At first glance, the African elephant doesn’t look like it has much in common with us humans. We support around 70-80 kg of weight on two legs, while it carries around four to six tonnes on four. We grasp objects with opposable thumbs, while it uses its trunk. We need axes and chainsaws to knock down a tree, but it can just use its head. Yet among these differences, there is common ground. We’re both long-lived animals with rich social lives. And we have very, very large brains (well, mostly).
But all that intelligence doesn’t come cheaply. Large brains are gas-guzzling organs and they need a lot of energy. Faced with similarly pressing fuel demands, humans and elephants have developed similar adaptations in a set of genes used in our mitochondria – small power plants that supply energy to our cells. The genes in question are “aerobic energy metabolism (AEM)” genes – they govern how the mitochondria metabolise nutrients in food, in the presence of oxygen.
We already knew that the evolution of AEM genes has accelerated greatly since our ancestors split away from those of other monkeys and apes. While other mutations were reshaping our brain and nervous system, these altered AEM genes helped to provide our growing cortex with much-needed energy.
Now, Morris Goodman from Wayne State University has found evidence that the same thing happened in the evolution of modern elephants. It’s a good thing too – our brain accounts for a fifth of our total demand for oxygen but the elephant’s brain is even more demanding. It’s the largest of any land mammal, it’s four times the size of our own and it requires four times as much oxygen.
Goodman was only recently furnished with the tools that made his discovery possible – the full genome sequences of a number of oddball mammals, including the lesser hedgehog tenrec (Echinops telfairi). As its name suggests, the tenrec looks like a hedgehog, but it’s actually more closely related to elephants. Both species belong to a major group of mammals called the afrotherians, which also include aardvarks and manatees.
Goodman compared the genomes of 15 species including humans, elephants, tenrecs and eight other mammals and looked for genetic signatures of adaptive evolution. The genetic code is such as that a gene can accumulate many changes that don’t actually affect the structure of the protein it encodes. These are called “synonymous mutations” and they are effectively silent. Some genetic changes do, however, alter protein structure and these “non-synonymous mutations” are more significant and more dramatic, for even small tweaks to a protein’s shape can greatly alter its effectiveness. A high ratio of non-synonymous mutations compared to synonymous ones is a telltale sign that a gene has been the target of natural selection.
And sure enough, elephants have more than twice as many genes with high ratios of non-synonymous mutations to synonymous ones than tenrecs do, particularly among the AEM genes used in the mitochondria. In the same way, humans have more of such genes compared to mice (which are as closely related to us, as tenrecs are to elephants).
These changes have taken place against a background of less mutation, not more. Our lineage, and that of elephants, has seen slower rates of evolution among protein-coding genes, probably due to the fact that the duration of our lives and generations have increased. Goodman speculates that with lower mutation rates, we’d be less prone to developing costly faults in our DNA every time it was copied anew.
Overall, his conclusion was clear – in the animals with larger brains, a suite of AEM genes had gone through an accelerated burst of evolution compared to our mini-brained cousins. Six of our AEM genes that appear to have been strongly shaped by natural selection even have elephant counterparts that have gone through the same process.
Of course, humans and elephants are much larger than mice and tenrecs. But our genetic legacy isn’t just a reflection of our bigger size, for Goodman confirmed that AEM genes hadn’t gone through a similar evolutionary spurt in animals like cows and dogs.
Goodman’s next challenge is to see what difference the substituted amino acids would have made to us and elephants and whether they make our brains more efficient at producing aerobic energy. He also wants to better understand the specific genes that have been shaped the convergent evolution of human and elephant brains over the course of evolution. That task should certainly become easier as more and more mammal genomes are published.
Reference: PNAS doi:10.1073/pnas.0911239106
More on elephants:
We all have a personal bubble, an invisible zone of privacy around our bodies. When strangers cross this boundary, it makes us feel uncomfortable. But not all of us – Daniel Kennedy from the California Institute of Technology has been studying a woman known only as SM, who lacks any sense of personal space.
SM suffers from a rare genetic disorder called Urbach-Wiethe disease, that causes parts of the brain’s temporal lobes to harden and waste away. This brain damage has completely destroyed SM’s amygdalae, a pair of small, almond-shaped structures that help us to process emotions.
Kennedy asked her to say when she felt most comfortable as a female experimenter walked towards her. On average, she preferred a distance of around a foot, about half the usual two-foot gap that 20 other normal people demanded. SM’s lack of boundaries remained whether she walked towards her partner or vice versa, whether they were looking away or at each other, and whether they started close by or far apart.
The fact that SM had a boundary at all was probably because at close distances, it’s hard to see people. She said time and time again that she was actually comfortable at any distance, and during one trial, she actually walked all the way to her partner until they were actually touching. Even when they were making direct eye contact and touching nose-to-nose, she only rated the experience as 1 on a comfort scale of 1 to 10, where 1 is perfectly comfortable and 10 is a level of discomfort that only the British can survive. When a male stranger talked to her up close, she again rated the chat as a 1 (even though he gave it a 7).
