Tiny Blobs of Brain Cells Could Reveal How Your Mind Differs from a Neanderthal’s

In recent years, scientists have figured out how to grow blobs of hundreds of thousands of live human neurons that look — and act — something like a brain.

These so-called brain organoids have been used to study how brains develop into layers, how they begin to spontaneously make electrical waves and even how that development might change in zero gravity. Now researchers are using these pea-size clusters to explore our evolutionary past.

In a study published on Thursday, a team of scientists describe how a gene likely carried by Neanderthals and our other ancient cousins triggered striking changes in the anatomy and function of brain organoids.

As dramatic as the changes are, the scientists say it’s too soon to know what these changes mean for the evolution of the modern human brain. “It’s more of a proof of concept,” said Katerina Semendeferi, a co-author of the new study and an evolutionary anthropologist at the University of California San Diego.

To build on the findings, she and her co-author, Alysson Muotri, have established the UC San Diego Archealization Center, a group of researchers focused on studying organoids and making new ones with other ancient genes. “Now we have a beginning, and we can start exploring,” Dr. Semendeferi said.

Dr. Muotri began working with brain organoids more than a decade ago. To understand how Zika produces birth defects, for example, he and his colleagues infected brain organoids with the virus, which prevented the organoids from developing their cortex-like layers.

In other studies, the researchers studied how genetic mutations help give rise to disorders like autism. They transformed skin samples from volunteers with developmental disorders and transformed the tissue into stem cells. They then grew those stem cells into brain organoids. Organoids from people with Rett Syndrome, a genetic disorder that results in intellectual disability and repetitive hand movements, grew few connections between neurons.

Dr. Semendeferi has been using organoids to better understand the evolution of human brains. In previous work, she and her colleagues have found that in apes, neurons developing in the cerebral cortex stay close to each other, whereas in humans, cells can crawl away across long distances. “It’s a completely different organization,” she said.

But these comparisons stretch across a vast gulf in evolutionary time. Our ancestors split off from chimpanzees roughly seven million years ago. For millions of years after that, our ancestors were bipedal apes, gradually attaining larger heights and brains, and evolving into Neanderthals, Denisovans and other hominins.

It’s been difficult to track the evolutionary changes of the brain along the way. Our own lineage split from that of Neanderthals and Denisovans about 600,000 years ago. After that split, fossils show, our brains eventually grew more rounded. But what that means for the 80 billion neurons inside has been hard to know.

Dr. Muotri and Dr. Semendeferi teamed up with evolutionary biologists who study fossilized DNA. Those researchers have been able to reconstruct the entire genome of Neanderthals by piecing together genetic fragments from their bones. Other fossils have yielded genomes of the Denisovans, who split off from Neanderthals 400,000 years ago and lived for thousands of generations in Asia.

The evolutionary biologists identified 61 genes that may have played a crucial role in the evolution of modern humans. Each of those genes has a mutation that’s unique to our species, arising some time in the last 600,000 years, and likely had a major impact on the proteins encoded by these genes.

Dr. Muotri and his colleagues wondered what would happen to a brain organoid if they took out one of those mutations, changing a gene back to the way it was in our distant ancestors’ genomes. The difference between an ancestral organoid and an ordinary one might offer clues to how the mutation influenced our evolution.

It took years for the scientists to get the experiment off the ground, however. They struggled to find a way to precisely alter genes in stem cells before coaxing them to turn into organoids.

Once they had figured out a successful method, they had to choose a gene. The scientists worried that they might pick a gene for their first experiment that would do nothing to the organoid. They mulled how to increase their odds of success.

“Our analysis made us say, ‘Let’s get a gene that changes a lot of other genes,’” said Dr. Muotri.

One gene on the list looked particularly promising in that regard: NOVA1, which makes a protein that then guides the production of proteins from a number of other genes. The fact that it is mainly active only in the developing brain made it more attractive. And humans have a mutation in NOVA1 not found in other vertebrates, living or extinct.

Dr. Muotri’s colleague, Cleber Trujillo, grew a batch of organoids carrying the ancestral version of the NOVA1 gene. After placing one under a microscope next to an ordinary brain organoid, he invited Dr. Muotri take a look.

The ancestral NOVA1 organoid had a noticeably different appearance, with a bumpy popcorn texture instead of a smooth spherical surface. “At that point, things started,” Dr. Muotri recalled. “I said, ‘OK, it’s doing something.’”

The proportion of different types of brain cells was also different in the ancestral organoids. And the neurons in the ancestral organoids began firing spikes of electrical activity a few weeks earlier in their development than modern human ones did. But it also took longer for the electrical spikes to get organized into waves.

Other experts were surprised that a single genetic mutation could have such obvious effects on the organoids. They had expected subtle shifts that might be difficult to observe.

“It looks like the authors found a needle in a haystack based on an extremely elegant study design,” said Philipp Gunz, a paleoanthropologist at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, who was not involved in the research.

Simon Fisher, the director of the Max Planck Institute for Psycholinguistics in the Netherlands, said the results must have come from a mix of hard work and some good luck. “There must have been some degree of serendipity,” he said.

Although the researchers don’t know what the changes in the organoids mean for our evolutionary history, Dr. Muotri suspects that there may be connections to the kind of thinking made possible by different kinds of brains. “The true answer is, I don’t know,” he said. “But everything that we see at very early stages in neurodevelopment might have an implication later on in life.”

