Gravitational waves are providing new hints about how black holes get their kicks.

The Advanced Laser Interferometer Gravitational-Wave Observatory’s detection of spacetime ripples from two merging black holes on December 26, 2015, indicated that one black hole was spinning like a tilted top as it orbited with its companion (SN: 7/9/16, p. 8). That off-kilter spin could mean that the stellar explosion that produced the black hole gave it a strong kick, physicist Richard O’Shaughnessy and colleagues report in a paper in press in Physical Review Letters.

Scientists aren’t sure how black holes like those detected by LIGO pair up (SN Online: 6/19/16). Two neighboring stars may have obliterated themselves in a pair of explosions called supernovas, producing two black holes. But that scenario should lead to black holes that spin in the same plane as their orbit. It would take a sizeable jolt from the supernova, of about 50 kilometers per second, to account for the cockeyed spin, the researchers conclude.

Computer simulations of supernovas predict smaller black hole boosts, making for a cosmological conundrum. “This will be a serious challenge for supernova modelers to explain,” O’Shaughnessy, of the Rochester Institute of Technology in New York, said June 5 in a news conference in Austin, Texas, at a meeting of the American Astronomical Society.

Fossil DNA may be rewriting the history of elephant evolution.

The first genetic analysis of DNA from fossils of straight-tusked elephants reveals that the extinct animals most closely resembled modern African forest elephants. This suggests that straight-tusked elephants were part of the African, not Asian, elephant lineage, scientists report online June 6 in eLife.

Straight-tusked elephants roamed Europe and Asia until about 30,000 years ago. Much like modern Asian elephants, they sported high foreheads and double-domed skulls. These features convinced scientists for decades that straight-tusked and Asian elephants were sister species, says Adrian Lister, a paleobiologist at the Natural History Museum in London who was not involved in the study.
For the new study, researchers extracted and decoded DNA from the bones of four straight-tusked elephants found in Germany. The fossils ranged from around 120,000 to 240,000 years old. The genetic material in most fossils more than 100,000 years old is too decayed to analyze. But the elephant fossils were unearthed in a lake basin and a quarry, where the bones would have been quickly covered with sediment that preserved them, says study author Michael Hofreiter of the University of Potsdam in Germany.

Hofreiter’s team compared the ancient animals’ DNA with the genomes of the three living elephant species — Asian, African savanna and African forest — and found that straight-tusked genetics were most similar to African forest elephants.

When the researchers told elephant experts what they’d found, “Everybody was like, ‘This can’t possibly be true!’” says study coauthor Beth Shapiro of the University of California, Santa Cruz. “Then it gradually became, ‘Oh yeah, I see.… The way we’ve been thinking about this is wrong.’”

If straight-tusked elephants were closely related to African forest elephants, then the African lineage wasn’t confined to Africa — where all elephant species originated — as paleontologists previously thought. It also raises questions about why straight-tusked elephants bore so little resemblance to today’s African elephants, which have low foreheads and single-domed skulls.
Accounting for this new finding may not be as simple as moving one branch on the elephant family tree, Lister says. It’s possible that straight-tusked elephants really were a sister species of Asian elephants, but they exhibit genetic similarities to African forest elephants from interbreeding before the straight-tusked species left Africa.

It’s also possible that a common ancestor of Asian, African and straight-tusked elephants had particular genetic traits that were, for some reason, only retained by African and straight-tusked elephants, he says.

Lister and colleagues are now reexamining data on straight-tusked skeletons to reconcile the species’ skeletal features with the new information on their DNA. “I will feel most comfortable if we can understand these genetic relationships in terms of the [physical] differences between all these species,” he says. “Then we’ll have a complete story.”

When we brought our first baby home from the hospital, our pediatrician advised us to have her sleep in our room. We put our tiny new roommate in a crib near our bed (though other containers that were flat, firm and free of blankets, pillows or stuffed animals would have worked, too).

