’ve never been in direct contact with trypanosomes.
Hecht’s discovery suggests that T.cruzi is an unexpected source of genetic diversity in our species. It’s certainly not the only parasite to do this. Viruses have been infiltrating our genes since time immemorial and a massive part of our genome has a viral origin. These events, where viruses joined our family tree, provided raw material for natural selection. Some viral genes wreaked havoc by disrupting important genes, while others were eventually domesticated to act as helpful, even necessary, parts of our genome.
But T.cruzi is a different story. Despite its microscopic, single-celled nature, it’s a vastly complex creature compared to a simple virus. And it continues to breach our DNA today. Now that we’re getting technically better at detecting such “horizontal gene transfers“, we may find that many other parasites are also smuggling their genes into ours. In Hecht’s words, the “human population may be a patchwork of all the organisms to which it has ever been exposed.”
This is an updated version of the first post I wrote this year. The scientists in question were looking at ways of recruiting bacteria in the fight against mosquito-borne diseases, such as dengue fever. They’ve just published new results that expand on their earlier experiments.
Mosquitoes are incredibly successful parasites and cause millions of human deaths every year through the infections they spread. But they are no match for the most successful parasite of all – a bacterium called Wolbachia. It infects around 60% of the world’s insect species and it could be our newest recruit in the fight against malaria, dengue fever and other mosquito-borne infections.
Wolbachia doesn’t usually infect mosquitoes but Scott O’Neill from the University of Queensland is leading a team of researchers who are trying to enlist it. Earlier this year, they published the story of their first success. They had developed a strain that not only infects mozzies, but halves the lifespans of infected females. Now, as the year comes to an end, they’re back with another piece of good news – their life-shortening bacteria also guard the mosquitoes from other infections.
It protects them against a species of Plasmodium, related to the parasite that causes malaria in humans, as well as the viruses responsible for dengue fever and Chikungunya. Infected insects are less likely to carry parasites that cause human disease, and those that do won’t live long enough to spread them. It’s a significant double-whammy that could have a lot of potential in controlling mosquito-borne diseases.
At 13 metres in length, Tyrannosaurus rex had little to fear from other predators. But it was occasionally attacked by an enemy far smaller than itself. In a wonderful piece of forensic palaeontology, Ewan Wolff from the University of Wisconsin has shown that the tyrant lizard king was often infected by a microscopic parasite, whose relatives still infect the birds of today. Potentially transmitted through bites from other tyrannosaurs, the parasite could have starved the infected animals to death.
Many of the large meat-eating dinosaurs have wounds on their heads that were clearly inflicted during fights with their own kind. Bite marks and long gouges caused by teeth raking bone are both fairly common, but both types of injuries show signs of healing – unlike the marks found on prey, these bites weren’t inflicted to kill. But tyrannosaurs also show a second type of injury – smooth-edged pits and holes, particularly in the jaw, where the bone has been eaten away. Some are small; others are centimetres across. They weren’t made by any tooth and they don’t match the shape of any mouth.
They do, however, bear a striking resemblance to injuries found in the beaks of modern birds, particularly falcons, pigeons and chickens. In birds, these injuries are the result of trichomonosis, a disease spread by a parasite called Trichomonas gallinae. The parasite creates ulcers throughout the bird’s mouth and throat, and erodes its jawbones.
Based on the strikingly similar size, shape and locations of the Tyrannosaurus pits and holes, Wolff thinks that the prehistoric predator was afflicted by a very similar contagion and even mounted a similar immune response. It’s yet further evidence of the close relationships between modern birds and their dinosaur ancestors. They may even have been attacked by the very same parasite, although based solely on the scars left behind, that’s impossible to determine.
Viruses and bacteria often act as parasites, infecting a host, reproducing at its expense and causing disease and death. But not always – sometimes, their infections are positively beneficial and on rare occasions, they can actually defend their hosts from parasitism rather than playing the role themselves.
In the body of one species of aphid, a bacterium and a virus have formed a unlikely partnership to defend their host from a lethal wasp called Aphidius ervi. The wasp turns aphids into living larders for its larvae, laying eggs inside unfortunate animals that are eventually eaten from the inside out. But the pea aphid (Acyrthosiphon pisum) has a defence – some individuals are infected by guardian bacteria (Hamiltonella defensa) that save their host by somehow killing the developing wasp larvae.
H.defensa can be passed down from mother to daughter or even sexually transmitted. Infection rates go up dramatically when aphids are threatened by parasitic wasps. But not all strains are the same; some provide substantially more protection than others and Kerry Oliver from the University of Georgia has found out why.
