A DNA test has found that a blonde-haired, blue-eyed child taken from a Roma family by Dublin's police force is their biological daughter, according to Sky News.

The child had been taken from her parents on Monday, after a neighbor contacted the authorities to report that the child was "living with a large Roma family but looked nothing like any of her supposed siblings," according to the Sunday World.

Doubts had already been raised about the child in Dublin, with The Irish Times reporting that the parents had produced both a birth certificate and a passport to support their claims.

However, the Irish case had followed the removal of another blonde girl from a Roma camp near the town of Larissa in central Greece. That girl, named "Maria," was found not to be a genetic match to the couple who claimed to be her parents.

Together these stories sparked a continent-wide controversy about the possibility that Roma gangs were responsible for the trafficking of stolen children. Many observers, however, worried that the case was leading to a witch hunt against Europe's Roma communities, historically some of the most isolated and persecuted people in Europe.

This is actually the second time this month that Irish police took a child from a Roma family and later returned him, the previous one being a 2-year-old boy in the Midlands region of Ireland. The Guardian reports that it is not clear if a DNA test influenced this decision.

Traveler support group Pavee Point has complained about the Irish cases, saying that the removal of children from their families was being treated as "a matter of first resort and not as a matter of last resort."

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Face shape is largely determined by genetics, yet no two faces are entirely alike. How do genes bring about faces with subtle differences while avoiding dramatic disruptions and facial malformations such as cleft lip and palate? The answer may be in the "junk DNA," a new study has found.

Noncoding DNA, sometimes called junk DNA, refers to sequences in a genome that don't produce proteins, some of which are thought to have no known biological function.

Studying mice, researchers identified more than 4,000 small regions in the genome that are likely a type of noncoding DNA called enhancers, which amplify the expression of a gene. In this case, these regions were active while the face of a mouse embryo developed, according to the study, detailed in the Oct. 25 issue of the journal Science.

Most of these enhancer sequences are found in humans as well, so it is likely that they have similar face-shaping functions in humans, the researchers said. [5 Face-Shaping Genes Identified]

"Our results suggest it is likely there are thousands of enhancers in the human genome that are somehow involved in craniofacial development," study researcher Axel Visel, a geneticist at Lawrence Berkeley National Laboratory's genomics division, said in a statement. "We don't know yet what all of these enhancers do, but we do know that they are out there and they are important for craniofacial development."

To test whether these enhancers are indeed important in shaping the face, the researchers deleted three of the enhancers in mice and compared them with normal mice at 8 weeks of age. The results showed that each enhancer deletion caused a distinct set of differences in the shape of the face — for instance, causing an increase or decrease in facial length and an increase or decrease in the width of various parts of the face, such as the base of the skull or the palate.

In the study, to avoid the challenge of recognizing individual mouse faces, the researchers created 3D images using a process called microcomputed tomography to link changes in face shape with alterations in the function of each of the enhancers.

Identifying enhancers that regulate a gene's activity is challenging, because such enhancers aren't necessarily located next to their target gene; rather, they could be acting from "long-distance" locations in the genome.

Many of the genetic defects that cause facial flaws such as clefts of the lip or palate have been identified, but only a small number of genes have been implicated in normal variation of the face's shape, the researchers said.

Studying genes that drive normal facial variations would offer an opportunity for human geneticists to look for mutations specifically in enhancers that may play a role in birth defects, Visel said.

Email Bahar Gholipouror follow her @alterwired. Follow LiveScience @livescience, Facebook& Google+. Original article on LiveScience.

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New research shows that not all of our body's tissues age at the same rate. Steve Horvath, a geneticist at UCLA's medical school, has discovered a new way to measure the biological age of human tissue, according to a study published last week in the journal Genome Biology.

To create the measurement, Horvath looked at data from 8,000 samples of 51 different cells and tissues. He studied methylation — a process that changes the structure of DNA and turns genes on and off. Newborn cells are turned into specialized tissues this way.

But once tissue-specific cells are created, they also get exposed to things that age them and add methyltations and other modifications to their DNA. For example, heart cells have gone through different changes to their DNA than skin cells have.

"My goal in inventing this clock is to help scientists improve their understanding of what speeds up and slows down the human aging process,"Horvath said in a press release.

The ticking rate of our biological clock does not stay the same throughout our life. Horvath discovered that the clock moves much faster when we're first born and our bodies are growing rapidly. The clock slows down and adopts a more constant rate by the time we turn 20.

He also found that different tissues from the same person age at different rates, breasts being some of the "oldest" tissues in the body. Horvath found that healthy breast tissue is about two to three years older than the rest of a woman's body, but healthy tissue near cancerous tissue is on average 12 years older than a woman's body.

Most of the breast tissue samples in his study were cancerous tissues, and there is a possibility that cancer made the DNA age older than healthy breast tissue would normally be. This might be the reason the woman's breast tissue in the diagram below is so much older than the rest of her tissues. To test this further, Horvath said more healthy breast tissue samples will need to be collected and measured from all different stages of a woman's life: before puberty, after puberty, pregnancy, and menopause. 

Horvath measured the age of cancer cells too. The biological clock showed that tumor tissue is on average 36 years older than normal, healthy human tissue. This might explain why cancer becomes a bigger risk the older we get. The study also showed that a woman's breast tissue ages several years faster than the rest of her body and may explain why breast cancer is the most common type of cancer in women.

These DNA ages of tissues are different for men and women. In the future, the clock will become more accurate as more data samples are analyzed, but for now here's a body snapshot of how our different tissues fare over time based on one woman and one man.

SEE ALSO: Women's Breasts Age Faster Than Other Parts Of Their Bodies

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The DNA gleaned from two ancient Siberian skeletons is related to that of modern-day Native Americans and western Eurasians, new research suggests.

The genetic material from the ancient Siberians provides additional evidence that the ancestors of Native Americans made the arduous trek from Siberia across the Bering Strait into the Americas.

But it also reveals there were multiple waves of migrations in Asia around this time, said Mark Hubbe, a biological anthropologist at The Ohio State University who was not involved in the study. [Top 10 Mysteries of the First Humans]

"This brings a new level of complexity to what we think happened in Asia," Hubbe told LiveScience.

Ancient migrations

Several genetic clues indicate that Native Americans came from a population that once inhabited Siberia and crossed the Bering Strait between 20,000 and 15,000 years ago.