The advice aims to reduce the risk of sleep-related deaths, including sudden infant death syndrome, or SIDS. Studies suggest that in their first year of life, babies who bunk with their parents (but not in the same bed) are less likely to die from SIDS than babies who sleep in their own room. The reasons aren’t clear, but scientists suspect it has to do with lighter sleep: Babies who sleep near parents might more readily wake themselves up and avoid the deep sleep that’s a risk factor for SIDS.

That’s an important reason to keep babies close. Room sharing also makes sense from a logistical standpoint. Middle of the night feedings and diaper changes are easier when there’s less distance between you and the babe.

But babies get older. They start snoring a little louder and eating less frequently, and it’s quite natural to wonder how long this room sharing should last. That’s a question without a great answer. In November 2016, the American Academy of Pediatrics task force on SIDS updated its sleep guidelines. The earlier recommendation was that babies ought to sleep in parents’ bedrooms for an entire year. The new suggestion softens that a bit to say infants should be there for “ideally for the first year of life, but at least for the first 6 months.”

Rachel Moon, a SIDS expert at the University of Virginia in Charlottesville who helped write the revised AAP guidelines, says that the update “gives parents a little more latitude after the first 6 months.” The vast majority of SIDS deaths happen in the first six months of life, but the studies that have found benefits for room sharing lumped together data from the entire first year. That makes it hard to say how protective room sharing is for babies between 6 and 12 months of age.

But a new study raises a reason why babies ought to get evicted before their first birthday: They may get more sleep at night in their own rooms. Babies who were sleeping in their own rooms at ages 4 or 9 months got more nighttime sleep than babies the same ages who roomed with parents, researchers reported online June 5 in Pediatrics.

The team asked hundreds of mothers to take sleep surveys when their children were 4, 9, 12 and 30 months old. Some of the 230 children slept in their own rooms when they were younger than 4 months, others moved to their own rooms between 4 and 9 months, and the rest were still sharing their parents’ rooms at 9 months.
At 9 months, babies who had been sleeping alone since 4 months of age slept an average of 40 minutes more than room sharers. The researchers found no differences in sleep duration between the groups of babies at age 12 months. By 30 months of age, though, children who had been sleeping in their own rooms by either 4 or 9 months of age slept on average 45 minutes longer at night than children who had been sharing their parents’ rooms at 9 months. (Important caveat: At 30 months, total daily sleep time didn’t differ between the groups. The former room sharers were making up for missed nighttime sleep with naps.)

Parents who want their babies age 6 months and older to sleep in their own room ought to be encouraged to make the move, says study coauthor Ian Paul, a pediatrician at Penn State. “The guidelines should reflect data, not opinion,” Paul says.

He suspects that sharing a bedroom with babies interferes with everyone’s sleep because normal nocturnal rustlings turn into full-blown wake-ups. Babies and adults alike experience brief arousals during sleep. But when parents are right next to babies, they’re more likely to respond to their children’s brief arousals, which then wakes the baby up more. “This then sets up the expectation from the baby that these arousals will be met with a parent reaction, causing a bad cycle to develop,” he says.

There was another difference that turned up between the two groups of babies. Babies who roomed with parents were four times more likely to be moved into their parents’ beds at some point during the night than babies who slept in their own rooms. Bed sharing is a big risk factor for sleep-related infant deaths.

But Moon cautions that the Pediatrics study is preliminary, and doesn’t warrant a change in the AAP guidelines. She and coauthors point out in an accompanying commentary that other factors might be behind the difference in sleep between the two groups of babies. For instance, babies who slept in their own room were more likely to have consistent bedtime routines, be put to bed drowsy but awake, and have bedtimes of 8 p.m. or earlier. Those are all signs of good “sleep hygiene” for babies, and might be contributing to the longer sleep times. “We know that consistent bedtime routine and consistent bedtime are very important in terms of sleep quality in children,” Moon says. “They could very well make a difference.”