At the new research center, Dr. Semendeferi plans to carry out careful anatomical studies on brain organoids and compare them to human fetal brains. That comparison will help make sense of the changes seen in the ancestral NOVA1 organoid.

And Dr. Muotri’s team is working through the list of 60 other genes, to create more organoids for Dr. Semendeferi to examine. It’s possible that the researchers may not be so lucky as they were on their first try and won’t see much difference with some genes.

“But others might be similar to NOVA1 and point to something new — some new biology that allows us to reconstruct an evolutionary path that helped us to become who we are,” Dr. Muotri said.

SARS-CoV-2 is following the evolutionary rule book

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Natural selection is a powerful force. In circumstances that are still disputed, it took a bat coronavirus and adapted it to people instead. The result has spread around the globe. Now, in two independent but coincidental events, it has modified that virus still further, creating new variants which are displacing the original versions. It looks possible that one or other of these novel viruses will itself soon become a dominant form of sars-cov-2.

Knowledge of both became widespread in mid-December. In Britain, a set of researchers called the Covid-19 Genomics uk Consortium (cog-uk) published the genetic sequence of variant b.1.1.7, and nervtag, a group that studies emerging viral threats, advised the government that this version of the virus was 67-75% more transmissible than those already circulating in the country. In South Africa, meanwhile, Salim Abdool Kalim, a leading epidemiologist, briefed the country on all three television channels about a variant called 501.v2 which, by then, was accounting for almost 90% of new covid-19 infections in the province of Western Cape.

Britain responded on December 19th, by tightening restrictions already in place. South Africa’s response came on December 28th, in the wake of its millionth recorded case of the illness, with measures that extended a night-time curfew by two hours and reimposed a ban on the sale of alcohol. Other countries have reacted by discouraging even more forcefully than before any travel between themselves and Britain and South Africa. At least in the case of b.1.1.7, though, this has merely shut the stable door after the horse has bolted. That variant has now been detected in a score of countries besides Britain—and from these new sites, or from Britain, it will spread still further. Isolated cases of 501.v2 outside South Africa have been reported, too, from Australia, Britain, Japan and Switzerland.

So far, the evidence suggests that despite their extra transmissibility, neither new variant is more dangerous on a case-by-case basis than existing versions of the virus. In this, both are travelling the path predicted by evolutionary biologists to lead to long-term success for a new pathogen—which is to become more contagious (which increases the chance of onward transmission) rather than more deadly (which reduces it). And the speed with which they have spread is impressive.

The first sample of b.1.1.7 was collected on September 20th, to the south-east of London. The second was found the following day in London itself. A few weeks later, at the beginning of November, b.1.1.7 accounted for 28% of new infections in London. By the first week of December that had risen to 62%. It is probably now above 90%.

Variant 501.v2 has a similar history. It began in the Eastern Cape, the first samples dating from mid-October, and has since spread to other coastal provinces.

The rapid rise of b.1.1.7 and 501.v2 raises several questions. One is why these particular variants have been so successful. A second is what circumstances they arose in. A third is whether they will resist any of the new vaccines in which such store is now being placed.

The answers to the first of these questions lie in the variants’ genomes. cog-uk’s investigation of b.1.1.7 shows that it differs meaningfully from the original version of sars-cov-2 in 17 places. That is a lot. Moreover, several of these differences are in the gene for spike, the protein by which coronaviruses attach themselves to their cellular prey. Three of the spike mutations particularly caught the researchers’ eyes.

One, n501y, affects the 501st link in spike’s amino-acid chain. This link is part of a structure called the receptor-binding domain, which stretches from links 319 to 541. It is one of six key contact points that help lock spike onto its target, a protein called ace2 which occurs on the surface membranes of certain cells lining the airways of the lungs. The letters in the mutation’s name refer to the replacement of an amino acid called asparagine (“n”, in biological shorthand) by one called tyrosine (“y”). That matters because previous laboratory work has shown that the change in chemical properties which this substitution causes binds the two proteins together more tightly than normal. Perhaps tellingly, this particular mutation (though no other) is shared with 501.v2.

Golden spike

b.1.1.7’s other two intriguing spike mutations are 69-70del, which knocks two amino acids out of the chain altogether, and p681h, which substitutes yet another amino acid, histidine, for one called proline at chain-link 681. The double-deletion attracted the researchers’ attention for several reasons, not the least being that it was also found in a viral variant which afflicted some farmed mink in Denmark in November, causing worries about an animal reservoir of the disease developing. The substitution is reckoned significant because it is at one end of a part of the protein called the s1/s2 furin-cleavage site (links 681-688), which helps activate spike in preparation for its encounter with the target cell. This site is absent from the spike proteins of related coronaviruses, such as the original sars, and may be one reason why sars-cov-2 is so infective.

The South African variant, 501.v2, has only three meaningful mutations, and all are in spike’s receptor-binding domain. Besides n501y, they are k417n and e484k (k and e are amino acids called lysine and glutamic acid). These two other links are now the subject of intense scrutiny.

Even three meaningful mutations is quite a lot for a variant to have. Just one would be more usual. The 17 found in b.1.1.7 therefore constitute a huge anomaly. How this plethora of changes came together in a single virus is thus the second question which needs an answer.

The authors of the cog-uk paper have a suggestion. This is that, rather than being a chance accumulation of changes, b.1.1.7 might itself be the consequence of an evolutionary process—but one that happened in a single human being rather than a population. They observe that some people develop chronic covid-19 infections because their immune systems do not work properly and so cannot clear the infection. These unfortunates, they hypothesise, may act as incubators for novel viral variants.