Between 1928 and 1958, Russian scientists excavated a Siberian site in Mal'ta, Russia, near Lake Baikal, and unearthed a trove of Venus figurines along with the skeleton of a juvenile, all dating back approximately 24,000 years. The figurines were intriguing, because they were similar in style to ones made by European hunter-gatherers.

European relatives

To trace the ancestry of these ancient people, Maanasa Raghavan, a researcher at the University of Copenhagen in Denmark, and colleagues managed to extract DNA from the ancient skeleton.

The team found that the mitochondrial DNA, or genetic material carried in the cytoplasm of cells that is passed through the maternal line, came from a lineage known as U, which is rare or extinct now, but was once common in hunter-gatherers from Europe during the Paleolithic Period.

The team also sequenced the male sex chromosome (Y chromosome), which traces the paternal lineage of the skeleton. On the paternal side, the ancient boy came from a lineage known as R, which is now found in southern Siberia and western Eurasia. The R lineage is also a sister group to one common in Native Americans.

The researchers estimate that between 14 and 38 percent of Native American ancestry could come from this ancestral population, with the remaining portion coming from ancient East Asians.

DNA from a 17,000-year-old skeleton found in south central Siberia showed signs of being from the same genetic lineage as the Ma'lta specimen.

Previously, researchers had thought that people migrated from Europe into east Asia, and then entered Siberia from the south in a fairly linear expansion, Hubbe said. But the new results suggest the Siberian inhabitants may have come from the West, he said. That suggests Asia experienced multiple, crisscrossing waves of migration, he said.

However, because the skeletons are so old, it's important to rule out the possibility that the DNA was contaminated, Theodore Schurr, an anthropologist at the University of Pennsylvania who was not involved in the study, wrote in an email.

And having so few ancient samples paints a very limited picture of a complicated genetic history.

"Although these results are intriguing and important, we should be cautious in inferring too much from just two genomes," said Jennifer Raff, an anthropologist at the University of Texas at Austin who was not involved in the study. "I would certainly like to see a more geographically and temporally widespread sampling of Siberian genomes in order to better understand their population history."

The findings were published today (Nov. 20) in the journal Nature.

SEE ALSO: Improve Your Health By Eating The Right Ratio Of These Fats

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It's that time of the year. In addition to listing the biggest science breakthroughs of 2013, the editors of the journal Science have named their "areas to watch in 2014."

Here are their four predictions about things to come in the months ahead.

1. A new era of neutrino detection.

If 2013 was the year of the Higgs boson, then 2014 will be the year of the neutrino. The nearly massless particle has no electric charge, but can be found everywhere, passing through our bodies and entire planets every second. Because neutrinos are invisible and interact weakly with other particles, they are hard to detect. But if pinned down, the elusive particles serve as silent messengers for radiation, which can be helpful in the hunt for cosmic rays and possibly monitoring nuclear weapons in the future. This year, scientists at the IceCube Neutrino Observatory, an underground telescope in Antarctica, detected high-energy neutrinos from beyond our solar system for the first time, an achievement that scientists hailed for opening up a "new era of neutrino astronomy."

2. A better way to study and treat diseases using genome sequencing.

In 2014, more and more researchers and doctors will use genome sequencing to treat cancer patients, newborns with life-threatening problems, and even healthy patients, an advancement made possible by cheap and faster sequencing machines. Sequencing advances will help us know and understand the genome — the strands of DNA that give our cells the instructions that influence everything from our hair color to diseases. When a patient's genome is analyzed, the knowledge gained can lead to more effective, customized medical treatments. Knowing what changes to the genome make cells cancerous can help oncologists defeat the tumor with tailor-made chemotherapy.

3. The end of research on chimpanzees.

2013 was a liberating year for chimpanzees, and it's only going to get better. In June, the U.S. government announced it would release all but 50 chimpanzees used for research to sanctuaries. Around the same time, the U.S. Fish and Wildlife Service proposed that captive chimps be listed as endangered, which would make it harder for labs to use the animals for research and to test new drugs. Both decisions reflect growing public opposition to the use of chimpanzees in experiments.

4. New details about the universe.

How did the universe begin, and then become what it is today? Those are just some of the questions that the European Space Agency's Planck space telescope aims to answer after more than four years of studying cosmic microwave background (CMB) — radiation from the Big Bang that preserves a picture of what the universe was like when it was only 380,000 years old. Astronomers released the most detailed picture of the universe as baby in March. The telescope was turned off into October 2013, but a new map that could potentially "contain traces of gravity waves that rippled through the universe in the first sliver of a second," is forthcoming.

SEE ALSO: The Biggest Scientific Breakthroughs Of 2013

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Once upon a time in the 1960s, scientists thought the human genome might contain as many as 2 million genes, units of DNA that code for proteins.

But ever since then, the estimated number has been steadily shrinking. A new study suggests that the human genome could contain as few as 19,000 protein-coding genes, fewer than nematode worms.

By the time the Human Genome Project began in the late 1990s, the Physics arXiv Blog reports, the highest estimates of the number of protein-coding genes put the number at 100,000, and estimates continue to fall:

In 2001, the initial sequence of the human genome cut the figure dramatically. The International Human Genome Sequencing Consortium put it at 30,000 while a rival group led by Craig Venter estimated the number at 26,000. In 2004, the final draft of the human genome reduced the figure even further to around 24,500 and in 2007 further analysis suggested that it was more like 20,500. And that’s where the figure has sat. Until now.

Researchers came up with the new estimate, detailed in a paper submitted to Molecular Biology and Evolution, by performing a variety of analyses such as filtering "out the human genes that are not present in other species and do not have a structure likely to code for a protein."

Of course, research has shown that more complex organisms don't require more genes. As Medium points out, a water flea has 31,000 genes, the most in any animal, while the record for the largest genome is thought to be held by a rare flowering plant native to Japan called Paris japonica.

All this raises the question: How does the human genome create as much complexity as it does: for instance the brain? Nobody knows exactly, but the answer would be invaluable. Non-coding regions of DNA, which make up a majority of the genome, play a huge role that is only just beginning to be understood.

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The genetic analysis of a male hunter-gatherer who lived in modern-day Spain around 7,000 years ago suggests that the man had dark skin and hair, but blue eyes.

Here's an artist's impression of what that man might have looked like:

The new genetic analysis was performed on DNA extracted from the tooth of a male skeleton, called La Brana 1, found in 2006 in a cave system in the Cantabrian Mountains of Spain. The findings from this analysis, published Jan. 26 in the journal Nature, are surprising because it shows that the light skin of Europeans evolved much more recently than once thought.