H.defensa‘s is only defensive when it itself is infected by a virus – a bacteriophage called APSE (or “A.pisum secondary endosymbiont” in full). APSE produces toxins that are suspected to target the tissues of animals, such as those of invading wasp grubs. The phage infects the bacteria, which in turn infect the aphids – it’s this initial step that protects against the wasps.
Swine flu has made the world all too aware of the possibility of diseases making the leap from animal hosts to human ones. Now, we know that another disease made a similar transition from chimpanzees to humans, several thousand years ago. This particular infection is caused by a parasite, and a very familiar and dangerous one – Plasmodium falciparum, the agent responsible for malaria.
Transmitted by the bite of mosquitoes, P.falciparum infects over 500 million people every year. Its closest relative is a related parasite, Plasmodium reichenowi, which infects chimpanzees. Leading an international research team, Stephen Rich from the University of Massachussetts has discovered that P.reichenowi is no mere relative – it’s actually P.falciparum‘s ancestor.
Rich compared the genes of the two species to build a Plasmodium family tree, which showed that all of the 133 known strains of P.falciparum, from all parts of the world, are united one a single branch on the P.reichenowi lineage. The stem of that branch represents a single event where P.reichenowi crossed the species barrier from chimps to humans.
The new study was possible because of eight newly collected samples of P.reichenowi from wild and captive chimps. Until now, only a single sample of this species had ever been isolated. Armed with fresh samples, the team focused their attention on three genes – cytB, clpC and 18s rRNA. They found that those of P.reichenowi are very varied, much more so than its genetically uniform cousin P.falciparum (even though we have over 16 times as many samples of the latter). Chances are that any two samples of P.reichenowi are more genetically distinct that either one is to P.falcarium.
In Lake Alexandrina, New Zealand, a population of snails is under threat from a parasitic flatworm, a fluke aptly known as Microphallus. The fluke chemically castrates its snail host and uses its body as a living incubator for its larvae. But the snails have a weapon against these body-snatching foes – sex.
The New Zealand mud snail Potamopyrgus antipodarum is found throughout island’s freshwater habitats. They breed either sexually or asexually through cloning, and the two strategies vary in prevalence throughout the lake. In the shallower waters round its margins, sex is the name of the game, but in the deeper waters towards the lake’s centre, snails are more likely to opt for cloning.
Kayla King from Indiana University has shown that it’s the concentration of the local parasites that drives this gradient of sex. The flukes spend their adult lives in ducks and they rely on the birds inadvertently scooping up their larvae while feeding. In Lake Alexandrina, ducks only feed in the shallow waters around the lake’s margins so these areas are hotspots for parasites, and for co-evolutionary wars between them and their snail hosts. Sex provides the snails with the genetic ammunition they need to stay in the game.
The snails and their parasites beautifully support and illustrate the principles of the Red Queen hypothesis, which suggests that one of the chief benefits of sex lies in providing the genetic innovation necessary to outfox parasites in evolutionary arms races.
Yasunori Kano from the University of Miyazaki has found that the babies of Neritina asperulata, a tiny snail just 3 millimetres across, hitchhike on the back of a larger species Neritina pulligera. This living bus is about 2 centimetres long, and dwarfs its passengers by more than seven times.
The hitchhiking snail is a special sort of parasite, and one that Kano thinks has never been described before. They don’t use their hosts as a snack, a home, an incubator or a foster parent – they simply treat them as a vehicle. Other parasites may unwittingly migrate in the bodies of their hosts, but there’s no evidence that these travels are intentional. N.asperulata, on the other hand, is completely dependent on the movements of other host snails. Without them, it would never get to the small rivers it needs to complete its life cycle.
Conspiracy theories, TV thrillers and airport novels are full of the idea that the world is secretly run by a hidden society. We have come up with many names for this shadowy cabal of puppet-masters – the Illuminati, the Freemasons, and more. But a better name would be ‘parasites’.
Every animal and plant is afflicted by parasites. The vast majority are simple, degenerate creatures, small in size and limited in intelligence. They affect our health and development, and even our behaviour and culture. And by pulling the strings of key species, parasites can change the face of entire habitats.In a typical school textbook, an ecosystem consists of plants that feed plant-eaters, who in turn, line the bowels of predators. But parasites influence all of these levels, and as such, they can change the structures of entire communities.
The idea that nature is secretly manipulated by these tiny, brainless creatures is unsettling but manipulate us, they do. And by changing the behaviour of their hosts, parasites can change the face of entire habitats. Chelsea Wood and colleagues from Dartmouth College have found compelling evidence for this, by showing that a tiny flatworm can alter the structure of a tidal habitat by infecting small marine snails.