So that’s where we are. Some things are clear, like putting your baby to sleep on her back on a flat, firm surface clear of objects and having your baby nearby during the first six months. But other decisions come with skimpier science, and whether to evict your 6-month-old is one of them. Because science can take you only so far, it may just come down to the snoring, stirring and sleep deprivation.

BOSTON — Some aspects of speech are as Southern as pecan pie. Consider the vowel shift that makes the word pie sound more like “pah.” While that pronunciation is found from Florida to Texas, a new study reveals a surprising diversity in Southern vowel pronunciation that’s linked to a speaker’s age, social class, gender, race and geography.

The research, presented June 29 at a meeting of the Acoustical Society of America, could help software developers create better speech recognition tools for smartphones and other devices.
To understand the medley of southern vowel sounds, linguist Margaret Renwick of the University of Georgia in Athens dove into the Digital Archive of Southern Speech. The archive comprises almost 400 hours of interviews with 64 native Southerners representing a mix of ethnicities, social classes, education levels and ages.

Renwick’s analysis of more than 300,000 vowel sounds finds, for example, that Southern upper middle class women are often at the extreme end of variation in pronunciation. While Southern men and women are equally likely to shift the vowel in bet to “bay-ut,” upper middle class Southern women are more likely to stretch the vowel sound in bit to “bee-ut.” They are also most likely to pronounce bait as bite. The finding that women are more inclined to draw a sound out into two syllables — or change it entirely — is in line with other research suggesting that women are linguistic innovators, and less likely to adhere to the norms of standard American English, Renwick said.

With a final rip, an iceberg roughly the size of Delaware has broken off Antarctica’s Larsen C ice shelf. Anticipated for weeks, the fracture is one of the largest calving events ever recorded.

On July 12, satellite images confirmed a nearly 5,800-square-kilometer, 1-trillion-metric-ton chunk of ice, equivalent to 12 percent of Larsen C’s total area, split from the ice shelf. “[We] have been surprised how long it took for the rift to break through the final few kilometers of ice,” Adrian Luckman, a glaciologist at Swansea University in Wales, said in a blogpost for Project MIDAS, which has been tracking the effects of a warming climate on the ice shelf. Now the focus will shift to the stability of the remaining ice shelf and the fate of the giant iceberg.
Scientists had been monitoring Larsen C since 2014, when they noticed that a crack in the ice shelf had grown roughly 20 kilometers in less than nine months (SN: 7/25/15, p. 8). After a relative lull in 2015, the crack grew another 40 kilometers in 2016 and then 10 more in the first half of January 2017, bringing its total length to 175 kilometers. At that point, its tip was 20 kilometers from the Weddell Sea.
The crack grew another 17 kilometers between May 25 and May 31 — at times traveling parallel to the edge and ultimately putting it within 13 kilometers of the ice front. Then, in late June, the outer part of the ice shelf picked up speed, putting new pressure on the crack and the entire shelf. “It won’t be long now,” Project Midas tweeted June 30. Added Luckman, also in a tweet: “The remaining ice is strained near to breaking point.”

Yet the vigil lasted nearly two more weeks. By July 6, the crack had come within 5 kilometers of the edge of the ice. Then, sometime between July 10 and July 12, it finally reached the water, allowing the huge hunk of ice to splinter off into the sea.
The ice loss dramatically alters the landscape of Larsen C, Luckman notes. “Maps will need to be redrawn.” And that could be the least of the trouble ahead, says Adam Booth, a geophysicist at the University of Leeds in England also with Project MIDAS. “The calving event is significant because it is likely a precursor to something much bigger, potentially the collapse of the whole Larsen C ice shelf,” Booth says. The same thing happened to the neighboring Larsen B ice shelf in 2002, after it calved a Rhode Island-sized iceberg (SN: 3/30/02, p. 197).

“Glaciologists are keen to see how Larsen C will react,” says Luckman.

A complete collapse of Larsen C could have implications for sea level rise. Antarctica’s ice shelves act as buttresses, helping to slow the flow of the continent’s ice into the ocean. Since these shelves float on the water, calving icebergs don’t directly raise sea level. But calving or the collapse of an ice shelf allows glaciers and ice streams further inland to flow into the ocean, which can contribute to sea level rise.