The theory goes like this. At first, such a patient’s lack of natural immunity relaxes pressure on the virus, permitting the multiplication of mutations which would otherwise be culled by the immune system. However, treatment for chronic covid-19 often involves what is known as convalescent plasma. This is serum gathered from recovered covid patients, which is therefore rich in antibodies against sars-cov-2. As a therapy, that approach frequently works. But administering such a cocktail of antibodies applies a strong selection pressure to what is now a diverse viral population in the patient’s body. This, the cog-uk researchers reckon, may result in the success of mutational combinations which would not otherwise have seen the light of day. It is possible that b.1.1.7 is one of these.

The answer to the third question—whether either new variant will resist the vaccines now being rolled out—is “probably not”. It would be a long-odds coincidence if mutations which spread in the absence of a vaccine nevertheless protected the virus carrying them from the immune response raised by that vaccine.

This is no guarantee for the future, though. The swift emergence of these two variants shows evolution’s power. If there is a combination of mutations that can get around the immune response which a vaccine induces, then there is a fair chance that nature will find it.

As Scientists Pinpoint the Genetic Reason for Lactose Intolerance, Unknowns Remain

Researchers have identified the genetic basis of lactose intolerance, the inability of most adults in the world to digest the principal sugar in milk. The finding, published today in the journal Nature Genetics, may lead to the development of a more accurate test for the condition.

Lactose intolerance can cause bloating and indigestion from consuming milk or milk products. More than 30 million Americans, mostly black or Asian, are prone to the condition.

Though lactose intolerance may sound like a disorder, it is in fact natural. In most people the gene for lactase, the enzyme that digests lactose, is switched on at birth and switched off at the age of weaning.

In most Europeans, however, the lactase gene remains active. With the domestication of cattle and goats in the Near East some 10,000 years ago, the ability to digest lactose throughout life could have conferred some nutritional advantage. Biologists speculate that a mutation that prolonged the gene’s activity was suddenly favored and spread throughout the population.

But one finding has baffled biologists: the gene for the lactase enzyme and the gene’s promoter, a neighboring region of DNA that controls the activity of the gene, show no significant difference between populations whose adults can digest lactose and those whose adults cannot

Now a team of Finnish and American biologists reports that it has identified two single-unit DNA changes that correlate strongly with the presence or absence of adult lactase activity.

The changes were found by studying the sequence of DNA units near the lactase gene in nine Finnish families. About 20 percent of Scandinavians are lactose intolerant, and Finnish scientists had collected elaborate pedigrees of the trait, allowing the precise DNA changes to be identified, said Dr. Leena Peltonen, an author of the study who works at the University of Helsinki.

A genetic test based on the finding will enable lactose intolerance to be diagnosed from the DNA in a drop of blood, Dr. Peltonen said. Now, the condition is recognized by measuring he hydrogen generated from undigested lactose by the bacteria in the gut.

But some experts do not see any particular need for a genetic test, because they do not regard lactose intolerance as a clinically serious condition. Dr. Michael D. Levitt of the Minneapolis Veterans Affairs Medical Center, whose specialty is the study of intestinal gas, said that in most people an inactive lactase gene was rarely a problem unless they drank large amounts of milk.

Many people who believe they have problems digesting lactose actually have irritable bowel syndrome, Dr. Levitt said.

Dr. Levitt, who invented the hydrogen test for lactose intolerance, said concern about the condition was ”mostly an American phenomenon, and the rest of the world is not much interested in it.” He says the concern about lactose has arisen because ”there is a tremendous amount of irritable bowel syndrome, and people would like to find a cause for it.”

Dr. Stephen James, an official of the National Institute of Diabetes and Digestive and Kidney Diseases, agrees that doctors and patients sometimes get diverted into a hunt for minute traces of lactose in the diet when the real problem is irritable bowel syndrome, a poorly understood condition for which there is no test except ruling out everything else.

The authors of the new report say the two DNA units that switch off the lactase gene are in the 9th and 13th introns in a neighboring gene whose role strangely has nothing to do with lactose metabolism. Introns are the spacer regions of DNA that separate the information-coding parts of a gene. Because the cell cuts out and discards the introns when a gene is activated, these disposable pieces of DNA have long been ignored. Now it seems they play unexpected roles in gene control.

In the default human condition, in which the lactase gene is programmed to turn off after weaning, people have C in the 9th intron position of both their maternal and paternal DNA and G in both the 13th intron positions. But changing the C to a T and the G to an A in either or both sets of a person’s DNA keeps the gene from switching off in the cells that line the intestine. (The four letters of the DNA alphabet are A, T, C and G, and one full set of DNA is inherited from each parent.)

This article was originally published in The New York Times. Read the original article.

Lactose Tolerance in East Africa Points to Recent Evolution

A surprisingly recent instance of human evolution has been detected among the peoples of East Africa. It is the ability to digest milk in adulthood, conferred by genetic changes that occurred as recently as 3,000 years ago, a team of geneticists has found.

The finding is a striking example of a cultural practice — the raising of dairy cattle — feeding back into the human genome. It also seems to be one of the first instances of convergent human evolution to be documented at the genetic level. Convergent evolution refers to two or more populations acquiring the same trait independently.

