This is the second of two interviews, to accompany my latest New Scientist feature on how birds sense magnetic fields. Thorsten Ritz was one of two scientists who blew this field of research open in 2000, with a landmark paper that suggested how migrating birds could detect the faint traces of the Earths’ magnetic field. My interview with his partner, Klaus Schulten, is elsewhere on the blog, along with more background on the topic.
These interviews are meant to provide bonus extras to the other freelance writing I do, acting as a home for great material that would otherwise be cut and lost. And Ritz’s interview is great material. He talks eloquently about the science of the magnetic sense but more importantly, he talks about what it’s like to work in this field – the reasons why progress has been slow, the thrill of crossing disciplines, and the feeling of doing “19th-century science”. I’ve edited the transcript for length, but it’s still long – if you read any of it, read that second half (starting from the fourth question).
It’s now winter in Europe and many small birds are well on their way to warmer climes, migrating over large tracts of land in search of better weather. Along the way, they keep their course with a remarkable supersense – the ability to sense magnetic fields.
This sense is known as magnetoreception. It sounds like a party for an X-Men villain, and it’s also the subject of my latest feature, out in this week’s issue of New Scientist. I talk about how birds sense magnetic fields, using a compass in the eye and a map in the beak. I look at why the magnetic sense has been so fiendishly difficult to study and why it has taken five decades to unravel some of its details.
For the full details, you’ll have to read the feature, but this is the quick version: when light enters the eyes of birds, it excites a molecule called cryptochrome, shunting it into a state when it can be affected by the earth’s magnetic field. The upshot is that you can ‘blind’ a bird to magnetic fields by covering its eyes (and sometimes, just the right one). It’s possible that they may even be able to see the fields as patterns overlaid on top of their normal vision.
One of the reasons that magnetoreception is such a tricky topic (for scientists as well as science writers!) is that it straddles incredible diverse fields of research, including quantum physics, neuroscience and animal behaviour. Only a few scientists can bridge such divides, and I had the pleasure of interviewing two of them for my piece: Klaus Schulten and Thorsten Ritz. Both gave eloquent, insightful and funny interviews that were inevitably pared down into a few short quotes for the feature. Fortunately, I have all the space I need to make that material publicly available.
First up is Schulten, who talks with marvellous clarity about the early days of the research and where it expects it to go. He was warm and jovial, and gave a great insight into how discoveries are made – by connecting dots that no one else can see. I’ve edited it very gently for length, but the words are all his.
I’ve just flown from London to North Carolina, a trip of around 6,200km. As flights go, it’s a pathetic one, a mere jaunt in the park compared to the epic voyage of the Arctic tern. Every year, this greatest of animal travellers makes a 70,000 km round-trip, in a relentless, globe-trotting pursuit of daylight. In summer, it spends its time in the sun-soaked Arctic and in winter, it heads for the equally bright climes of Antarctica. In its 30 years of life, this champion aeronaut flies more than 2.4 million kilometres – the equivalent of three return journeys to the Moon.
The Arctic tern’s marathon flight is fairly familiar, but estimating the length of such a massive trek isn’t easy. It would be charitable to forgive scientists for getting it wrong, given that they had to rely on observations at sea and capturing banded birds at different places. But few would have predicted just how wrong the textbook figures are. They typically suggest that the tern covers 40,000km in a year. The bird should be insulted – in reality, it flies almost twice that amount.
Its true itinerary has only just been revealed through the use of tiny tracking devices. Similar machines have already exposed the travel plans of larger seabirds like albatrosses, petrels and shearwaters. But these gadgets been too large and clunky to attach to smaller fliers – strapping a 400g recorder to a 100g bird isn’t going to give you an accurate picture of its flying abilities.
Carsten Egevang from Denmark’s Aarhus University changed all of that by developing tiny geolocators, less than 1g in weight. These locators can track the movements of migrating birds by recording the amount of light falling upon it at different points in its journey, and they’ve already been baptised by recording the entire migration of songbirds. Egevang strapped them to the leg of 50 terns, and managed to retrieve 11 of them the following season, when the birds returned.
The feather is an extraordinary biological invention and the key to the success of modern birds. It has to be light and flexible to give birds fine control over their airborne movements, but tough and strong enough to withstand the massive forces generated by high-speed flight. It achieves this through a complicated internal structure that we are only just beginning to fully understand, with the aid of unlikely research assistants – fungi.