Calving of icebergs is common, and over several decades, the shelves usually recover to their original size. But in the last two decades, ice shelves have instead continued to lose ice until collapsing, probably as a result of rising temperatures due to climate change, researchers suspect. In 2014, researchers concluded the collapse of Larsen B was the result of warming (SN: 10/18/14, p. 9).

Some computer simulations suggest Larsen C could suffer the same fate, possibly within a few years to decades, Luckman says. Still, the calving event that feeds a potential collapse may be hard to pin on climate change. “Not all ice-related stories have a clear global warming origin,” Luckman notes. Larsen C’s calving, he says, “may simply be a natural event that would have happened regardless of human activity.”
Not everyone is convinced that Larsen C will fall apart completely. Researchers from Europe predict major changes to the shelf would happen only if it loses 55 percent of its ice. At that point, a significant amount of ice could ooze from glaciers into the ocean. Still, understanding what allowed the recent rift to grow and calve will “give us insight regarding other fractures or rifts on the shelf,” says geoscientist Dan McGrath of Colorado State University in Fort Collins. While McGrath says a collapse is “very unlikely,” he adds that “these other dormant rifts are in locations where if they reinitiated, the subsequent calving event would be worrisome for the shelf’s stability.”

Discrepancies in the predictions of Larsen C’s fate raise an important point, says Richard Alley, a geologist at Penn State. Researchers don’t understand ice shelf calving and collapsing enough predict how any one individual ice shelf will behave after a break.

“The Larsen C ice shelf is, of course, just one small part of Antarctica,” Booth says. “What is worrying is that we’re seeing trends in several ice shelves that tend towards decreasing stability. Should they continue along these trends, we could be seeing the start of increased mass loss from the Antarctic continent.”

A genetic-engineering tool designed to spread through a population like wildfire — eradicating disease and even whole invasive species — might be more easily thwarted than thought.

Resistance to the tools, called CRISPR gene drives, arose at high rates in experiments with Drosophila melanogaster fruit flies, researchers at Cornell University report July 20 in PLOS Genetics. Rates of resistance varied among strains of fruit flies collected around the world, from a low of about 4 percent in embryos from an Ithaca, N.Y., strain to a high of about 56 percent in Tasmanian fruit fly embryos.
“At these rates, the constructs would not start spreading in the population,” says coauthor Philipp Messer, a population geneticist. “It might require quite a bit more work to get a gene drive that works at all.”

Gene drives are basically genetic copy-and-paste machines. These self-perpetuating machines are inherited by more than 50 percent of offspring of an individual carrying a gene drive. Working perfectly, they could transmit to 100 percent of offspring.

In its simplest form, a CRISPR gene drive consists of a piece of DNA that encodes both an enzyme called Cas9, which acts as molecular scissors, and a guide RNA that tells the Cas9 enzyme where to cut. That cutting may disrupt important genes. Researchers are experimenting with this as a way to sterilize malaria-carrying mosquitoes (SN Online: 12/7/15).

Some gene drives also carry a genetic payload. For instance, another approach to fighting malaria is to develop drives that carry genes to “vaccinate” mosquitoes against the disease (SN: 12/26/15, p. 6). Other drives might carry genes that make fluorescent proteins to indicate the gene drive’s presence; Messer and colleagues used such markers to follow two gene drives in fruit flies bred in the lab.
When an organism carrying the tool mates with one that doesn’t, gene drives go to work. Inside the fertilized egg, guide RNAs shepherd Cas9 produced by the engineered mate to a spot where it cuts the other mate’s chromosome.

If everything works correctly, cells repair that break by copying the gene drive onto the cut chromosome. But the slice can also be fixed by gluing the cut ends back together. That regluing sometimes leads to mistakes that destroy Cas9’s cutting site, creating a chromosome that is resistant to the gene drive’s insertion.