Throughout most of human history, the ability to digest lactose, the principal sugar of milk, has been switched off after weaning because the lactase enzyme that breaks the sugar apart is no longer needed. But when cattle were first domesticated 9,000 years ago and people later started to consume their milk as well as their meat, natural selection would have favored anyone with a mutation that kept the lactase gene switched on.

Such a mutation is known to have arisen among an early cattle-raising people, the Funnel Beaker culture, which flourished 5,000 to 6,000 years ago in north-central Europe. People with a persistently active lactase gene have no problem digesting milk and are said to be lactose tolerant.

Almost all Dutch people and 99 percent of Swedes are lactose tolerant, but the mutation becomes progressively less common in Europeans who live at increasing distances from the ancient Funnel Beaker region.

Geneticists wondered if the lactose tolerance mutation in Europeans, identified in 2002, had arisen among pastoral peoples elsewhere. But it seemed to be largely absent from Africa, even though pastoral peoples there generally have some degree of tolerance.

A research team led by Dr. Sarah Tishkoff of the University of Maryland has now solved much of the puzzle. After testing for lactose tolerance and genetic makeup among 43 ethnic groups in East Africa, she and her colleagues have found three new mutations, all independent of one another and of the European mutation, that keep the lactase gene permanently switched on.

The principal mutation, found among Nilo-Saharan-speaking ethnic groups of Kenya and Tanzania, arose 2,700 to 6,800 years ago, according to genetic estimates, Dr. Tishkoff’s group reports today in the journal Nature Genetics. This fits well with archaeological evidence suggesting that pastoral peoples from the north reached northern Kenya about 4,500 years ago and southern Kenya and Tanzania 3,300 years ago.

Two other mutations were found, among the Beja people of northeastern Sudan and tribes of the same language family, Afro-Asiatic, in northern Kenya.

Genetic evidence shows that the mutations conferred an enormous selective advantage on their owners, enabling them to leave almost 10 times as many descendants as people without such mutations. The mutations have created “one of the strongest genetic signatures of natural selection yet reported in humans,” the researchers write.

The survival advantage was so powerful perhaps because those with the mutations not only gained extra energy from lactose but also, in drought conditions, would have benefited from the water in milk. People who were lactose intolerant could have risked losing water from diarrhea, Dr. Tishkoff said.

Diane Gifford-Gonzalez, an archaeologist at the University of California, Santa Cruz, said the new findings were “very exciting” because they “showed the speed with which a genetic mutation can be favored under conditions of strong natural selection, demonstrating the possible rate of evolutionary change in humans.”

The genetic data fitted in well, she said, with archaeological and linguistic evidence about the spread of pastoralism in Africa. The first clear evidence of cattle in Africa is from a site 8,000 years old in northwestern Sudan. Cattle there were domesticated independently from two other domestications, in the Near East and the Indus Valley of India.

Nilo-Saharan speakers in Sudan and their Cushitic-speaking neighbors in the Red Sea hills probably domesticated cattle at the same time, because each has an independent vocabulary for cattle items, said Dr. Christopher Ehret, an expert on African languages and history at the University of California, Los Angeles. Descendants of each group moved south and would have met again in Kenya, Dr. Ehret said.

Dr. Tishkoff detected lactose tolerance among Cushitic speakers and Nilo-Saharan groups in Kenya. Cushitic is a branch of Afro-Asiatic, the language family that includes Arabic, Hebrew and ancient Egyptian.

Dr. Jonathan Pritchard, a statistical geneticist at the University of Chicago and a co-author of the new article, said there were many signals of natural selection in the human genome but it was usually hard to know what was being selected for. In this case Dr. Tishkoff clearly defined the driving force, he said.

The mutations Dr. Tishkoff detected are not in the lactase gene itself but a nearby region of the DNA that controls the activation of the gene. The finding that different ethnic groups in East Africa have different mutations is one instance of their varied evolutionary history and their exposure to many different selective pressures, Dr. Tishkoff said.

“There is a lot of genetic variation between groups in Africa, reflecting the different environments in which they live, from deserts to tropics, and their exposure to very different selective forces,” she said.

People in different regions of the world have evolved independently since dispersing from the ancestral human population in northeast Africa 50,000 years ago, a process that has led to the emergence of different races. But much of this differentiation at the level of DNA may have led to the same physical result.

As Dr. Tishkoff has found in the case of lactose tolerance, evolution may use the different mutations available to it in each population to reach the same goal when each is subjected to the same selective pressure. “I think it’s reasonable to assume this will be a more general paradigm,” Dr. Pritchard said.

 

This article was originally published in The New York Times. Read the original article.

Narrower Skulls, Oblong Brains: How Neanderthal DNA Still Shapes Us

People who sign up for genetic testing from companies like 23andMe can find out how much of their DNA comes from Neanderthals. For those whose ancestry lies outside Africa, that number usually falls somewhere between 1 percent and 2 percent.

Scientists are still a long way from understanding what inheriting a Neanderthal gene means to people. Some Neanderthal genes may be helpful — improving our defenses against infections, for example — but other bits may leave carriers slightly more prone to certain diseases.

On Thursday, a team of scientists revealed that two pieces of Neanderthal DNA may have another effect: They may change the shape of our brains.

The study, published in the journal Current Biology, wasn’t designed to determine how Neanderthal genes influence thought — if they do so at all. Instead, the value of the research lies in its unprecedented glimpse into the genetic changes influencing the evolution of the human brain.

