Scientists say they’ve figured out a way to extract tiny traces of ancient human DNA from dirt in caves that lack skeletal remains.

The technique could be valuable for reconstructing human evolutionary history, according to the study published Thursday in the journal Science.

That’s because fossilized bones, currently the main source of ancient DNA, are scarce even at sites where circumstantial evidence points to a prehistoric human presence.

“There are many caves where stone tools are found but no bones,” said Matthias Meyer, a geneticist at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, who co-authored the study.

The researchers collected 85 sediment samples from seven caves in Europe and Russia that humans are known to have entered or even lived in between 14,000 and 550,000 years ago.

By refining a method previously used to find plant and animal DNA, they were able to search specifically for genetic material belonging to ancient humans and other mammals.

Scientists focused on mitochondrial DNA, which is passed down the maternal line, because it is particularly suited to telling apart closely related species. And by analyzing damaged molecules they were able to separate ancient genetic material from any contamination left behind by modern visitors

The researchers found evidence of 12 mammal families including extinct species such as woolly mammoth, woolly rhinoceros, cave bear and cave hyena.

By further enriching the samples for human-like DNA, however, the scientists were able to detect genetic traces of Denisovans — a mysterious lineage of ancient humans first discovered in a cave in Siberia — and Neanderthals from samples taken at four sites.

Crucially, one of the sites where they discovered Neanderthal DNA was a cave in Belgium, known as Trou Al’Wesse, where no human bones had ever been found, though stone artefacts and animal bones with cut marks strongly suggested people had visited it.

Eske Willerslev, who helped pioneer the search for DNA in sediment but wasn’t involved in the latest research, said the new study was an interesting step, but cautioned that it’s difficult to determine how old sediment samples found in caves are.

“In general (it) is very disturbed and unless you can show that’s not the case you have no idea of the date of the findings,” said Willerslev, an evolutionary geneticist at the University of Copenhagen, Denmark.

Meyer said the new method greatly increases the number of sites where archaeologists will be able to find genetic evidence to help fill gaps in the history of human evolution and migration, such as how widespread Neanderthal populations were and which stone tools they were able to make.

Scientists may also be able to greatly expand their limited knowledge of the Denisovans, whose DNA can still be found in Melanesians and Aboriginal Australians today, by using the new procedure.

“In principle, every cave where there’s evidence of human activity now offers this possibility,” Meyer told The Associated Press.—AP

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The inexpensive technique, which can have broad applications in monitoring and protecting aquatic life, was conducted in the East River, which is actually an inlet, and the Hudson River last year.

“By conducting a series of tests over time, collecting surface water from the same point on both the Hudson and East Rivers once a week for six months, we’ve successfully demonstrated a novel way to record fish migration,” said the researchers at New York’s Rockefeller University, whose work appeared in the latest issue of scientific journal PLOS One.

The weekly “snapshots” came from water samples filtered to concentrate the DNA left behind by the slimy surface of fish as they swim, or from their droppings. The DNA was then extracted and sequenced, with the results matched against an online public reference library.

The researchers’ data largely corresponded to findings from years of migration studies conducted by fishnet trawls, the traditional method of tracking marine migration. This is much more labor intensive, expensive and harmful to fish.

“Environmental DNA” sampling will be an easy way to estimate the population and distribution of fish and other aquatic species in bodies of water from rivers and lakes to seas and oceans, the authors said.

“It amazes me that we can get the same information from a small cup of water and a large net full of fish,” said Mark Stoeckle, lead author and senior research associate for the Program for the Human Environment at Rockefeller University.

“Our work also offers clear new insight into the durability of DNA in the water, which persists despite currents and tides with a ‘Goldilocks’ quality just right for research,” he said, telling AFP that experiments carried out in aquariums showed DNA survives for a few days or even a week.

Stoeckle’s study was inspired by French scientist Pierre Tabarlet of the University of Grenoble, who was the first to show that small volumes of water contained enough DNA fragments to detect dozens of species of fish.

The New York research obtained DNA from 42 species of fish, including 81 percent of those known to be common to the area, such as herring, striped bass and oyster toadfish — a flattened brown creature with bulging eyes and a mouthful of teeth.

Uncommon species were also detected, while some DNA came from fish frequently consumed by New Yorkers but not naturally present in the East and Hudson Rivers, such as salmon, tilapia and red snapper.

The researchers determined these latter samples likely entered the water after passing through humans and being discharged in wastewater.

The eDNA technique could allow researchers to identify endangered species sold in markets and restaurants, said Jesse Ausubel, another Rockefeller University researcher and study co-author.