Researchers previously believed that early Europeans lost the dark skin pigmentation of their African ancestors some 40,000 years ago as they began moving north to regions with less sunlight.

Lighter skin absorbs more ultraviolet rays, an important adaptation for making Vitamin D in sun-poor environments. Our body naturally produces Vitamin D when ultraviolet rays in sunshine strike the skin. Vitamin D is essential for the absorption of calcium, to keep our bones healthy.

Study co-author Carles Lalueza-Fox, a paleogenomics researcher at Pompeu Fabra University in Spain told LiveScience: "It was assumed that the lighter skin was something needed in high latitudes, to synthesize vitamin D in places where UV light is lower than in the tropics."

But La Brana's dark European skin, which was still around as late as 7,000 years ago, shows that the move to higher-latitudes may not be the reason that modern-day Europeans have fair skin. Instead, the cause could be linked to diet, researchers said.

The analysis is the first of a genome of a hunter-gather from the Mesolithic period — the time between 10,000 and 5,000 years ago — to be fully sequenced.

The Mesolithic period, or Middle Stone Age was followed by the Neolithic era, when hunter-gatherers became farmers and started eating a lot more grains.

This dietary switch could be the reason Europeans developed lighter skin.

"In the food-production theory, the cereal-rich diet of Neolithic farmers lacked vitamin D,"LiveScience explains, "so Europeans rapidly lost their dark-skin pigmentation only once they switched to agriculture, because it was only at that point that they had to synthesize vitamin D from the sun more readily."

In addition, the researchers found that the La Brana hunter-gather was lactose intolerant and not able to digest starchy food as well as Neolithic farmers, "supporting the hypotheses that these abilities were selected for during the later transition to agriculture," the authors wrote in their study.

SEE ALSO: What The Human Face Might Look Like 100,000 Years From Now

SEE ALSO: How Beer Created Civilization

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Current human DNA tests take two to three weeks to be completed, and must be sent into an accredited laboratory. But a new rapid test, which could analyze human DNA in 90 minutes in the field, is nearly complete, Pentagon and industry officials told USA Today.

The change to an exponentially faster, mobile test will have huge implications for for law enforcement, war crimes investigations and immigration, Chris Asplen, the executive director of the Global Alliance for Rapid DNA Testing, told the paper.

"When it comes to solving crime (not proving it in court but actually using DNA to find the killer, rapist, burglar, etc.) the value of DNA as an investigative tool is directly proportional to the speed at which it can be leveraged in any given investigation," Asplen said.

The Pentagon will finish evaluating the test by this June, prototypes of which are being developed by NetBio of Waltham, Mass. The departments of Homeland Security and Justice are working on their own tests.

Current laws that governs how DNA tests can be used — particularly the DNA Identification Act of 1994 — did not anticipate rapid analysis. "The language requires that only DNA tests done in an accredited laboratory may be entered" into a national database, Asplen said. "That language will have to changed."

[USA Today]

SEE ALSO: This Is A Picture Of A Strand Of DNA

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By comparing the Neanderthal genome to modern human DNA, the authors of two new studies, both published on Wednesday, show how DNA that humans have inherited from breeding with Neanderthals has shaped us.

Modern humans, Neanderthals, and their sister lineage, Denisovans, descended from a common ancestor. The ancestors of modern humans broke off from this single branch more than 500,000 years ago. The Neanderthals split from the Denisovans some time later. The Neanderthals formed their own lineage that lived in Europe and Asia from around 200,000 years ago to 30,000 years ago. There's also a period when scientists believe that Neanderthals and ancient humans overlapped and interbred.

Researchers from Harvard Medical School, who published their findings in Nature, previously showed that the ancestors of modern humans interbred with Neanderthals between 80,000 years ago and 40,000 years ago, before Neanderthals went extinct.

Any given person of European or Asian descent owes at least 1% of their DNA to the Neanderthal genome. 

How much Neanderthal is in all of us?

The Harvard team found that remnants of Neanderthal DNA are not distributed evenly across the modern human genome. Some regions are rich with Neanderthal DNA — suggesting these traits were important for survival as humans evolved — while other spots have little or no traces of Neanderthal genetic material.

In the Nature study, scientists compared the DNA of more than 800 people from Europe and East Asia and nearly 200 people from sub-Saharan Africa with the genome sequence of a 50,000-year-old Neanderthal fossil.

Indigenous Africans have little or no Neanderthal DNA since their ancestors did not breed with Neanderthals who lived in Europe and Asia, according to researchers. The Harvard team determined that specific genetic material was passed down from Neanderthals if it appeared in some non-Africans and the Neanderthal sequence, but not the sub-Saharan Africans.

A related study published in Science, led by Benjamin Vernot from the University of Washington, used a different technique to draw similar conclusions. They estimate that any living human today who is not from Africa inherited 1% to 3% of their genomes from Neanderthals, while the total amount of Neanderthal genome that survived across all modern populations is 20%, the report says.

The influence of the Neanderthal gene

The Harvard team found that Neanderthal genes are concentrated in parts of modern human DNA that affect the skin and hair. These inherited characteristics probably helped ancient humans to survive as they moved north out of Africa and into colder environments, where things like thicker hair and tougher skin would be useful.

The researchers also found remnants of Neanderthal DNA in modern humans that influence conditions like type 2 diabetes, Crohn's disease, lupus, biliary cirrhosis, and smoking behavior, but their impact on human health — whether it's good or bad — is not clear. 

"Every piece of this story that we uncover tells us more about our ancestors' genetic contributions to modern human health and disease," Irene A. Eckstrand of the National Institutes of Health's National Institute of General Medical Sciences, which partially funded the research published in Nature, said in a statement.

Missing Neanderthal DNA

The Harvard team also found regions of modern human DNA where hints of Neanderthal ancestry were practically non-existent, specifically in genes that are most active in the male testes and genes on the X chromosome — sex genes.

When Neanderthals and ancient humans hooked up after several hundred thousands of years of being apart, their genomes had changed enough that they were almost biologically incompatible, according to the Nature paper.

Some of the Neanderthal genes weren't the best fit with our human ancestors, and created problems like reduced fertility in male offspring, the researchers said. 

In order for neanderthal-human hybrids to breed with our human ancestors successfully, they had to eliminate these Neanderthals genes, which is why there are gaps in what Neanderthal DNA ended up in our genome.