“This study is surely a milestone,” said Emiliano Bruner, a paleoanthropologist researcher at Spain’s National Research Center on Human Evolution, who was not involved in the research.

Neanderthals and modern humans are evolutionary cousins whose ancestors diverged about 530,000 years ago, possibly somewhere in Africa. Neanderthals left Africa long before modern humans, and their bones were found across Europe, the Near East, and even Siberia.

Before they disappeared about 40,000 years ago, Neanderthals left behind signs of sophistication: spears used to hunt big game, for instance, and jewelry made of shells and eagle talons.

Yet scientists still wonder just how much like us these cousins were. Did they speak a full-blown language? Did they think in symbols?

One thing is clear: They were not short on brains. By measuring the volume inside Neanderthal skulls, researchers have found that their brains were as big as ours, on average, perhaps bigger.

But their brains did not mimic ours. “We have roundish brains,” said Philipp Gunz, a paleoanthropologist at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany. “All other human species have elongated brain cases.”

Dr. Gunz and his colleagues study CT scans of fossil skulls to track brain evolution. As it turns out, the oldest skulls of modern humans, dating back 300,000 years, held elongated brains — more like those of Neanderthals than our own.

Skulls from about 120,000 years ago show that brains had gotten somewhat rounder by then, but were still outside the range observed in people today.

But there’s a gap in the fossil record after that period; the next oldest skulls that Dr. Gunz and his colleagues have studied are just 36,000 years old. These have the distinctive roundedness of living humans.

Modern human skulls got rounder because certain regions of the brain changed size. At the back of the brain, for example, a part called the cerebellum dramatically expanded.

Dr. Gunz and his colleagues wondered what sort of genetic changes drove this shift. It occurred to them that an answer might be found in a natural experiment that took place about 60,000 years ago: the interbreeding of modern humans and Neanderthals.

As they left Africa, modern humans encountered and mated with Neanderthals, producing healthy children who inherited a set of chromosomes from each parent. Neanderthal DNA has persisted through the generations in people of non-African descent.

 

Did Neanderthal genes affect the shape of modern human brains? The effect of any one gene would be exquisitely subtle, and so Dr. Gunz and his colleagues needed to compare a lot of brains to find it.

Fortunately, a number of scientific teams had already begun building databases of brain scans and DNA from volunteers.

Dr. Gunz’s team studied 4,468 people in the Netherlands and Germany. They searched the DNA of the volunteers for over 50,000 common genetic markers inherited from ancient Neanderthals.

Then the researchers compared the shapes of people’s brains to see whether any Neanderthal gene variants were associated. Two genetic markers jumped out: People who carry them have unusual patterns of gene activity in their brains.

One marker is linked to a gene called PHLPP1. It’s unusually active in the cerebellum of people who carry the Neanderthal version. This gene controls the production of an insulating sleeve that wraps around neurons. Known as myelin, it is crucial for long-range communication in the brain.

The other marker is linked to a gene called UBR4, which in carriers is less active in a region deep in the brain called the putamen. UBR4 helps neurons divide in the brains of children.

These findings suggest that PHLPP1 and UBR4 evolved to work differently in modern human brains. The modern human version of PHLPP1 may have produced extra myelin in the cerebellum. And our version of UBR4 may have made neurons grow faster in the putamen.

Why these changes? Simon Fisher, a co-author of the new study at the Max Planck Institute for Psycholinguistics in the Netherlands, speculated that modern humans evolved more sophisticated powers of language. They may have also become better at making tools.

“Things like tool use and speech articulation are hugely dependent on motor circuitry,” said Dr. Fisher.

Both require the brain to send fast, precise commands to muscles. And it may be no coincidence that the cerebellum and putamen are crucial parts of our motor circuitry — the very regions that helped change the overall shape of the modern human brain.

What does this research mean for people who carry the Neanderthal versions of these brain-shaping genes? There are limits to what genetics can tell us, said John Anthony Capra, an evolutionary biologist at Vanderbilt University who was not involved in the study.

It’s very hard to predict people’s behavior from their genes, he noted — let alone try to account for a few Neanderthal genes. To learn what they are doing in the brain will require that scientists discern very faint signals amid the noise of the human genome.

“That’s a long way off, if ever possible,” Dr. Capra said

 

This article was originally published in The New York Times. Read the original article.

A species of spider that suckles its young

Superficially, individuals of a species of jumping spider called Toxeus magnus look like ants. This protects them from the attentions of spider wasps—a group of insects that catch and paralyse spiders in order to lay their eggs on the arachnids’ bodies, which thus act as a living larder for the wasps’ larvae. Ants are not, however, the only group of unrelated animals that T. magnus resembles. They are also quite like mammals. That, at least, is the conclusion of a study just published in Science by Quan Ruichang of the Xishuangbanna Tropical Botanical Garden, in Yunnan, China.

Female mammals produce milk to suckle their young. Before modern gene-based phylogeny developed, that was indeed the definition of a mammal. A few other types of animal do something similar. Pigeons, for example, generate a milklike secretion in their throats, which they feed to their squabs. But until now, only in mammals (or some of them, anyway) was lactation thought to be the basis of an extended relationship between parent and offspring. Dr Quan and his colleagues have changed that thinking.

Their study was stimulated by the observation that wild T. magnus seem to remain in the maternal nest far longer than most other spider species. They wondered why. They therefore brought some specimens into their laboratory for a closer look. This showed that the mother of a brood exudes fluid from her epigastric furrow, the canal through which she lays her eggs. For the first week of her hatchlings’ lives, she deposits this fluid in drops around the nest, from which the young spiders drink. After that, until they are about 40 days old, she suckles the spiderlings directly.