In the fruit fly experiments, some mistakes created resistance during or before fertilization. Others took place in early embryos because cells produced Cas9 for too long, allowing the enzyme to chop chromosomes again and again, Messer and colleagues discovered. That was especially a problem when females produced Cas9, they found.

Some uses of gene drives, such as those that would sterilize or kill mosquitoes, can’t tolerate any amount of resistance no matter when it arises, Messer says. Because those types of gene drives damage the organism’s fertility or viability, mosquitoes carrying resistance would have an advantage and quickly outcompete insects vulnerable to the drives.

In a separate study posted June 14 at BioRxiv.org, Messer and colleagues tested several approaches to overcoming gene drive resistance. They found that using multiple guide RNAs and turning on Cas9 only in males could reduce resistance rates.

“This is a very important and elegant set of experiments,” says MIT evolutionary engineer Kevin Esvelt.

But the conclusions aren’t news to most gene drive researchers.

“We’re aware of all these problems, and the essence of how to deal with them hasn’t been changed by these studies,” says geneticist Ethan Bier of the University of California, San Diego. Bier and lab colleague Valentino Gantz created the first gene drive in fruit flies in 2015, and have worked with other researchers to develop gene drives that would prevent mosquitoes from carrying malaria (SN: 12/12/15, p. 16).

Messer’s group is, however, the first to experimentally confirm predictions about resistance and how to avoid it, Esvelt says. “They show what’s been apparent to some people in the field for a very long time.”

Some people might think that high rates of resistance mean that gene drives are safe to release because they won’t spread easily in the wild. But that notion is misguided, says Bier. Even if a gene drive is able to affect only a small percentage of a local pest population, it could still spread around the world, Esvelt adds. “It could still screw us all over in the current form.”

Researchers should continue to conduct gene drive experiments under tight containment, he and Bier caution.

For a glue that holds up inside the body, turn to the humble slug, Arion subfuscus. A new super-sticky material mimics slug slime’s ability to stick on slick wet surfaces and could lead to more effective medical adhesives.

The material has two parts: a sticky layer that attaches to a surface, and a shock-absorbing layer that reduces strain. That makes the adhesive less likely to snap off.

Researchers tested the material as a surgical adhesive in a number of different scenarios: It stuck to pig skin and liver. It latched on to a beating pig’s heart, even when the surface was coated in blood. It sealed up a heart defect, preventing liquid from leaking even when the organ was inflated and deflated tens of thousands of times. And it was less toxic in the body than a commonly used commercialized tissue adhesive, researchers report July 28 in Science.

The researchers hope the material could someday be used in surgical procedures in place of invasive sutures and staples.

The company mice keep can change their behavior. In some ways, genetically normal littermates behave like mice that carry an autism-related mutation, despite not having the mutation themselves, scientists report.

The results, published July 31 in eNeuro, suggest that the social environment influences behavior in complex and important ways, says neuroscientist Alice Luo Clayton of the Simons Foundation Autism Research Initiative in New York City. The finding comes from looking past the mutated mice to their nonmutated littermates, which are usually not a subject of scrutiny. “People almost never look at it from that direction,” says Clayton, who wasn’t involved in the study.
Researchers initially planned to investigate the social behavior of mice that carried a mutation found in some people with autism. Studying nonmutated mice wasn’t part of the plan. “We stumbled into this,” says study coauthor Stéphane Baudouin, a neurobiologist at Cardiff University in Wales.

Baudouin and colleagues studied groups of mice that had been genetically modified to lack neuroligin-3, a gene that is mutated in some people with autism. Without the gene, the mice didn’t have Neuroligin-3 in their brains, a protein that helps nerve cells communicate. Along with other behavioral quirks, these mice didn’t show interest in sniffing other mice, as expected. But Baudouin noticed that the behavior of the nonmutated control mice who lived with the neuroligin-3 mutants also seemed off. He suspected that the behavior of the mutated mice might be to blame.