Regions of the modern human genome where Neanderthal DNA is absent suggests that "the introduction of some of these Neanderthal mutations was harmful to the ancestors of non-Africans and that these mutations were later removed by the action of natural selection," Sriram Sankararaman, lead author of the Nature paper from Harvard Medical School, said in a statement

SEE ALSO: DNA Of Ancient Human Spawns New Theory Of Why Europeans Became White

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As of Feb. 3, 2014, both state governments and the U.S. government have exonerated 1,304 innocent prisoners since 1989, according to a new report from the National Registry for Exonerations. And 87 of them were freed in 2013 alone — the highest number ever recorded. 

Contrary to what people may think, DNA testing isn't behind most of these exonerations. Instead, judges and prosecutors have become increasingly willing to reconsider old convictions even without new DNA evidence, potentially because of  growing awareness about wrongful convictions.

"The trend I've seen the most obviously is more prosecutors and judges are less freaked out about a prisoner's potential innocence and more willing to look into the matter now," University of Michigan law professor and editor of the National Registry of Exonerations Samuel Gross told Business Insider.

When DNA evidence became admissible in court in 1985, it shocked the system, especially in cases of sexual assault, according to Gross. Because DNA evidence has freed some inmates with lengthy sentences, people might assume testing leads to most exonerations today.

But there have always been more non-DNA exonerations than DNA exonerations. The gap has actually increased over time, as this graph shows:

Although we see a rapid increase in the number of total exonerations since 2011, the number of DNA exonerations (blue line) has dropped steadily for the last three years, while the number of non-DNA exonerations (red line) spiked during the same period. 

One major factor, according to the National Registry for Exonerations, is driving the increase in non-DNA convictions: greater cooperation from law enforcement, especially under often ignored circumstances like those without biological evidence, cases with light sentences, and judgements based on plea bargains. 

Not everyone agrees that greater cooperation from law enforcement is a recent development though.

"We always reviewed big cases, multiple murders or high-profile cases," Scott Burns, executive director of the National District Attorneys Association told NPR. "What you're seeing now is that it's institutionalized — it's given a name, probably a line item on a budget in a large office — and that's good as well."

Regardless of reasons for the increase in exonerations, the type of crime also plays an interesting role. Consider the chart below:

Of the 87 exonerations in 2013, 17%, a record number, occurred in cases in which the defendants pleaded guilty, according to the report. These circumstances most likely arise during plea bargains, when defendants plead guilty in exchange for reduced sentences. For some time now, the vast majority of defendants across the U.S. end up pleading out, Gross pointed out.

Naturally, legal resources first go to prisoners facing execution (8% of exonerations, according to the report) or life in prison. As a result, the great majority of known exonerations apply to murder and rape, "the most serious common crimes of violence with the harshest sentences," according to the report.

Gross also noted exonerations in murder and rape cases decreased for the first time in 2013. 

Researchers also considered timing when interpreting the stats. The charts below shows the average time an exonerated prisoner will spend behind bars based on his or her crime.

As you'll see from the data, inmates exonerated in 2013 spent an average of about 12 years in prison. That means in recent years prosecutors and judges became more willing to look into cases more than a decade old.

"This is really a journey into the past — around the turn of the century," Gross explained.

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At 18, Elana Simon has beaten cancer and is even a co-author of a study about her disease, which was published Thursday in the journal Science.

Six years ago, Simon was diagnosed with a rare liver cancer, called fibrolameller. Simon's cancer was caught in time and she had surgery to remove the tumor, according to the Associated Press. But hers was a lucky case. Because the disease only affects about 200 people in the United States each year, it's not well understood, making it difficult to detect and treat.

So while still in high school, Simon took it upon herself to begin researching the difference between these tumor cells and healthy liver tissues. The teenager got help from her father, Sanford Simon, who runs a laboratory at Rockefeller University and is the study's senior author, as well as her pediatric surgeon, Michael LaQuaglia of Memorial Sloan Kettering. The New York Genome Center was also involved in the research.

Researchers obtained 15 tumor samples that had been surgically removed from people with fibrolamellar cancer and sequenced their genomes.

One mutation — which was present in all 15 patients — really popped out. It involved a piece of DNA that "had been broken and rejoined, creating a mutated gene that had the potential to wreak havoc in the bodies of individuals with the gene," according to a media release from Rockefeller University.

Researchers are now trying to understanding how the broken gene causes the tumors by testing how it changes human liver cells in the lab.

The results are encouraging, but this hardly the end of the mystery. According to the Wall Street Journal, La Quaglia says that "finding such a mutation doesn't mean it definitely causes the cancer and more research needs to be done to establish its role."

Simon, now cancer-free and finishing up her senior year in high school, plans to attend Harvard in the fall, according to the WSJ. 

SEE ALSO: What Cheap Genome Sequencing Means For The Future Of Medicine

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Wiping fingerprints and cleaning up stray hairs may not be enough to remove evidence that you've been at a crime scene.

According to microbial ecologist Rob Knight, speaking at TED 2014 in Vancouver on Wednesday, the bacteria on your hands leave a "print" on a computer mouse that can be identified with up to 95% certainty— and potentially used by forensic investigators. 

Two humans have 99.9% similar DNA, but could have wildly different bacteria living on their skin. The species of bacteria found on their palms would only be about 13% similar, according to a study that Knight co-authored in 2010.

The study tested whether or not skin bacteria could be easily recovered from surfaces like keyboards and computer mice — and if that bacteria would identify the individuals who had left it behind. 

Back in 2010, the new technique was 70-90% accurate, but Knight's talk suggests that the rate of accuracy is rapidly improving. 

How your bacteria to identify you

When blood, hair, semen, saliva, or tissue is found at a crime scene, investigators can use it to examine the DNA of the human who left it behind. A good DNA sample is considered incredibly accurate evidence, but samples can be damaged, misleading, or improperly handled. In some cases, it's impossible to find DNA at a crime scene at all. 

But if someone leaves behind traces of their skin's unique bacterial colonies when they touch things, the DNA from those traces could potentially be matched back to the individual it came from. Such a match could serve was a confirmation of human DNA evidence or provide new leads in cases where no DNA exists. 

To test this theory, Knight and his collaborators compared the bacteria living on three keyboards to the bacteria living on their owners' fingers. They were different enough to show who had used which keyboard.

Then they checked other public keyboards, to see if the original three volunteers in the study could be linked to any of those. They couldn't be.

The unique bacterial traces that researchers had swabbed from the keyboards were still there, even after sitting in an average temperature room for two weeks — suggesting that the sampling technique might be usable in slow-moving forensic investigations. Or crime scenes stumbled on after the fact.