SM has been working with this group of researchers, led by Ralph Adolphs, for over a decade but her comfort didn’t stem from simply knowing her partner well. When Kennedy tested two other people who also knew the scientists equally well, but didn’t have damaged amygdalae, they were much less accommodating with their personal space than SM was. Nor did SM simply put her discomfort to heel – she knew that Kennedy was “up to something”, but so did the male stranger and that did nothing to allay his discomfort.
In fact, it was clear that SM understood the concept of personal space. She thought it was smaller than most people’s, and she said that she didn’t want to make other people too uncomfortable by standing too close to them. She estimated that people feel most comfortable about 1.5 feet apart – that’s an underestimate but it’s still larger than her own preference.
Kennedy’s experiments suggest that our sense of personal space comes from the amydgala. Indeed, when he scanned the brains of a small group of volunteers, their amygdalae were more active when someone was standing close to the scanner than when they were keeping their distance.
Kennedy thinks that the amygdala, with its pivotal role in emotional processing, governs the emotional kick we feel when people enter our personal zone. Without it, we remain unfazed by close proximity. What’s less clear is how this affect changes as we get to know people better. Why is it that friends and loved ones are allowed (or positively encouraged) to stay nearer than strangers are?
Other aspects of SM’s ability to deal with emotions are off-kilter too. For a start, she knows no fear – not in a Batman way, but in the sense that she can’t recognise the emotion in the eyes of others Way back in 1994, Adolphs’ group showed that SM can reasonably recognise the emotions in most facial expressions, but she falters when the face in question is afraid. And even though she’s a talented artist, she can’t draw a scared face, once claiming that she didn’t know what such a face would look like.
Now, Naotsugu Tsuchiya, working in Adolphs’ team, has found that SM’s knowledge of fear is a little more complicated. When asked to classify angry and fearful faces, or threatening and harmless scenes, SM did so completely normally when she had to do it quickly. Even though she felt that the scared faces were less intense than volunteers with intact amygdalae, she classified them correctly, with similar reaction times.
In a similar experiment, Tsuchiya showed SM faces that had been gradually morphed from fearful to neutral expressions. When she had unlimited time, it took much more severe expressions for her to recognise a face as fearful. But when she had to quickly pick scared faces from a set, her performances were indistinguishable from other people.
This means that the amygdala isn’t always necessary to know fear. It’s not needed for the earliest stages where our brain starts to process fearful images below the level of our consciousness. Instead, Tsuchiya suggests that after this first level of analysis is over, the amygdala helps us to use the results to make social judgments – to explicitly recognise fear for what it is and to assess the relevance of those first subconscious twinges.
Reference: Nature Neuroscience doi:10.1038/nn.2381 and 10.1038/nn.2380
More on the amygdala:
In martial arts classes, students are often taught to treat weapons as extensions of their own body. But this is more than just a metaphor. It turns out that when we use tools – not just swords and spears, but toothbrushes and rakes as well – our brain treats them as temporary body parts.
According to some psychologists, our brains rely on a mental representation of our bodies called the “body schema”, which allows us to coordinate our various parts and to interact with the world around us. Now, Lucilla Cardinali from INSERM, France has found that we incorporate tools into this mental plan after using them for just a few minutes. It’s confirmation of an idea that has been kicking around for almost a century.
She recruited 14 volunteers and asked them to grab a block in the middle of a table, that was always the same distance away. Then, they had to repeat the same actions with a grabber – a long, mechanical lever tipped with a two-fingered “hand” – and then a third time, with their own hand again.
Small LEDs on the volunteers’ hands allowed Cardinali to track their movements and calculate the speed and acceleration of their arms. She found that they reached for the block differently after they had been accustomed to the grabber, taking longer to accelerate their hands more slowly and to seize the block (although once they actually touched the blocks, they grasped them in just the same way as before). The delays even affected the speed at which they pointed at the block, a behaviour that wasn’t “trained” by the grabber.
Be it in sports or comedy, they say that timing is everything. In evolution, it’s no different. Many of the innovations that have separated us from other apes may have arisen not through creating new genetic material, but by subtly shifting how the existing lot is used.
Take our brains, for example. In the brains of humans, chimps and many other mammals, the genes that are switched on in the brain change dramatically in the first few years of life. But Mehmet Somel from the Max Planck Institute for Evolutionary Anthropology has found that a small but select squad of genes, involved in the development of nerve cells, are activated much later in our brains than in those of other primates.
This genetic delay mirrors other physical shifts in timing that separate humans from other apes. Chimpanzees, for example, become sexually mature by the age of 8 or 9; we take five more years to reach the same point of development.