At a microscopic level, feathers are made of a protein called beta-keratin. The same protein also forms the beaks and claws of birds, and the scales and shells of reptiles. It’s close (but less rigid) relative, alpha-keratin, makes up the nails, claws and hairs of mammals. Zoom out, and we see that feathers have a central shaft called the rachis with two vanes on either side. Each vane is composed of barbs that branch off the rachis. Even thinner barbules branch off from the barbs, and are held together by small hooks that give the feather its shape.
What’s much less clear is how the keratin fibres and filaments are organised into the rachis, barbs and barbules. To work that out, scientists would typically slice the rachis in cross-sections and look at it under an electron microscope. But feathers don’t give up their secrets so easily. Their fibres are stuck together with a chemical glue that makes them virtually impossible to separate. Imagine gluing a bundle of matches together and cutting them cross-ways. You could see the fibres that make up the component matches, but if they were glued together tightly enough, you wouldn’t be able to tell where one match started and another began. So it is with feathers and their keratin.
Theagarten Lingham-Soliar from the University of Kwazulu-Natal solved the problem by recruiting fungi as research assistants. He used four species, which like to grow on keratin, to digest the complex molecules that glue individual filaments together. The process was very slow. Even after a year, the feathers seemed in pretty good shape and it was only after 18 months that they had broken down enough to be studied under the microscope.
Today, a new paper published in Nature adds another chapter to the story of FOXP2, a gene with important roles in speech and language. The FOXP2 story is a fascinating tale that I covered in New Scientist last year. It’s one of the pieces I’m proudest of so I’m reprinting it here with kind permission from Roger Highfield, and with edits incorporating new discoveries since the time of writing.
The FOXP2 Story (2009 edition)
Imagine an orchestra full of eager musicians which, thanks to an incompetent conductor, produces nothing more than an unrelieved cacophony. You’re starting to appreciate the problem faced by a British family known as KE. About half of its members have severe difficulties with language. They have trouble with grammar, writing and comprehension, but above all they find it hard to coordinate the complex sequences of face and mouth movements necessary for fluid speech.
Thanks to a single genetic mutation, the conductor cannot conduct, and the result is linguistic chaos. In 2001, geneticists looking for the root of the problem tracked it down to a mutation in a gene they named FOXP2. Normally, FOXP2 coordinates the expression of other genes, but in affected members of the KE family, it was broken.
It had long been suspected that language has some basis in genetics, but this was the first time that a specific gene had been implicated in a speech and language disorder. Overeager journalists quickly dubbed FOXP2 “the language gene” or the “grammar gene”. Noting that complex language is a characteristically human trait, some even speculated that FOXP2 might account for our unique position in the animal kingdom. Scientists were less gushing but equally excited – the discovery sparked a frenzy of research aiming to uncover the gene’s role.
Several years on, and it is clear that talk of a “language gene” was premature and simplistic. Nevertheless, FOXP2 tells an intriguing story. “When we were first looking for the gene, people were saying that it would be specific to humans since it was involved in language,” recalls Simon Fisher at the University of Oxford, who was part of the team that identified FOXP2 in the KE family. In fact, the gene evolved before the dinosaurs and is still found in many animals today: species from birds to bats to bees have their own versions, many of which are remarkably similar to ours. “It gives us a really important lesson,” says Fisher. “Speech and language didn’t just pop up out of nowhere. They’re built on very highly conserved and evolutionarily ancient pathways.”
Two amino acids, two hundred thousand years
The first team to compare FOXP2 in different species was led by Wolfgang Enard from the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany. In 2001, they looked at the protein that FOXP2 codes for, called FOXP2, and found that our version differs from those of chimpanzees, gorillas and rhesus macaques by two amino acids out of a total of 715, and from that of mice by three. This means that the human version of FOXP2 evolved recently and rapidly: only one amino acid changed in the 130 million years since the mouse lineage split from that of primates, but we have picked up two further differences since we diverged from chimps, and this seems to have happened only with the evolution of our own species at most 200,000 years ago.
The similarity between the human protein FOXP2 and that of other mammals puts it among the top 5 per cent of the most conserved of all our proteins. What’s more, different human populations show virtually no variation in their FOXP2 gene sequences. Last year, Enard’s colleague Svante Pääbo made the discovery that Neanderthals also had an identical gene, prompting questions over their linguistic abilities (see “Neanderthal echoes below).
“People sometimes think that the mutated FOXP2 in the KE family is a throwback to the chimpanzee version, but that’s not the case,” says Fisher. The KEs have the characteristically human form of the gene. Their mutation affects a part of the FOXP2 protein that interacts with DNA, which explains why it has trouble orchestrating the activity of other genes.