In a follow up study the researchers tested the hands and computer mice of nine additional people and let the computer mice sit untouched for more than 12 hours before collecting bacterial samples.

In every case, the bacteria on the mouse matched up with the bacteria on its owner's hand, significantly more so than with samples from 270 hands that had never touched the mouse.

Proceed with caution

The authors of the study caution that forensic analysis requires considerable testing and refinement before it can be regularly used in criminal investigations. And right now, a good DNA sample is still more accurate.

But they said that their results show that analyzing bacteria could provide independent confirmation of other forensic findings like fingerprints or human DNA, and could provide evidence in cases where those don't exist. In the future, a refined version of microbe-based forensics could potentially provide a more "personally identifying" picture of an individual than other commonly accepted techniques.

Plus, this technology has already been tested where it counts, as Knight explained in his TED talk. "It was featured on CSI Miami, so you really know it's true," he said.

SEE ALSO: The 40 Science Experts Will Completely Revamp Your Social Media Feed

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In the not-too-distant future, it may be possible to create a digital mugshot from DNA.

Researchers from Pennsylvania State University, led by anthropologist Mark Shriver, published a study this week on their attempts to understand how our genetic code influences our facial structure.

That research, say the authors of the study, will one day make it possible to predict criminals’ appearances based only on, say, a strand of hair left at a crime scene.

Although things like sex, skin tone, and eye and hair colors are relatively easy to predict from DNA, facial structures have always been more of a mystery. Faces are complicated, and how one part is shaped can strongly influence other parts of the face. To tackle such a complex project, the researchers took pictures of 532 people of mixed European and West African ancestry from three different regions. They then made 3D images of those faces, overlaying each of them with 7,000 data points to determine variation among faces. Nature explains what they did next:

Next, the authors compared the volunteers’ genomes to identify points at which the DNA differed by a single base, called a single nucleotide polymorphism (SNP). To narrow down the search, they focused on genes thought to be involved in facial development, such as those that shape the head in early embryonic development, and those that are mutated in disorders associated with features such as cleft palate. Then, taking into account the person’s sex and ancestry, they calculated the statistical likelihood that a given SNP was involved in determining a particular facial feature.

In the end, the scientists found 24 SNPs on 20 different genes, all of which control facial structure to some extent. Of course, a person’s entire appearance isn’t solely dictated by his or her DNA, and current methods for testing DNA are by no means falling by the wayside. “Human facial diversity is substantial, complex, and largely scientifically unexplained,” write the researchers in the study’s abstract, published in PLOS Genetics. Still, their predictive model can already create a crude facial model based only on genetic code, and the project’s usefulness for detectives is already being tested. Shriver is already working with police to find a serial rapist in Pennsylvania.

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Scientists have inserted DNA-based nanobots into a living cockroach, which are able to perform logical operations. Researchers say the nanobots could eventually be able to carry out complex programs, to diagnose and treat disease.

These DNA machines (or origami robots, so-called since they can unfold and deliver drugs stored within) carry fluorescent markers, allowing researchers to tell where in the roach's body they are traveling and what they are doing. Incredibly, the "accuracy of delivery and control of the nanobots is equivalent to a computer system,"New Scientist reported. A study describing the advance was published this week in Nature Nanotechnology.

The nanobots can interact with one another, and were shown to be able to perform simple logical operations, for example releasing a molecule stored within upon command. Or, as the researchers put it: "The interactions generate logical outputs, which are relayed to switch molecular payloads on or off." It's a little hard to believe or wrap your head around, but then again, scientists for years have been able to use DNA to store large amounts of information, and DNA bots are nothing new. The researchers get the bots to work by exploiting the bind properties of DNA:

When it meets a certain kind of protein, DNA unravels into two complementary strands. By creating particular sequences, the strands can be made to unravel on contact with specific molecules – say, those on a diseased cell. When the molecule unravels, out drops the package wrapped inside.

"This is the first time that biological therapy has been able to match how a computer processor works," study co-author Ido Bachelet, from the Institute of Nanotechnology and Advanced Materials at Bar Ilan University in Israel, told New Scientist. The scientists said it should be possible to improve the computing power of the nanobots to approach that of an "8-bit computer, equivalent to a Commodore 64 or Atari 800 from the 1980s."

While the bots cannot currently be inserted into mammals, due to their more advanced immune systems that can recognize and target these foreign particles, they can probably be modified to do so. "There is no reason why preliminary trials on humans can't start within five years," Bachelet said.

[New Scientist]

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New genetic evidence casts further doubt on the authenticity of a grisly French relic: a gourd long believed to be stained with the blood of Louis XVI.

Scientists sequenced the genome from dried blood inside the 200-year-old gourd and found that it didn't match with the DNA signatures of the king's ancestry, nor did it seem to carry the code for Louis XVI's celebrated traits, like his imposing height and blue eyes.

Deposed during the French Revolution, Louis XVI was executed by guillotine in January 1793, months before his wife, Marie Antoinette, fell victim to the Reign of Terror, too.

According to legend, witnesses soaked up the king's blood with handkerchiefs after his beheading. An inscription on the elaborately decorated gourd claims the vessel held one of those bloody cloths. [See Photos of Louis XVI's Embalmed Head & Gourd]

Last year, a group of scientists compared the DNA signatures from blood found in the gourd with the DNA of three modern male relatives of Louis XVI from different branches of the Bourbon line. The Y chromosomes from the three men matched one another, but not the blood. This revelation, published in the European Journal of Human Genetics, sparked a new investigation.

"When the Y chromosome of three living Bourbons was decoded, and we saw that it did not match with the DNA recovered from the pumpkin in 2010, we decided to sequence the complete genome and to make a functional interpretation in order to see if the blood could actually belong to Louis XVI," Carles Lalueza-Fox, of the Spanish National Research Council (CSIC), said in a statement.

Based on their newly sequenced genome, Lalueza-Fox and colleagues think whomever the blood in the gourd belonged to didn't look like Louis XVI in terms of physical appearance or genealogical heritage.

Louis XVI was known for his towering stature; he may have stood over 6 feet (185?centimeters) tall. Though scientists do not entirely understand the genetic basis for height, Lalueza-Fox and colleagues wrote that the genome pieced together from the gourd blood was not consistent with that of a very tall person, but rather better matched someone with only slightly above-average height for the day. The king also had blue eyes, while the person who left their blood on the gourd more likely had brown eyes, the researchers say.