These delays are signs of an evolutionary process called “neoteny“, where a species’ growth slows down to the point where adults retain many of the features previously seen juveniles. You can see neoteny at work in some domestic dog breeds, which are remarkably similar to baby wolves, or the axolotl salamander, which keeps the gills of a larva even as it becomes a sexually mature adult. And some scientists, like the late Stephen Jay Gould, have suggested that neoteny has played a major role in human evolution too.
As adults, we share many of the physical features of immature chimps. Our bone structures, including flat faces and small jaws, are similar to those of juvenile chimps, as is our patchy distribution of hair. A slower rate of development may even have shaped our vaunted intelligence, by stretching out the time when we are most receptive to new skills and knowledge. Somel’s research supports this idea by showing that since our evolutionary split from chimpanzees, the activation of some important brain genes has been delayed to the very start of adolescence.
A couple of weeks ago, I wrote about propranolol, a drug that can erase the emotion of fearful memories. When volunteers take the drug before recalling a scary memory about a spider, it dulled the emotional sting of future recollections. It’s not, however, a mind-wiping pill in the traditional science-fiction sense, and it can’t erase memories as was so widely reported by the hysterical mainstream media.
The research that’s published today is a different story. Jin-Hee Han from the University of Toronto has indeed found a way to erase a specific fearful memory, but despite the superficial similarities, this is a very different story to the propranolol saga. For a start, Han worked in mice not humans. And unlike the propranolol researchers, who were interested in developing ways of treating people with post-traumatic stress disorder, Han’s goal was to understand how memories are stored in the brain. Erasing them was just a step towards doing that.
Han’s found that a protein called CREB is a molecular beacon that singles out neurons involved in remembering fearful experiences. When a rat experiences something scary, the CREB-neurons in a part of its brain called the amygdala are responsible for storing that memory – for producing what neuroscientists call its “trace”. When Han killed the amygdala’s CREB-neurons, he triggered selective amnesia in the rats, abolishing the specific fears they had been trained to feel. The memory loss was permanent.
This is a major piece of work. Scientists have long believed that memories are represented by specific collections of neurons. But these neurons don’t occur in a neat, tidy clump; they’re often widely spread out, which makes finding the cells that make up any particular memory incredibly challenging. Han has done this by using the CREB protein as a marker. And in doing so, he had highlighted the vital role of this protein in our memories.
I stress again that this isn’t about erasing memories in and of itself. Doing so is just a means to an end – identifying a group of neurons involved in storing a specific memory. For reasons that should become clear in this article, Han’s technique isn’t exactly feasible in humans! Whether this will stop the inevitable run-for-the-hills editorials is perhaps unlikely, but enough speculation: on with the details.
The trauma of child abuse can last a lifetime, leading to a higher risk of anxiety, depression and suicide further down the line. This link seems obvious, but a group of Canadian scientists have found that it has a genetic basis.
By studying the brains of suicide victims, Patrick McGowan from the Douglas Mental Health University Institute, found that child abuse modifies a gene called NR3C1 that affects a person’s ability to deal with stress. The changes it wrought were “epigenetic”, meaning that the gene’s DNA sequence wasn’t altered but it’s structure was modified to make it less active. These types of changes are very long-lasting, which strongly suggests that the trauma of child abuse could be permanently inscribed onto a person’s genes.
Child abuse, from neglect to physical abuse, affects the workings of an important group of organs called the “hypothalamic-pituitary-adrenal axis” or HPA. This trinity consists of the hypothalamus, a funnel-shaped part of the brain; the pituitary gland, which sits beneath it; and the adrenal glands, which sit above the kidneys. All three organs secrete hormones. Through these chemicals, the HPA axis controls our reactions to stressful situations, triggering a number of physiological changes that prime our bodies for action.
The NR3C1 gene is part of this system. It produces a protein called the glucocorticoid receptor, which sticks to cortisol, the so-called “stress hormone”. Cortisol is produced by the adrenal glands in response to stress, and when it latches on to its receptor, it triggers a chain reaction that deactivates the HPA axis. In this way, our body automatically limits its own response to stressful situations.
Without enough glucocorticoid receptors, this self-control goes awry, which means that the HPA is active in normal situations, as well as stressful ones. No surprise then, that some scientists have found a link between low levels of this receptor and schizophrenia, mood disorders and suicide. So, childhood trauma alters the way the body reacts to stress, which affects a person’s risk of suicide or mental disorders later in life. Now, McGowan’s group have revealed part of the genetic (well, epigenetic) basis behind this link.
Chimpanzees may not be able to recite Hamlet or giving rousing speeches but there is no doubt that they are excellent communicators. They exchange a wide variety of sophisticated calls and gestures that carry meaning and can be tailored to different audiences.
The sophistication of chimp communication doesn’t stop there. Jared Taglialatela from the Yerkes National Primate Research Center has found that chimp signals and human speech are both strongly influenced by the same area in the left half of the brain – a region called the inferior frontal gyrus (IFG).