Next steps involve refining the technology by comparing more eDNA results against the findings from traditional studies carried out with nets and sonar.

“It is unclear, for example, if 100 DNA ‘reads’ indicate the presence of one fish or 10 fish,” researchers said.

Ausubel said that stage will take five to 10 years but “the upside potential is just enormous.”

“It could easily improve the rationality with which fish quotas are set and the quality and reliability of their monitoring around the world,” he said.

For Tony MacDonald, director of the Urban Coast Institute at Monmouth University, the science of eDNA sampling “represents a potentially important advance in our capability to detect, understand and more effectively and efficiently manage fisheries and marine biodiversity.”—AFP

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Despite ethical and safety concerns, investors are attracted by synthetic biology’s wide market potential and the plummeting cost of DNA synthesis, which is industrialising the writing of the genetic code that determines how organisms function.

While existing biotechnology is already used to make medicines like insulin and genetically modified crops, synthesizing whole genes or genomes gives an opportunity for far more extensive changes.

Matt Ocko, a Silicon Valley venture capitalist whose past investments include Facebook, Uber and Zynga , believes the emerging industry has passed the “epiphany” moment needed to prove it can deliver economic value.

“Synthetic biology companies are now becoming more like the disruptive, industrial-scale value propositions that define any technology business,” he said.

“The things that sustain and accelerate this industry are today more effective, lower cost, more precise and more repeatable. That makes it easier to extract disruptive value.”

Ocko, whose Data Collective firm has invested in companies including organism design firm Gingko Bioworks and bioengineer Zymergen, is not alone.

Other tech veterans backing the new wave of “synbio” start-ups include Jerry Yang, Marc Andreessen, Peter Thiel and Eric Schmidt, famous for their roles at Yahoo, Netscape, PayPal and Google respectively.

UNCERTAINTIES REMAIN

Experts meeting in London this week said the science toolkit was improving fast and the cost of synthesising DNA was now 100 times cheaper than in 2003, although uncertainties remain about regulation and the public’s appetite for tinkering with life.

The global conference hosted by Imperial College London, bringing together scientists and money people, comes four weeks after researchers announced they were close to building a complete artificial genome for baker’s yeast.

This ambitious project has brought complex artificial life a big step closer because yeast is a eukaryote, an organism whose cells contain a nucleus, just like human cells.

The yeast work shows how DNA can be manipulated on a large scale, with genetic code increasingly treated like a programming language in which binary 1s and 0s are replaced by DNA’s four chemical building blocks, abbreviated as A, T, G, C.

A growing emphasis on computing is closing the gap between biology and traditional tech, even though this is an area that remains unpredictable, variable and complex.

“The intersection of biology and technology is a difficult place to be because of different cultures and languages, but I think we are breaking through some of those barriers,” said Thomas Bostick, former head of the U.S. Army Corps of Engineers who now leads biotech firm Intrexon’s environment unit.

The idea that engineering life can be broken down into data and coding is part of the appeal for tech investors.

“DNA is seen as the next programmable matter and that is what a lot of the Silicon Valley investors are excited about,” said John Cumbers, founder of synthetic biology network SynBioBeta.

“They’ve witnessed the power of software over the last 25 years and they are looking for the next big thing.”

Data from SynBioBeta shows a record $1.21 billion was invested in the sector worldwide in 2016, a threefold increase from five years earlier, while the number of firms in the sector has almost doubled to 411. For a graphic see http://tmsnrt.rs/2n3VYuO

A range of companies are springing up, from those producing new chemicals for industry to providers of DNA synthesis and related software, like U.S.-based Twist Bioscience and Britain’s Synthace.

Work is also advancing by leaps and bounds in the complementary area of gene editing now being embraced by many of the world’s top drugmakers.

CHANGE OF TACK

The current product focus represents a change of tack from the first widely tipped application of synthetic biology in making biofuels from engineered algae.

In the event, algal biofuel proved a lot harder to scale up than expected and a tumbling oil price during the Great Recession of the late 2000s undercut the business model.

Drew Endy of Stanford University believes the case for using synthetic biology to take on gasoline never stacked up.

“Why would you bank your whole platform on a bulk high-volume, low-price, low-margin product? It’s baffling, not strategic,” he said.

Today’s synbio firms are looking at more niche and expensive products, such as potent painkillers and cancer medicines made in yeast cells – or fabrics with novel properties, although some have only reached demonstration stage.

California-based Bolt Threads recently debuted a limited edition $314 necktie made from yeast-derived spider’s silk and Japanese rival Spiber has made a concept piece spider-silk parka jacket.