What's more, the genome had some markers of northern Italian heritage. This finding "cannot be easily reconciled with the known Louis XVI family history, given that just one in 16 great-great-grandparents — Victor Amadeus II, Duque of Savoy (1666–1732) — has some possible northern Italian ancestry," the researchers wrote.

The findings were published online today (April 24) in the journal Scientific Reports.

Follow Megan Gannon on Twitter and Google+. Follow us @livescience, Facebook & Google+. Original article on Live Science.

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The first living organism to carry and pass down to future generations an expanded genetic code has been created by American scientists, paving the way for a host of new life forms whose cells carry synthetic DNA that looks nothing like the normal genetic code of natural organisms.

Researchers say the work challenges the dogma that the molecules of life making up DNA are "special".

Organisms that carry the beefed-up DNA code could be designed to churn out new forms of drugs that otherwise could not be made, they have claimed.

"This has very important implications for our understanding of life," said Floyd Romesberg, whose team created the organism at the Scripps Research Institute in La Jolla, California. "For so long people have thought that DNA was the way it was because it had to be, that it was somehow the perfect molecule."

From the moment life gained a foothold on Earth the diversity of organisms has been written in a DNA code of four letters. The latest study moves life beyond G, T, C and A – the molecules or bases that pair up in the DNA helix – and introduces two new letters of life: X and Y.

Romesberg started out with E coli, a bug normally found in soil and carried by people. Into this he inserted a loop of genetic material that carried normal DNA and two synthetic DNA bases. Though known as X and Y for simplicity, the artificial DNA bases have much longer chemical names, which themselves abbreviate to d5SICS and dNaM.

In living organisms, G, T, C and A come together to form two base pairs, G-C and T-A. The extra synthetic DNA forms a third base pair, X-Y, according to the study in Nature. These base pairs are used to make genes, which cells use as templates for making proteins.

Romesberg found that when the modified bacteria divided they passed on the natural DNA as expected. But they also replicated the synthetic code and passed that on to the next generation. That generation of bugs did the same.

"What we have now, for the first time, is an organism that stably harbours a third base pair, and it is utterly different to the natural ones," Romesberg said. For now the synthetic DNA does not do anything in the cell. It just sits there. But Romesberg now wants to tweak the organism so that it can put the artificial DNA to good use.

"This is just a beautiful piece of work," said Martin Fussenegger, a synthetic biologist at ETH Zurich. "DNA replication is really the cream of the crop of evolution which operates the same way in all living systems. Seeing that this machinery works with synthetic base pairs is just fascinating."

The possibilities for such organisms are still up for grabs. The synthetic DNA code could be used to build biological circuits in cells which do not interfere with the natural biological function; scientists could make cells which use the DNA to manufacture proteins not known to exist in nature. The development could lead to a vast range of protein-based drugs.

The field of synthetic biology has been controversial in the past. Some observers have raised concerns that scientists could create artificial organisms which could then escape from laboratories and spark an environmental or health disaster.

More than 10 years ago, the scientsist Eckard Wimmer, at Stony Brook University, in New York, recreated the polio virus from scratch to highlight the dangers.

Romesberg said that organisms carrying his "unnatural" DNA code had a built-in safety mechanism. The modified bugs could only survive if they were fed the chemicals they needed to replicate the synthetic DNA. Experiments in the lab showed that without these chemicals, the bugs steadily lost the synthetic DNA as they could no longer make it.

"There are a lot of people concerned about synthetic biology because it deals with life, and those concerns are completely justified," Romesberg said. "Society needs to understand what it is and make rational decisions about what it wants."

Ross Thyer, at the University of Texas, in Austin, suggested the synthetic DNA could become an essential part of an organism's own DNA. "Human engineering would result in an organism which permanently contains an expanded genetic alphabet, something that, to our knowledge, no naturally occurring life form has accomplished.

"What would such an organism do with an expanded genetic alphabet? We don't know. Could it lead to more sophisticated storage of biological information? More complicated or subtle regulatory networks? These are all questions we can look forward to exploring."

This article originally appeared on guardian.co.uk

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DNA tests have shown that hair samples claimed to have come from yetis, sasquatch and bigfoot actually came from other species currently in the area or from their ancestors.

Two Himalayan alleged “yeti” samples tested by scientists have been found to have come from an ancient bear.

This is the first systematic DNA survey of these elusive primates to be published in a peer-reviewed journal.

Most samples attributed to yeti/sasquatch were identified as known species living in their normal geographical range.

Dr Brian Sykes of the University of Oxford and colleagues report their findings in theProceeding of the Royal Society B.

Dr Sykes says the results end decades of ambiguity about sample identification.

In an editorial in the Royal Society, Norman MacLeod of the UK Natural History Museum says cryptozoologists, or those who seek ancient creatures thought to be extinct or to be legends such as mermaids, must now either accept these findings or show where they are in error.

Cryptozoology supporters have claimed that the scientific establishment has failed to live up to the tenets of its own philosophy by not acknowledging the evidence they have offered for the existence of large species presently unknown to science.

MacLeod says the evidence is typically anecdotal observations recounted by individuals backed up on occasion by photographic and/or sound recordings, usually of quite poor quality.

MacLeod says scientific researchers have regarded this as hopelessly ambiguous and not suitable for rigorous hypothesis testing.

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Researchers have known for a while that many people alive today carry genes from human species other than Homo sapiens--the result of ancient interbreeding with Neanderthals and Denisovans. They have even worked out that this admixed DNA must often be doing something particularly useful, because its pattern suggests natural selection is actively retaining it. The specifics, though, have not been clear. But in one case they now are, for it is because of these occasional Denisovan ancestors that Tibetans thrive in Tibet.

The plateau of Tibet is one of the most hostile places people inhabit. The air is thin and the weather cold. The locals, nevertheless, do well. And Rasmus Nielsen of the University of California, Berkeley, and his colleagues at BGI, a Chinese DNA-sequencing laboratory, suggest in this week's Nature that one of the genes which lets them do so is Denisovan.

The Denisovans are a mysterious branch of Homo. They were identified in 2010 by an analysis of the DNA of a bone discovered in a cave (occupied in the 18th century by a hermit called Denis) in the Altai Mountains in Russia. This bone was thought, when found, to be either Neanderthal or modern human, but the analysis showed it was neither. In the wake of that finding, a small percentage of Denisovan DNA has been discovered in various groups of people in Asia and the Pacific islands, Tibetans among them.