Experiments that measured the growth and survival of young spiders, some of which involved sealing the mother’s epigastric furrow using typing-correction fluid, showed that the spiderlings did, indeed, depend on the secretion for nutrition. They relied on it completely until they were 20 days old, at which point they started leaving the nest to hunt on their own account. Even after this, though, the fluid formed an important dietary supplement until they were about 40 days old. And chemical analysis showed that it is a rich source of nutrients. It contains four times as much protein as cow’s milk does.

Even when weaned, young spiders, like many young mammals, returned home regularly after they had been out searching for food of their own—and experiments that removed the mother showed she was in some way contributing to their health and survival even then. Young spiders continued to return until they were 60 days old, and thus sexually mature. At that point, the mother started attacking returning sons, thus driving them away—presumably to avoid the risk of them mating with their sisters and producing inbred offspring. Daughters, though, she continued to tolerate. At what point those daughters, too, left to set up shop by themselves the study did not investigate.

Whether epigastric lactation and its consequent prolongation of family life is confined to T. magnus, or is more widespread among jumping spiders, remains to be looked at. But unless the strategy has evolved very recently it seems likely that at least some of T. magnus’s relatives will also employ it. Either way, Dr Quan’s discoveries serve as a reminder that if something works well in one part of the animal kingdom, the chances are that it will do so elsewhere, too.

 

 

 

This article was originally published in The Economist. Read the original article.

Yes, the Octopus Is Smart as Heck. But Why?

To demonstrate how smart an octopus can be, Piero Amodio points to a YouTube video. It shows an octopus pulling two halves of a coconut shell together to hide inside. Later the animal stacks the shells together like nesting bowls — and carts them away.

“It suggests the octopus is carrying these tools around because it has some understanding they may be useful in the future,” said Mr. Amodio, a graduate student studying animal intelligence at the University of Cambridge in Britain.

But his amazement is mixed with puzzlement.

For decades, researchers have studied how certain animals evolved to be intelligent, among them apes, elephants, dolphins and even some birds, such as crows and parrots.

But all the scientific theories fail when it comes to cephalopods, a group that includes octopuses, squid and cuttlefish. Despite feats of creativity, they lack some hallmarks of intelligence seen in other species.

“It’s an apparent paradox that’s been largely overlooked in the past,” said Mr. Amodio. He and five other experts on animal intelligence explore this paradox in a paper published this month in the journal Trends in Ecology and Evolution.

For scientists who study animal behavior, intelligence is not about acing a calculus test or taking a car apart and putting it back together. Intelligence comprises sophisticated cognitive skills that help an animal thrive.

That may include the ability to come up with solutions to the problem of finding food, for example, or a knack for planning for some challenge in the future. Intelligent animals don’t rely on fixed responses to survive — they can invent new behaviors on the fly.

To measure animal intelligence, scientists observe creatures in the wild — watching a dolphin stick a sponge on its beak to avoid getting cuts from sharp rocks and coral, for example. Or they bring animals into the lab and offer them puzzles to solve, such as rewarding crows when they learn to rip paper into strips of just the right size.

Only a few species stand out in these studies, and by comparing them, scientists have identified some shared factors. The animals have big brains relative to their body size, they live for a long time, and they can form long-lasting social bonds.

Those similarities have led to some promising explanations for how certain animals evolved to be smart.

One is known as the ecological intelligence hypothesis. It holds that intelligence evolves as an adaptation for finding food. While some animals have a reliable food supply, others have to cope with unpredictability.

“If you eat fruit, you have to remember where the fruiting trees are and when they’re ripe,” said Mr. Amadio. “It can be much more cognitively challenging than eating leaves.”

Tools allow animals to get to food that they couldn’t reach otherwise. And if they can make plans for the future, they can store food to survive hard times.

Other researchers have argued for what’s known as the social intelligence hypothesis: Smarter animals “cooperate and learn from other members of the same species,” said Mr. Amadio.

Together, these forces appear to have encouraged the development of bigger, more powerful brains.

Smart animals also tend to live for a long time, and it’s possible that bigger brains drove the evolution of longevity. It takes years for juveniles to develop these complex organs, during which time they need help from adults to get enough food.

Cephalopods behave in ways that certainly suggest they’re highly intelligent. An octopus named Inky, for example, made a notorious escape recently from the National Aquarium of New Zealand, exiting his enclosure and slithering into a floor drain and, apparently, out to sea.

Cuttlefish can scare off predators by forming eyespots on their bodies in order to look like giant fish. But they only use this trick against predators that rely on vision to find prey. If a predator that depends on smell shows up, the cuttlefish are smart enough just to flee.

Octopuses show the same flexibility when scientists bring them into labs. In one study, researchers at Hebrew University presented octopuses with an L-shaped box with food inside. The animals figured out how to push and pull the morsel through a tiny hole in the wall of their tank.

Another feature that cephalopods share with other smart animals is a relatively big brain. But that’s where the similarities appear to end. Most of the neurons that do the computing, for example, are in the octopus’s arms.

Most strikingly, cephalopods die young. Some may live as long as two years, while others only last a few months. Nor do cephalopods form social bonds.

They get together to mate, but males and females don’t stay together for long or care for their young. While chimpanzees and dolphins may live in societies of dozens of other animals, cephalopods seem to be loners.