Boston-based Gingko Bioworks, meanwhile, is developing a rose oil for French fragrance house Robertet and Switzerland’s Evolva has developed a vanillin, or vanilla extract, that, unlike most vanilla flavouring, is not made from petrochemicals.

In some areas – especially anything to do with food or the environment – synthetic biology is already running into criticism. Friends of the Earth was quick to condemn the new yeast-derived vanillin as “extreme” genetic engineering.

Other controversies appear inevitable as synthetic biologists push the envelope with more extreme projects, such as a Harvard team’s “Jurassic Park”-style proposal to resurrect the woolly mammoth by adapting the Asian elephant genome.

Intrexon’s Bostick, whose firm is releasing millions of genetically manipulated mosquitoes in Brazil in a bid to slash populations of Zika-carrying insects, believes each synthetic biology scheme has to prove its benefits outweigh the risks.

“There are always pros and cons, and we owe people a fair and balanced assessment.”—Reuters

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These “mini brains” offer insight into the processes with which individual nerve cells organise themselves into our highly complex tissues, the researchers said.

“The method thus opens up completely new opportunities for investigating disorders in the architecture of the developing human brain,” said lead researcher Julia Ladewig from the Institute of Reconstructive Neurobiology at the University of Bonn in Germany.

For the study, the researchers converted skin cells from patients into so-called induced pluripotent stem cells.

From these ‘jack-of-all-trades’ cells, they generated the brain organoids, according to the study published in the journal Cell Reports.

In their work, the scientists investigated the Miller-Dieker syndrome. This hereditary disorder is attributed to a chromosome defect.

As a consequence, patients present malformations of important parts of their brain.

“In patients, the surface of the brain is hardly grooved but instead more or less smooth,” Vira Iefremova, who is also from University of Bonn, explained.

What causes these changes has so far only been known in part.

The researchers produced induced pluripotent stem cells from skin cells from Miller-Dieker patients, from which they then grew brain organoids.

“We were able to show that the stem cells divide differently in these patients,” Philipp Koch, Associate Professor at the University of Bonn.

“In healthy people, the stem cells initially extensively multiply and form organised, densely packed layers. Only a small proportion of them becomes differentiated and develops into nerve cells,” Koch said.

The researchers believe that organoids could herald a new era in brain research.

“And if we better understand the development of our brain, new treatment options for disorders of the brain can presumably arise from this over the long term,” Ladewig said.—IANS

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Lifestyle and heredity get the most blame but new research suggests random chance plays a bigger role than people realize: Healthy cells naturally make mistakes when they multiply, unavoidable typos in DNA that can leave new cells carrying cancer-prone genetic mutations.

How big? About two-thirds of the mutations that occur in various forms of cancer are due to those random copying errors, researchers at Johns Hopkins University reported Thursday in the journal Science.

Whoa: That doesn’t mean most cases of cancer are due solely to “bad luck.” It takes multiple mutations to turn cells into tumors — and a lot of cancer is preventable, the Hopkins team stressed, if people take proven protective steps.

Thursday’s report is an estimate, based on a math model, that is sure to be hotly debated by scientists who say those unavoidable mistakes of nature play a much smaller role.

But whatever the ultimate number, the research offers a peek at how cancer may begin.

And it should help with the “why me” question from people who have “done everything we know can be done to prevent cancer but they still get it,” said Hopkins’ Dr. Bert Vogelstein, a pioneer in cancer genetics who co-authored the study. “They need to understand that these cancers would have occurred no matter what they did.”

GENE MUTATIONS CAUSE CANCER BUT WHAT CAUSES THE MUTATIONS?

You might inherit some mutations, like flaws in BRCA genes that are infamous for causing aggressive breast and ovarian cancers in certain families.

More commonly, damage is caused by what scientists call environmental factors — the assault on DNA from the world around us and how we live our lives. There’s a long list of risks: Cigarette smoke, UV light from the sun, other forms of radiation, certain hormones or viruses, an unhealthy diet, obesity and lack of exercise.

Then there are those random copy errors in cells — what Vogelstein calls our baseline rate of genetic mutations that will occur no matter how healthy we live.

One way to think of it: If we all have some mutations lurking in our cells anyway, that’s yet another reason to avoid known risks that could push us over the edge.

HOW CELLS MAKE TYPOS

New cells are formed when an existing cell divides and copies its DNA, one cell turning into two. Every time DNA is copied, about three random mutations occur, Vogelstein said.

We all harbor these kinds of mutations and most don’t hurt us because they’re in genes that have nothing to do with cancer or the body’s defense mechanisms spot and fix the damage, said Dr. Otis Brawley of the American Cancer Society, who wasn’t involved in the new research.