There must have been some evolutionary advantage associated with the human form of FOXP2, otherwise the two mutations would not have spread so quickly and comprehensively through the population. What this advantage was, and how it may have related to the rise of language, is more difficult to say. Nevertheless, clues are starting to emerge as we get a better picture of what FOXP2 does – not just in humans but in other animals too.
During development, the gene is expressed in the lungs, oesophagus and heart, but what interests language researchers is its role in the brain. Here there is remarkable similarity across species: from humans to finches to crocodiles, FOXP2 is active in the same regions. With no shortage of animal models to work with, several teams have chosen songbirds due to the similarities between their songs and human language: both build complex sequences from basic components such as syllables and riffs, and both forms of vocalisation are learned through imitation and practice during critical windows of development.
All bird species have very similar versions of FOXP2. In the zebra finch, its protein is 98 per cent identical to ours, differing by just eight amino acids. It is particularly active in a part of the basal ganglia dubbed “area X”, which is involved in song learning. Constance Scharff at the Max Planck Institute for Molecular Genetics in Berlin, Germany, reported that finches’ levels of FOXP2 expression in area X are highest during early life, which is when most of their song learning takes place. In canaries, which learn songs throughout their lives, levels of the protein shoot up annually and peak during the late summer months, which happens to be when they remodel their songs.
So what would happen to a bird’s songs if levels of the FOXP2 protein in its area X were to plummet during a crucial learning window? Scharff found out by injecting young finches with a tailored piece of RNA that inhibited the expression of the FOXP2 gene. The birds had difficulties in developing new tunes and their songs became garbled: they contained the same component “syllables” as the tunes of their tutors, but with syllables rearranged, left out, repeated incorrectly or sung at the wrong pitch.
The cacophony produced by these finches bears uncanny similarities to the distorted speech of the afflicted KE family members, making it tempting to pigeonhole FOXP2 as a vocal learning gene – influencing the ability to learn new communication sounds by imitating others. But that is no more accurate than calling it a “language gene”. For a start, songbird FOXP2 has no characteristic differences to the gene in non-songbirds. What’s more, among other species that show vocal learning, such as whales, dolphins and elephants, there are no characteristic patterns of mutation in their FOXP2 that they all share.
Instead, consensus is emerging that FOXP2 probably plays a more fundamental role in the brain. Its presence in the basal ganglia and cerebellums of different animals provides a clue as to what that role might be. Both regions help to produce precise sequences of muscle movements. Not only that, they are also able to integrate information coming in from the senses with motor commands sent from other parts of the brain. Such basic sensory-motor coordination would be vital for both birdsong and human speech. So could this be the key to understanding FOXP2?
New work by Fisher and his colleagues supports this idea. In 2008, his team engineered mice to carry the same FOXP2 mutation that affects the KE family, rendering the protein useless. Mice with two copies of the dysfunctional FOXP2 had shortened lives, characterised by motor disorders, growth problems and small cerebellums. Mice with one normal copy of FOXP2 and one faulty copy (as is the case in the affected members of the KE family) seemed outwardly healthy and capable of vocalisation, but had subtle defects.
For example, they found it difficult to acquire new motor skills such as learning to run faster on a tilted running wheel. An examination of their brains revealed the problem. The synapses connecting neurons within the cerebellum, and those in a part of the basal ganglia called the striatum in particular, were severely flawed. The signals that crossed these synapses failed to develop the long-term changes that are crucial for memory and learning. The opposite happened when the team engineered mice to produce a version of FOXP2 with the two characteristically human mutations. Their basal ganglia had neurons with longer outgrowths (dendrites) that were better able to strengthen or weaken the connections between them.
A battery of over 300 physical and mental tests showed that the altered mice were generally healthy. While they couldn’t speak like their cartoon equals, their central nervous system developed in different ways, and they showed changes in parts of the brain where FOXP2 is usually expressed (switched on) in humans.
Their squeaks were also subtly transformed. When mouse babies are moved away from their nest, they make ultrasonic distress calls that are too high for us to hear, but that their mothers pick up loudly and clearly. The altered Foxp2 gene subtly changed the structure of these alarm calls. We won’t know what this means until we get a better understanding of the similarities between mouse calls and human speech.