The gene Dr Nielsen has been investigating is a version of EPAS-1. This encodes part of a protein called hypoxia-inducible transcription factor 2-alpha. Transcription factors activate other genes, and this one (as its name suggests) does so in response to low oxygen levels. When that happens, it is responsible for stimulating the production of red blood cells, the growth of capillaries and the production of proteins involved in energy generation.

Everybody has some version of EPAS-1, and so everybody can acclimatise to high altitude. But such acclimatisation comes at a price: the extra red cells make blood stickier and more likely to clot, which increases the risk of thrombosis. Except, curiously, in Tibetans. They are well acclimatised without having noticeably raised red-cell counts. And that effect has been tracked down to the particular version of EPAS-1 in their chromosomes.

Dr Nielsen and his team wanted to study the Tibetan version more closely, so they sequenced both it and the area around it in detail. When they did this they discovered that the block of DNA it inhabits is so similar to its Denisovan equivalent that it must originally have come from a mating (maybe more than one) between a Denisovan and Homo sapiens.

Moreover, it is pretty much only Tibetans who have this version of the gene. Dr Nielsen established in 2010 that about 90% of them do, compared with fewer than 10% of their Han Chinese neighbours. He estimated that the altitude-friendly version became this widespread in Tibet in a mere 3,000 years.

His latest study also looked at other groups with Denisovan genes, and could find no trace at all in them of the Denisovan form of EPAS-1. Probably, it is useless or worse at low altitudes, so natural selection has removed it. But, though the Altai Mountains are not as high as Tibet, it might well have been useful there.

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Jay Johnson's DNA was cut into pieces. Tiny molecular scissors chopped it into slices the cell couldn't readily repair. The cell did its best at a speedy patch-up job, but the gene was left effectively useless. As the battered remnants were about to be infused back into Johnson's body, he sat in the quiet hospital room at the University of Pennsylvania and contemplated his fate. "God, if this really works," he thought, "this will be amazing."

Jay Johnson was part of a clinical trial testing a radical technology that precisely cuts and modifies DNA that may cure his HIV. The new treatment is being tested on diseases long thought to be beyond the reach of genetic therapies, including HIV, brain cancer, and Alzheimer's disease. Inspired by nature and engineered by researchers, scientists have discovered three classes of proteins that cut and paste DNA, all known by their somewhat cumbersome acronyms: ZFNs, TALENs and CRISPRs.

ZFNs: Zinc Finger Nucleases

When exploring the genetic code of the African clawed frog, scientists noted an odd protein tightly bound to the frog's DNA. When they mapped the 3D architecture of the protein, they were surprised to see elongated loops resembling fingers, grasping the frog's genes with extraordinary strength. Holding the loops together was a stable zinc ion. Because of its unusual hand-like structure, they named the protein zinc finger.

A decade later Srinivasan Chandrasegaran, then a postdoctoral fellow at Johns Hopkins, wondered how he could make practical use of the sticky proteins. The problem was that each zinc finger recognized only a tiny chunk of DNA, about three bases. This kept the collection from being specific enough to target genes in people. If he wanted to use the proteins to target a specific piece of DNA, he needed more length. Chandra, as his friends called him, had a simple solution. He stitched six of the proteins together so that instead of just three bases, he had eighteen, enough to recognize a fragment of a gene.

But binding the DNA wasn't enough. He also had to figure out a way to alter it. Chandra decided to borrow an enzyme used by bacteria to cut out viruses from their genetic code. Called restriction endonucleases, this clever defense mechanism is an ideal way to cut DNA. Chandra chose the FokI restriction enzyme, known for its ability to make a clean break. Chandra combined the DNA gripping ability of the zinc fingers with the DNA cutting enzyme. A zinc finger nuclease (ZFN) was born.

To make the technology safe in humans, two ZFNs are delivered directly to the nucleus of the cell, where they bind to two separate pieces of DNA surrounding their genetic 'prey.' Then the cutting enzymes dimerize, locking onto each other. Only after they're locked together can the enzymes engage, snipping through the DNA. The cell has trouble repairing this kind of double-stranded break, so the end result is a mangled and dysfunctional gene. A similar process can be used to repair a gene instead of breaking it, allowing genetic material to be inserted into the cell. In a major breakthrough, scientists using this method can now target just about any gene.

A small California biotech, Sangamo Biosciences, has developed ZFNs commercially. Sangamo is currently conducting clinical trials for therapies for everything from HIV to hemophilia to Alzheimer's disease.

Breakthroughs seem imminent. In March, an article published in the New England Journal of Medicine reported results from a Phase II clinical trial for HIV. This trial treated HIV by cutting the CCR5 gene. CCR5 is kind of like an appendix--it's not necessary for human health. On the other hand, it's vital for HIV. The vast majority of HIV strains need the CCR5 receptor to enter human cells. Thanks to a mutation called Δ32, people with a defective gene are resistant to the virus, which is another reason why Sangamo hopes they can treat HIV by carving up the gene. Their study found that in the 12 people tested, the technology is safe. It's still very early, but the data is promising, showing a rise in cells modified by the ZFNs corresponding to a decrease in HIV. Jay Johnson is one of the 12 receiving this cutting edge therapy in hopes of curing his HIV.

TALENs: Transcriptor Activator-Like Effector Nucleases

While ZFNs came from a small, aquatic frog, TALENs were adapted from bacteria, specifically a plant pathogen named Xanthomomas, which preys upon the plant's genetic code.

Feng Zhang was a graduate student at MIT and frustrated by the complexity of genome modification. Because ZFNs grasp DNA with their finger-like elongations, they are difficult to design and expensive to produce. To get around this problem, Zhang turned to TALENs.

There are no finger-like structures in these proteins. Instead the DNA binding is reminiscent of how it occurs naturally in our cells. The amino acids that make up the TALEN precisely align with the DNA sequences they cut. Changing the amino acids in the TALEN changes which sequences it binds to, making customized alterations of the proteins far simpler. Even better, each TALEN recognizes 17 bases of DNA, plenty long enough to recognize a piece of human DNA. That's part of the reason TALENs have taken the lead from ZFNs.

TALENs use the same FokI enzyme that cuts through DNA in ZFNs, which makes it relatively easy to design a TALEN capable of specifically binding human DNA. In both processes, two binding agents flank the gene and then move in, the enzyme creating a double-stranded break the cell can't recover from.