But sometimes the errors hit the wrong spot and damage genes that can spur cancerous growth or genes that help the cell spot and fix problems. Then the damaged cells can survive to copy themselves, allowing important mutations to gradually build up over time. That’s one reason the risk of cancer increases with age.

THE STUDY FINDINGS

Thursday’s study follows 2015 research by Vogelstein and statistician Cristian Tomasetti that introduced the idea that a lot of cancer may be due to “bad luck,” because those random DNA copying mistakes are more common in some kinds of cancer than others. Cancer prevention advocates worried the idea might sway people to give up on healthier lifestyles.

This time around, the duo analyzed mutations involved in 32 types of cancer to estimate that 66 percent of the gene flaws are due to random copy errors. Environmental and lifestyle factors account for another 29 percent, while inherited genes made up just 5 percent of the mutations.

DIFFERENT ORGANS, DIFFERENT RISKS

The same person can harbor a mix of mutations sparked by random DNA mistakes, heredity or environmental factors. And which is the most common factor differs by cancer, the Hopkins team said.

For example, they estimate that random cell errors account for 77 percent of critical mutations in pancreatic cancer — while still finding some caused by lifestyle risks like smoking. And the random DNA mistakes caused nearly all the mutations leading to childhood cancers, which is not surprising because youngsters have had little time to be exposed to environmental risks.

In contrast, most lung cancer mutations were the result of lifestyle factors, mainly from smoking. And while lung tissue doesn’t multiply frequently, the small number of mutations caused by chance DNA errors might explain rare cases of never-smokers who still get sick.

“This paper is a good paper,” said the cancer society’s Brawley. “It gives prevention its due respect.”

OTHER SCIENTISTS SEE MORE TO THE STORY

Estimates from Britain suggest 42 percent of cancers are potentially preventable with a healthy lifestyle, and the Hopkins team says their mutation research backs that idea.

But Dr. Yusuf Hannun, Stony Brook University’s cancer center director, contends that’s just the number known to be preventable today — researchers may discover additional environmental risks we can guard against in the future.

He said the Hopkins paper exaggerates the effect of the unavoidable DNA mistakes. His own 2015 research concluded they account for 10 to 30 percent of cancer cases.—AP

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The gene, known as TMEM106B, accelerates normal brain aging in older people by up to 12 years, said the report in the journal Cell Systems.

The gene generally starts to affect people around 65, particularly in the frontal cortex, which is responsible for higher mental processes like concentration, planning, judgment and creativity.

“If you look at a group of seniors, some will look older than their peers and some will look younger,” said co-author Asa Abeliovich, professor of pathology and neurology in the Taub Institute for Alzheimer’s Disease and the Aging Brain at Columbia University Medical Center.

“People who have two ‘bad’ copies of this gene have a frontal cortex that, by various biological measures, appears 12 years older that those who have two normal copies.”

Researchers found the gene by analyzing genetic data from autopsied human brain samples taken from 1,904 people without any apparent disease.

Until age 65, “everybody’s in the same boat, and then there’s some yet-to-be-defined stress that kicks in,” said Abeliovich.

“If you have two good copies of the gene, you respond well to that stress. If you have two bad copies, your brain ages quickly.”

Other individual genes have been previously found which raise the risk of neurodegenerative disorders, such as apolipoprotein E (APOE) for Alzheimer’s disease.—AFP

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The international team used computers to create laboratory-made versions of the threadlike structures that carry genetic code inside cells.

Synthesizing genomes may alarm some who see biotechnologists “playing God” but scientists view it as a logical extension of existing genetic engineering that is already used routinely to make drugs like insulin, as well as genetically modified crops.

The international group previously took seven years to build the first yeast chromosome in 2014. The addition of another five demonstrates accelerating progress in the field of synthetic biology, which promises a new era of designer life-forms.

New strains of synthetic yeast could be put to work to produce novel medicines, chemicals and biofuels. The work also serves as a foundation for a more ambitious project to synthesize a human genome in the next 10 years.

Yeast is surprisingly closely related to humans at the genetic level, sharing 26 percent of its genes with our species, although the human genome is around 250 times larger.

While other teams have synthesized bacterial and viral DNA, the Synthetic Yeast Genome Project is the first to do this in a eukaryote, an organism whose cells contain a nucleus, like human cells.

Writing in the journal Science on Thursday, scientists from the United States, China, Britain and France involved in the latest work reported that the yeast containing artificial genetic material was fit and healthy, just like normal yeast.