For now, the two groups of engineered mice tentatively support the idea that human-specific changes to FOXP2 affect aspects of speech, and strongly support the idea that they affect aspects of learning. “This shows, for the first time, that the [human-specific] amino-acid changes do indeed have functional effects, and that they are particularly relevant to the brain,” explains Fisher. “FOXP2 may have some deeply conserved role in neural circuits involved in learning and producing complex patterns of movement.” He suspects that mutant versions of FOXP2 disrupt these circuits and cause different problems in different species.
Pääbo agrees. “Language defects may be where problems with motor coordination show up most clearly in humans, since articulation is the most complex set of movements we make in our daily life,” he says. These circuits could underpin the origins of human speech, creating a biological platform for the evolution of both vocal learning in animals and spoken language in humans.
Holy diversity, Batman
The link between FOXP2 and sensory-motor coordination is bolstered further by research in bats. Sequencing the gene in 13 species of bats, Shuyi Zhang and colleagues from the East China Normal University in Shanghai discovered that it shows incredible diversity. Why would bats have such variable forms of FOXP2 when it is normally so unwavering in other species?
Zhang suspects that the answer lies in echolocation. He notes that the different versions seem to correspond with different systems of sonar navigation used by the various bat species. Although other mammals that use echolocation, such as whales and dolphins, do not have special versions of FOXP2, he points out that since they emit their sonar through their foreheads, these navigation systems have fewer moving parts. Furthermore, they need far less sensory-motor coordination than flying bats, which vocalise their ultrasonic pulses and adjust their flight every few milliseconds, based on their interpretation of the echoes they receive.
These bats suggest that FOXP2 is no more specific to basic communication than it is to language, and findings from other species tell a similar tale. Nevertheless, the discovery that this is an ancient gene that has assumed a variety of roles does nothing to diminish the importance of its latest incarnation in humans.
Since its discovery, no other gene has been convincingly implicated in overt language disorders. FOXP2 remains our only solid lead into the genetics of language. “It’s a molecular window into those kinds of pathways – but just one of a whole range of different genes that might be involved,” says Fisher. “It’s a starting point for us, but it’s not the whole story.” He has already used FOXP2 to hunt down other key players in language.
The executive’s minions
FOXP2 is a transcription factor, which activates some genes while suppressing others. Identifying its targets, particularly in the human brain, is the next obvious step. Working with Daniel Geschwind at the University of California, Los Angeles, Fisher has been trying to do just that, and their preliminary results indicate just what a massive job lies ahead. On their first foray alone, the team looked at about 5000 different genes and found that FOXP2 potentially regulates hundreds of these.
Some of these target genes control brain development in embryos and its continuing function in adults. Some affect the structural pattern of the developing brain and the growth of neurons. Others are involved in chemical signalling and the long-term changes in neural connections that enable to learning and adaptive behaviour. Some of the targets are of particular interest, including 47 genes that are expressed differently in human and chimpanzee brains, and a slightly overlapping set of 14 targets that have evolved particularly rapidly in humans.
Most intriguingly, Fisher says, “we have evidence that some FOXP2 targets are also implicated in language impairment.” Last year, Sonja Vernes in his group showed that FOXP2 switches off CNTNAP2, a gene involved in not one but two language disorders – specific language impairment (SLI) and autism. Both affect children, and both involve difficulties in picking up spoken language skills. The protein encoded by CNTNAP2 is deployed by nerve cells in the developing brain. It affects the connections between these cells and is particularly abundant in neural circuits that are involved in language.
Verne’s discovery is a sign that the true promise of FOXP2’s discovery is being fulfilled – the gene itself has been overly hyped, but its true worth lies in opening a door for more research into genes involved in language. It was the valuable clue that threw the case wide open. CNTNAP2 may be the first language disorder culprit revealed through FOXP2 and it’s unlikely to be the last.
Most recently, Dan Geschwind compared the network of genes that are targeted by FOXP2 in both chimps and humans. He found that the two human-specific amino acids within this executive protein have radically altered the set of genetic minions that it controls.
The genes that are directed by human FOXP2 are a varied cast of players that influence the development of the head and face, parts of the brain involved in motor skills, the growth of cartilage and connective tissues, and the development of the nervous system. All those roles fit with the idea that our version of FOXP2 has been a lynchpin in evolving the neural circuits and physical structures that are important for speech and language.
The FOXP2 story is far from complete, and every new discovery raises fresh questions just as it answers old ones. Already, this gene has already taught us important lessons about evolution and our place in the natural world. It shows that our much vaunted linguistic skills are more the result of genetic redeployment than out-and-out innovation. It seems that a quest to understand how we stand apart from other animals is instead leading to a deeper appreciation of what unites us.