Experiments confirmed this hunch. Usually, mice form strong social hierarchies, with the most aggressive and vocal males at the top. But in mixed groups of mutated and genetically normal male mice, there was no social hierarchy. “It’s flat,” Baudouin says.

Raised and housed together, the mutated and nonmutated mice all had less testosterone than nonmutated mice raised in genetically similar groups. The testosterone levels in both types of mice were comparable to those found in females — “one of the strongest and most surprising results,” Baudouin says.

The mice’s social curiosity was lacking, too. Usually, mice are interested in the smells of others, and will spend lots of time sniffing a cotton swab that had been swiped across the bedding of unfamiliar mice. But when given a choice of strange mouse scent or banana scent, the nonmutated littermates spent just as much time sniffing banana as did the mutant mice.
When Baudouin and colleagues added back the missing Neuroligin-3 protein to parts of the mutant mice’s brains, aspects of their behavior normalized. The mice became interested in the odor from another mouse’s bedding, for instance. These behaviors also shifted in the mice’s nonmutated littermates. That experiment suggests that the missing protein — and the resulting abnormal behavior of the mutants — was to blame for their littermates’ abnormal actions.

Still, it’s hard to tease apart the mice’s roles, says behavioral neuroscientist Mu Yang of Columbia University. “It is a shared environment, and there is no sure way to tell who is influencing whom, or whether both parties are being impacted.”

Female mice that completely lacked the neuroligin-3 gene also influenced the behaviors of littermates that carried one mutated version of the gene, other behavior tests revealed. More experiments are needed to determine whether the social environment affects male and female mice differently, and if so, whether those differences relate to autism, says Luo Clayton.

For the first time in the United States, researchers have used gene editing to repair a mutation in human embryos.

Molecular scissors known as CRISPR/Cas9 corrected a gene defect that can lead to heart failure. The gene editor fixed the mutation in about 72 percent of tested embryos, researchers report August 2 in Nature. That repair rate is much higher than expected. Work with skin cells reprogrammed to mimic embryos had suggested the mutation would be repaired in fewer than 30 percent of cells.
In addition, the researchers discovered a technical advance that may limit the production of patchwork embryos that aren’t fully edited. That’s important if CRISPR/Cas9 will ever be used to prevent genetic diseases, says study coauthor Shoukhrat Mitalipov, a reproductive and developmental biologist at Oregon Health & Science University in Portland. If even one cell in an early embryo is unedited, “that’s going to screw up the whole process,” says Mitalipov. He worked with colleagues in Oregon, California, Korea and China to develop the embryo-editing methods.

Researchers in other countries have edited human embryos to learn more about early human development or to answer other basic research questions (SN: 4/15/17, p. 16). But Mitalipov and colleagues explicitly conducted the experiments to improve the safety and efficiency of gene editing for eventual clinical trials, which would involve implanting edited embryos into women’s uteruses to establish pregnancy.
In the United States, such clinical trials are effectively banned by a rule that prevents the Food and Drug Administration from reviewing applications for any procedure that would introduce heritable changes in human embryos. Such tinkering with embryo DNA, called germline editing, is controversial because of fears that the technology will be used to create so-called designer babies.

“This paper is not announcing the dawn of the designer baby era,” says R. Alta Charo, a lawyer and bioethicist at the University of Wisconsin Law School in Madison. The researchers have not attempted to add any new genes or change traits, only to correct a disease-causing version of a gene.

In the study, sperm from a man who carries a mutation in the MYBPC3 gene was injected into eggs from women with healthy copies of that gene. Carrying just one mutant copy of the gene causes an inherited heart problem called hypertrophic cardiomyopathy (SN: 9/17/16, p. 8). That condition, which strikes about one in every 500 people worldwide, can cause sudden heart failure. Mutations in the MYBPC3 gene are responsible for about 40 percent of cases. Doctors can treat symptoms of the condition, but there is no cure.