While ZFNs have been around for a decade, TALENs are relatively new. They don't have the rigorous safety testing available in humans ZFNs do. But while the research is ongoing, where TALENs have proven useful is in disease modeling. Scientists have created disease cell lines, identical except for a single TALEN-created mutation. It's an ideal system for reverse genetics, tracing a lone genetic mutation to its effect in the cell. Disease models have now been made for hepatitis C, blood cholesterol levels, insulin sensitivity, and others. TALENs are effective at genome editing, and because of their innate simplicity, may can be used in humans.

CRISPRs: Clustered Regularly Interspaced Short Palindromic Repeats

The newest kids on the DNA chopping block are CRISPRs. Like TALENs, CRISPRs arise from bacterial defenses against viruses. They are are small repeating palindromes spaced throughout the bacterial genome. In between these repeating sequences are "guides," small chunks of genetic code that match those of the invaders. They lead the CRISPR to the right spot in the DNA. With their help, the CRISPRs bind to the target DNA, forming a tight structure with the intruder's genetic code. Instead of using the FokI nuclease like ZFNs and TALENs, CRISPRs use Cas9, a similar bacterial enzyme, capable of making deep cuts in DNA. But the effect of the enzyme is the same: because it creates a double-stranded break, the cell can't repair it. Just like with ZFNs and TALENs, the gene is taken out of commission. (Also like ZFNs and TALENs, DNA can be added at the cut site to potentially repair a gene.)

Of the three, CRISPRs have the most elegant design. There's no need for complicated protein structure here, just clean lines of genetic code tied to the cutting enzyme. The simplicity creates a streamlined cell delivery, which is a big advantage. Yet in some ways, the sheer simplicity is frightening. The system doesn't have the same safeguards that prevent against off-target effects, like if the protein goes rogue and potentially cuts at an unintended site.

Feng Zhang has been at the forefront of CRISPR development, rapidly producing mutant cell lines and mouse models. In just one year, researchers have used CRISPRs to target genes in models of cystic fibrosis, sickle cell anemia, and autism. While developing animal models of disease used to take months and even years, it's now being done in weeks.

CRISPR technology is moving ahead at lightning speed. This February, scientists in China published their study of CRISPRs in monkey embryos. They targeted physiological genes involved in development. The two infant primates are now under close observation. Remarkably, the researchers were able to alter two genes in a single step. Despite the worries of off-target effects, none have been observed. Instead, other fears have been raised. Some groups are concerned that this technology is likely to expand the role of animal testing. One thing is certain: With the use of CRISPRs in primate models, the technology is inching closer to use in humans.

The potential of CRISPRs is clear in a recent Nature Biotechnology study. Researchers at MIT used the technology to correct a mutation in the FAH gene in a mouse model of a rare human genetic disorder called tyrosinemia. The disorder causes an excess of the amino acid tyrosine, which can lead to liver failure and even death. Humans with the disease take a drug to control the production of the amino acid. In the mouse model, animals with the disorder controlled the disease with the same drug. But after CRISPRs were delivered to the animals, the modified cells proliferated, eventually making up one-third of all the animals' liver cells and ultimately curing the three mice tested.

Genomic surgery has the potential to treat an incredible variety of human disease. But along with this potential comes concerns, both ethical and scientific, of forever altering a person's DNA.

Back at the University of Pennsylvania hospital, Jay Johnson was optimistic as the needle pricked into his vein to deliver his own chopped up DNA back into his bloodstream. It took only a few minutes for the ZFN treated cells to be infused into his body. Ten minutes later he started to feel extremely cold. Twenty minutes later the cramping began. He felt like his "whole body was a big ball of knots." Jay Johnson was the only person in the group of twelve to experience an adverse reaction. His experience is an important reminder that these techniques are not just about the conceptual beauty and function of DNA-cutting proteins. When put into practice, the techniques are being used on people—who by necessity are guinea pigs for the emerging technology.

Still, despite his adverse reaction, Jay Johnson is healthy and would gladly sign up for another clinical trial. He's not fearful of the technique, only hopeful for the potential benefits. His participation in research is, he says, "Not only for myself, but for science."

This article originally appeared on Popular Science

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People may unsuspectingly choose friends who have some DNA sequences in common with them, a new analysis finds.

Researchers compared gene variations between nearly 2,000 people who were not biologically related, and found that friends had more gene variations in common than strangers.

The study lends a possible scientific backing for the well-worn clichés, "We're just like family," or "Friends are the family you choose," the researchers said.

"Humans are unique in that we create long-term connections with people of our species," said Nicholas Christakis, a social scientist at Yale University involved in the study. "Why do we do that? Why do we make friends? Not only that, we prefer the company of people we resemble."

The researchers did the study because they wanted "to provide a deep evolutionary account of the origins and significance of friendship," Christakis said.

The new study is based on data from the Framingham Heart Study, which is a large, ongoing study looking at heart disease risk factors in the people living in one town: Framingham, Massachusetts. The researchers looked at data on people's DNA, as well as who was friends with whom.

After analyzing almost 1.5 million markers of gene variations, the researchers found that pairs of friends had the same level of genetic relation as people did with a fourth cousin, or a great-great-great grandfather, which translates to about 1 percent of the human genome.

The most common gene shared by friends was the "olfactory" gene, which is involved in a person's sense of smell.

Although 1 percent may not sound like much, Christakis said in a statement, "to geneticists it is a significant number.

He said, "Most people don't even know who their fourth cousins are, yet we are somehow, among a myriad of possibilities, managing to select as friends the people who resemble our kin."

The findings suggest that choosing friends who share similar genes is a behavior that may have contributed to human evolution, the researchers said.

"Imagine you're the first person on the planet to evolve the capacity to speak," Christakis told Live Science. "Do you think that mutation would increase your Darwinian evolution? No. Because you would have no one to speak to."

The usefulness of a speech gene would depend on whether a friend shared the same gene, Christakis said. In other words, there's an advantage to people's genes evolving in relation to those of their friends.

The researchers acknowledged some caveats to their conclusions. For example, it may be that people form friendships with those of the same ethnicities, they said. But to take this into account, the researchers studied participants from a homogeneous group of people, from a Caucasian background.

The researchers compared pairs of strangers within this population as well as friends, using a "friendship score," which predicts whether two people could be friends based on their genetic background.

"What we're reporting is the difference between people who are friends, and people who could be friends, all from the same ancestry," said study researcher James Fowler, a professor of medical genetics at the University of California, San Diego.  

The study was published today (July 14) in the journal Proceedings of the National Academy of Sciences.

Follow Jillian Rose Lim @jillroselim & Google+. Follow us @livescience, Facebook & Google+. Original article on Live Science.

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