Mr. Amodio and his colleagues think the evolutionary history of cephalopods may explain this intelligence paradox. About half a billion years ago, their snaillike ancestors evolved to use their shells as a buoyancy device. They could load chambers in the shell with gas to float up and down in the ocean.

A cousin of cephalopods, the nautilus, still lives this way. Like cephalopods, it has tentacles. It also has a somewhat enlarged brain, although it doesn’t seem to be anywhere as intelligent as an octopus.

About 275 million years ago, the ancestor of today’s cephalopods lost the external shell. It’s not clear why, but it must have been liberating. Now the animals could start exploring places that had been off-limits to their shelled ancestors. Octopuses could slip into rocky crevices, for example, to hunt for prey.

On the other hand, losing their shells left cephalopods quite vulnerable to hungry predators. This threat may have driven cephalopods to become masters of disguise and escape. They did so by evolving big brains, the ability to solve new problems, and perhaps look into the future — knowing that coconut or clam shells may come in handy, for example.

An octopus pulls together two empty shells in order to hide off the coast of Sulawesi, Indonesia.CreditEthan Daniels, via Getty Images

Image
An octopus pulls together two empty shells in order to hide off the coast of Sulawesi, Indonesia.CreditEthan Daniels, via Getty Images

Yet intelligence is not the perfect solution for cephalopods, Mr. Amodio suggested. Sooner or later, they get eaten. Natural selection has turned them into a paradox: a short-lived, intelligent animal.

Mr. Amodio said that scientists still need to learn a lot more about cephalopods before they can know if this hypothesis is sound. But the research may do more than shine a light on octopuses and their cousins: It could give us a deeper understanding of intelligence in general.

“We can’t take for granted that there’s just one way to intelligence,” Mr. Amodio said. “There could be different paths.”

 

 

This article was originally published in The New York Times. Read the original article.

How Did We Get to Be Human?

I spoke recently to a scientist who was writing up a summary of what we know about human evolution. He should have had a head start, having written a similar article five years ago.

But when he looked at what he had written then, he realized that little of it was relevant. “I can’t use much of any of it,” he told me.

As a journalist, I can sympathize.

In recent years, scientists have offered a flood of insights into how we became human. Fairly often, the new evidence doesn’t square with what we thought we knew.

Instead, many of these findings demand that researchers ask new questions about the human past, and envision a more complex prehistory.

When Science Times debuted 40 years ago, scientists knew far less about how our ancestors branched off from other apes and evolved into new species, known as hominins.

Back then, the oldest known hominin fossil was a diminutive, small-brained female unearthed in Ethiopia named Lucy. Her species, now known as Australopithecus afarensis, existed from about 3.85 million years ago to about 2.95 million years ago.

Lucy and her kin still had apelike features, like long arms and curved hands. They could walk on the ground, but inefficiently. Running was out of the question.

Hominin evolution appeared to have taken a relatively direct path from her to modern humans. The earliest known members of our genus, Homo, were taller and had long legs for walking and running, as well as much larger brains. Eventually, early Homo gave rise to our own exceptional species, Homo sapiens.

Now, it’s clear that Lucy’s species wasn’t the beginning of our evolution; it was a branch that sprouted midway along the trunk of our family tree. Researchers have found fossils of hominins dating back over six million years. Those vestiges — a leg bone here, a crushed skull there — hint at even more apelike ancestors.

All this mixing and experimentation produced as many as 30 different sorts of hominins — that we know of. And one kind did not simply succeed another through history: For millions of years, several sorts of hominins coexisted.

Indeed, our own species shared this planet with near-relatives until just recently.

In 2017, researchers found the oldest known fossils of our species in Morocco, bones dating back about 300,000 years. At that time, Neanderthals also existed. They continued to live across Europe and Asia until 40,000 years ago.

At that time, too, Homo erectus, one of the oldest members of our genus, still clung to existence in what is now Indonesia. The species did not go extinct until at least 143,000 years ago.

Homo erectus and Neanderthals are hardly new to paleoanthropologists. Neanderthals came to light in 1851, and Homo erectus fossils were discovered in the 1890s. But still other hominins, recent research has shown, shared the planet with our own species.

In 2015, researchers unearthed 250,000-year-old fossils in a South African cave. Known as Homo naledi, this new species had a Lucy-sized brain, but it was also a complex structure in ways that resembled our own.

The wrist and other hand bones of Homo naledi were humanlike, while its long, curved fingers seemed more like an ape’s.

While Homo naledi thrived in Africa, another mysterious species could be found on an island now called Flores, in Indonesia. Known as Homo floresiensis, these hominins stood only three feet high and had brains even smaller than that of Homo naledi.

The species may have arrived on Flores as early as 700,000 years ago, and these hominins endured until at least 60,000 years ago. Homo floresiensis appears to have made stone tools, perhaps to hunt and butcher the dwarf elephants that once lived on the island.

Paleoanthropologists today are no longer limited to just examining the size and shape of fossils. Over the past 20 years, geneticists have learned how to extract DNA from bones dating back tens of thousands of years.

In one remarkable discovery in Siberia, researchers examining a nondescript pinkie bone discovered the genome of a separate line of hominins, now known as Denisovans.

As it turns out, we have had the planet to ourselves only in the past 40,000 years — a small fraction of Homo sapiens’ existence. Perhaps we outcompeted other species. Maybe they just had bad luck in evolution’s lottery.