Along with the man’s sperm, researchers injected into the egg the DNA-cutting enzyme Cas9 and a piece of RNA to direct the enzyme to snip the mutant copy of the gene. Another piece of DNA was also injected into the egg. That hunk of DNA was supposed to be a template that the fertilized egg could use to repair the breach made by Cas9. Instead, embryos used the mother’s healthy copy of the gene to repair the cut.

Embryos’ self-healing DNA came as a surprise, because gene editing in other types of cells usually requires an external template, Mitalipov says. The discovery could mean that it will be difficult for researchers to fix mutations in embryos if neither parent has a healthy copy of the gene. But the finding could be good news for those concerned about designer babies, because embryos may reject attempts to add new traits.

Timing the addition of CRISPR/Cas9 is important, the researchers also discovered. In their first experiments, the team added the gene editor a day after fertilizing the eggs. Of 54 injected embryos, 13 were patchwork, or mosaic, embryos with some repaired and some unrepaired cells. Such mosaic embryos probably arise when the fertilized egg copies its DNA before researchers add Cas9, Mitalipov says.

Injecting Cas9 along with the sperm — before an egg had a chance to replicate its DNA — produced only one patchwork embryo. That embryo had repaired the mutation in all its cells, but some cells used the mother’s DNA for repair while others used the template supplied by the researchers.

None of the tested embryos showed any signs that Cas9 was cutting where it shouldn’t be. “Off-target” cutting has been a safety concern with the gene editor because of the possibility of creating new DNA errors.

The study makes progress toward using gene editing to prevent genetic diseases, but there’s still has a long way to go before clinical testing can begin, says Janet Rossant, a developmental biologist at the Hospital for Sick Children and the University of Toronto. “We need to be sure this can be done reproducibly and effectively.”

I heard it for the first time a few days ago: “She’s copying me!” my 4-year-old wailed in a righteous complaint about her little sister. And she most certainly was copying, repeating the same nonsense word over and over. While it was distressing to my older kid, I thought it was funny that it took her so long to realize her sister copies almost everything she does.

This egregious violation occurred just after I had read about an experiment that pitted young kids against bonobos in a test to see who might copy other individuals more. I’ll get right to the punch line: Kids won, by a long shot. The results, published online July 24 in Child Development, show that despite imitation annoying older siblings everywhere, it’s actually really important.

“Imitation is one of the most essential skills for being human,” says study coauthor Zanna Clay, a comparative psychologist at the University of Birmingham and Durham University, both in England. Learning how to talk, operating the latest iPhone and figuring out how to buy bulk goods at the local co-op — these skills all rely on imitation. Not only that, but imitation is also important for cementing social relationships. My daughter notwithstanding, “Humans like to be imitated, and we like those who imitate us,” Clay says.
Clay and her colleague Claudio Tennie tested just how strong the urge to imitate is in 77 children ages 3 to 5 and a group of 46 bonobos ages 3 to 29. In one-on-one trials, the researchers sat next to the kids and bonobos with a small wooden box about the size of a hand. Inside was a treat: a sticker for the kids and a bit of apple for the bonobos.

Before opening the box, the researcher performed nonsensical actions over it, either rubbing the box with the back of the hand and doing a wrist twist in the air or tracing a cross into the top of the box and then tracing the edges.

These hand motions were totally irrelevant to the actual opening of the box. Nonetheless, after seeing the gestures, the vast majority of the kids made the same motions before trying to open their own box. Not a single bonobo, though, copied the irrelevant actions.
What the bonobos did — not copying the meaningless gestures — “is the rational thing to do,” says Clay. “Yet the irrational thing that the kids did is part of the reason why human cultures have evolved so rapidly and so diversely.”

Such excessive imitation, called overimitation, is a special form of copying in which people perform actions that clearly serve no purpose. It may be behind rituals, social norms and language that keep our societies running smoothly.

And it may be unique to humans: Other studies have failed to spot overimitation among chimpanzees and orangutans. These findings hint that our powerful urge to imitate even nonsensical gestures may be one of the things that separate humans from other apes.