Jef Boeke of New York University’s Langone Medical Center, one of the lead researchers, said this adaptability augured well for building a raft of different designer genomes to address unmet needs in medicine and industry.

“(It) suggests that we can continue to be even bolder in our future designs and make more dramatic changes and really explore the limits of what you can do with a genome to have the yeast do our bidding and make more useful products,” he said.

Tom Ellis of Imperial College London said it was “a landmark moment for the worldâ€s biggest synthetic biology project”.

Genomes are made up of DNA, a sequence of four different chemical building blocks abbreviated as A, T, G, C. Scientists have learnt to manipulate pairings of these chemicals to rewrite genetic code.

The natural baker’s yeast genome consists of 12 million base pairs but the synthetic version is about 8 percent smaller as scientists have removed some non-coding “junk” DNA.

Techniques for synthesizing DNA are improving all the time and costs are falling. Today, the cost of making each base pair of DNA chemicals is around 10 cents, which researchers said would allow the synthesis of whole genomes to become routine.—Reuters

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The study showed that a gene called ATF4 plays a key role in Parkinson’s disease, acting as a ‘switch’ for genes that control mitochondrial metabolism for neuron health.

When the expression of ATF4 is reduced in flies, expression of these mitochondrial genes drops.

This drop results in dramatic locomotor defects, decreased lifespan, and dysfunctional mitochondria in the brain.

“Interestingly, when we overexpressed these mitochondrial genes in fly models of Parkinson’s, mitochondrial function was re-established, and neuron loss was avoided,” said Miguel Martins from the University of Leicester in London.

By discovering the gene networks that orchestrate this process, the researchers have singled out new therapeutic targets that could prevent neuron loss.

Some forms of Parkinson’s are caused by mutations in the genes PINK1 and PARKIN.

Fruit flies with mutations in these genes accumulate defective mitochondria and exhibit Parkinson’s-like changes, including loss of neurons, the researchers said.

For the study, published in the journal Cell Death and Differentiation, the team used PINK1 and PARKIN mutant flies to search for other critical Parkinson’s genes and using a bioinformatics approach discovered that the ATF4 gene plays a key role.

“Studying the roles of these genes in human neurons could lead to tailored interventions that could one day prevent or delay the neuronal loss seen in Parkinson’s,” Martins added.

Previous studies have showed several genes that protect neurons in Parkinson’s disease, creating possibilities for new treatment options.—IANS

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Using gene-editing techniques, this could help to boost breeding of endangered birds, as well as improving production of commercial hens, researchers wrote in the study published in the journal Development.

A team led by the University of Edinburgh’s Roslin Institute used a genetic tool called TALEN to delete a section of chicken DNA. They targeted part of a gene called DDX4, which is crucial for bird fertility.

“These chickens are a first step in saving and protecting rare poultry breeds from loss in order to preserve future biodiversity of our poultry from both economic and climate stresses,” said lead researcher Mike McGrew from the University of Edinburgh’s Roslin Institute.

Researchers noted that donor primordial germ cells from other breeds could be implanted into the gene-edited chickens as they are developing inside an egg.

The surrogate hens would then grow up to produce eggs containing all of the genetic information from the donor breeds.

The surrogate chickens are the first gene-edited birds to be produced in Europe.—IANS

Image: The Roslin Institute

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A beacon is an online web service that allows researchers to determine whether an institution has particular genomic data in its data set.

The aim of the Indian beacon is to address the gap in shared Indian genomics data, which helps scientists better understand disease and develop more effective drug delivery systems and therapeutics.

“Genomics is the science that will define healthcare in our lifetime. Solving healthcare problems at scale is exceptionally important for India to ensure quality of life for our 1.3 billion citizens. Cutting-edge genomics will provide truly innovative solutions that will benefit individuals and the population as a whole,” said Dinesh Patnaik, Indian deputy high commissioner to the UK, at the launch in Cambridge.

The Indian beacon joins those already on the Wellcome Genome Campus supplied by EMBL-EBI and the Wellcome Trust Sanger Institute in Hinxton, Cambridgeshire.

Cambridge-based Global Gene Corp (GCC) is based at the Wellcome Genome Campus and is co-founded by alumni from the Indian Institute of Technology, Harvard and National University of Singapore with the mission to “democratise genomics”.

Sumit Jamuar, chairman & CEO of GCC, creator of the ggcINDIA beacon, said: “Indian genomics data is one of the biggest missing pieces in the genomics puzzle. The promise of precision medicine can only be realised with usable and sharable genomics data.

“As a member of GA4GH, our ggcINDIA beacon will start to address the lack of shared Indian genomics data to enable researchers globally to accelerate development of precision medicine.”—PTI

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