But in one way, we are still living with them. Both Neanderthals and Denisovans interbred with our ancestors some 60,000 years ago, and billions of people today carry their DNA. Still mosaics, after all this time.

This article was originally published in The New York Times.  Read the original article.

The microscopic structure of a cat’s tongue helps keep its fur clean

T.s. eliot’s mystery cat, Macavity, besides being a criminal mastermind able to evade the combined ranks of British law enforcement, had a coat that was “dusty from neglect”. Criminality is one thing, but this truly strains the imagination. Real cats are champion groomers.

Of the ten hours a day that a domestic cat deigns to remain awake, it spends a quarter licking dirt, fleas, blood and loose hairs from its fur. Cats’ tongues, specialised for this task, are covered in hundreds of backward-facing keratin spines. But exactly how these cone-shaped protuberances, called filiform papillae, work to give the animals such mastery over their cleanliness has remained unknown until now.

To crack the mystery Alexis Noel and David Hu, a pair of engineers at the Georgia Institute of Technology, in Atlanta, examined the grooming mechanisms of six feline species—from domestic pets and bobcats to snow leopards and lions. Studying the activity of tongues inside the mouths of living creatures proved tricky, so instead Dr Noel and Dr Hu built an automated grooming machine fitted out with tongues and furs from animals whose lives had ended at places such as the Tiger Haven in Tennessee, a sort of retirement home for rescued big cats. They attached the tongues to a mechanical arm and made them “lick” the furs. High-resolution cameras and scanners took pictures.

The two researchers found that the filiform papillae were shaped not, as had previously been thought, like solid cones. Rather, they resembled tiny scoops. Each had a small groove—named a cavo papilla by the team—at its tip.

This structure permits surface tension to wick saliva from a cat’s mouth and release it into the farthest recesses of the animal’s fur. During each lick, about half of the saliva on the tongue is so transferred. Saliva serves as a multi-purpose cleaning agent and the cavo papillae also assist the absorption, for the return journey, of any dirt or blood that needs removing. The cat’s tongue therefore “acts like a loofah and a sponge at the same time”, says Dr Hu.

The pair’s findings, just published in the Proceedings of the National Academy of Sciences, could inspire new ways to clean complex hairy surfaces. The authors themselves demonstrated one such application, which they call the tongue-inspired grooming (tigr) brush. To make this they employed 3d printing to create structures, shaped like cat papillae, attached to a silicone base. The tigr brush pulled on cat hairs and fur with less force than existing brushes, and was easier to clean. Such a brush could also be used to spread medicines deep into a cat’s fur or onto its skin, without the usual distressing practice of having to shave the animal first.

 

 

This article was originally published in The Economist. Read the original article.

Chemists find a recipe that may have jump-started life on Earth

In the molecular dance that gave birth to life on Earth, RNA appears to be a central player. But the origins of the molecule, which can store genetic information as DNA does and speed chemical reactions as proteins do, remain a mystery. Now, a team of researchers has shown for the first time that a set of simple starting materials, which were likely present on early Earth, can produce all four of RNA’s chemical building blocks.

Those building blocks—cytosine, uracil, adenine, and guanine—have previously been re-created in the lab from other starting materials. In 2009, chemists led by John Sutherland at the University of Cambridge in the United Kingdom devised a set of five compounds likely present on early Earth that could give rise to cytosine and uracil, collectively known as pyrimidines. Then, 2 years ago, researchers led by Thomas Carell, a chemist at Ludwig Maximilian University in Munich, Germany, reported that his team had an equally easy way to form adenine and guanine, the building blocks known as purines. But the two sets of chemical reactions were different. No one knew how the conditions for making both pairs of building blocks could have occurred in the same place at the same time.

Now, Carell says he may have the answer. On Tuesday, at the Origins of Life Workshop here, he reported that he and his colleagues have come up with a simple set of reactions that could have given rise to all four RNA bases.

Carell’s story starts with only six molecular building blocks—oxygen, nitrogen, methane, ammonia, water, and hydrogen cyanide, all of which would have been present on early Earth. Other research groups had shown that these molecules could react to form somewhat more complex compounds than the ones Carell used.

To make the pyrimidines, Carell started with compounds called cyanoacetylene and hydroxylamine, which react to form compounds called amino-isoxazoles. These, in turn, react with another simple molecule, urea, to form compounds that then react with a sugar called ribose to make one last set of intermediate compounds.

Finally, in the presence of sulfur-containing compounds called thiols and trace amounts of iron or nickel salts, these intermediates transform into the pyrimidines cytosine and uracil. As a bonus, this last reaction is triggered when the metals in the salts harbor extra positive charges, which is precisely what occurs in the final step in a similar molecular cascade that produces the purines, adenine and guanine. Even better, the step that leads to all four nucleotides works in one pot, Carell says, offering for the first time a plausible explanation of how all of RNA’s building blocks could have arisen side by side.

“It looks pretty good to me,” says Steven Benner, a chemist with the Foundation for Applied Molecular Evolution in Alachua, Florida. The process provides a simple way to produce all four bases under conditions consistent with those believed present on early Earth, he says.

The process doesn’t solve all of RNA’s mysteries. For example, another chemical step still needs to “activate” each of RNA’s four building blocks to link them into the long chains that form genetic material and carry out chemical reactions. But making RNA under conditions like those present on early Earth now appears within reach.

 

 

This article was originally published in Science. Read the original article.