Box – Neanderthal echoes
The unique human version of the FOXP2 gives us a surprising link with one extinct species. Last year, Svante Pääbo’s group at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, extracted DNA from the bones of two Neanderthals, one of the first instances of geneticists exploring ancient skeletons for specific genes. They found that Neanderthal FOXP2 carries the same two mutations as those carried by us – mutations accrued since our lineage split from chimps between 6 and 5 million years ago.
Pääbo admits that he “struggled” to interpret the finding: the Neanderthal DNA suggests that the modern human’s version of FOXP2 arose much earlier than previously thought. Comparisons of gene sequences of modern humans with other living species had put the origins of human FOXP2 between 200,000 and 100,000 years ago, which matches archaeological estimates for the emergence of spoken language. However, Neanderthals split with humans around 400,000 years ago, so the discovery that they share our version of FOXP2 pushes the date of its emergence back at least that far.
“We believe there were two things that happened in the evolution of human FOXP2,” says Pääbo. “The two amino acid changes – which happened before the Neanderthal-human split – and some other change which we don’t know about that caused the selective sweep more recently.” In other words, the characteristic mutations that we see in human FOXP2 may indeed be more ancient than expected, but the mutated gene only became widespread and uniform later in human history. While many have interpreted Pääbo’s findings as evidence that Neanderthals could talk, he is more cautious. “There’s no reason to assume that they weren’t capable of spoken language, but there must be many other genes involved in speech that we yet don’t know about in Neanderthals.”
Walks through a forest are often made all the more enjoyable by the chance to watch brightly coloured birds flit between the trees. But birds are not just mere inhabitants of forests – in some parts of the world, they are the key to the trees’ survival.
The Serengeti is one such place. Since 1950, around 70-80% of riverside forests have disappeared from this area. Fires seem to be a particular problem, opening large gaps in the canopy that forests can’t seem to recover from. To understand why Gregory Sharam from the University of British Columbia has been monitoring the density of the forests since 1966. From 1997-2006, he studied 18 particular patches at varying stages of decline.
During this time, as the forest density declined, so too did the number of bird species in the area. The total number halved and fruit-eating species were especially hit, declining from 16 to 6 species. These fruit-eaters perform a valuable service for a wide variety of trees, eating their fruit and dispersing their unharmed seeds. In pristine forest, around 70% of all seeds on the forest floor have previously passed through the guts of birds. In fragmented open forest, that proportion falls to 3%.
Without fewer birds, seeds that simply fall to the ground become more important for the trees’ survival but these too suffer without their feathered friends. They are destroyed by seed-eating bruchid beetles. The beetles generally avoid seeds that are still on trees and for some reason, they also steer clear of seeds that have been previously eaten by birds. But seeds that naturally drop to the ground are fair game and as tree density fell, the beetles’ attack rate climbed from 20% to 90%.
In 1995, a palaeontologist called Mark Norrell reported an amazing discovery – the fossilised remains of a dinosaur called Troodon, sitting on top of a large clutch of eggs. The fossil was so well-preserved and its posture so unmistakeable that it provided strong proof that some dinosaurs incubated their eggs just as modern birds do. And since then, two other small predatory species – Oviraptor and Citipati – have been found in brooding positions on top of egg clutches.
But a subtler look at these fossils reveal much more about dinosaur parenting than the simple fact that it existed. To David Varricchio from Montana State University, they also tell us which parent took more responsibility for the young. Based on the size of the egg clutches and the bones of the parent, Varricchio thinks that it was the males that cared for the babies. And given that small, predatory dinosaurs were the ancestors of modern birds, fatherly care was probably also the norm for the earliest members of our feathered friends.
Of all the back-boned animal groups, none show a greater equality of parental care that the birds. Among mammals, the next generation is mainly the mother’s responsibility and fathers help out in less than 5% of species. By comparison, male birds help to care for eggs and chicks in over 90% of living species. But Varricchio (together with Norrell and others) argues that this joint parenting is not how the dynasty started off.
The team noted that the clutches so delicately incubated by Troodon, Oviraptor and Citipati contained a substantial number of eggs, about 22 to 30 eggs apiece. Compared to most of the 433 living birds and crocodilians whose clutch sizes have been studied, the dinosaurs were sitting on far more eggs than animals of their size normally do. The team found that species where both parents chip in, or where mum takes the lead, usually settle for smaller clutches. Only those where dad does almost all of the work tend to rear such large broods.