Woolly Mammoth DNA To Be Cloned, Then Joined With Elephant DNA To Create New Creature

A team of international scientists are extracting high quality DNA from the remains of a woolly mammoth that lived 43,000 years ago, with the aim of joining it with the DNA of an elephant, they told The Siberian Times Thursday. Results from the necropsy of the woolly mammoth in Yakutsk, Sakha Republic — due to wind up Saturday after more than 10 months of analysis — has caused “palpable excitement” within the team of scientists, hailing from Russia, the UK, the United States, Denmark, South Korea, and Moldova.

“The data we are about to receive will give us a high chance to clone the mammoth,” Radik Khayrullin, vice president of the Russian Association of Medical Anthropologists, told The Siberian Times in Yakutsk. He urged responsibility in any attempts to clone the woolly mammoth. “It is one thing to clone it for scientific purpose, and another to clone for the sake of curiosity,” he said. Geneticists are reportedly searching for an Asian elephant whose egg could be injected with cloned material from the woolly mammoth. That same or another female elephant would be the surrogate mother of the resulting fertilzed egg. Any resulting wooly mammoth/elephant hybrid baby would have to be female, since there is no y-chromosome material from the wooly mammoth, who was a female. At any rate, such a procedure would take decades to perfect, experts said.

Semyon Grigoriev, head of the Museum of Mammoths of the Institute of Applied Ecology of the North at the North Eastern Federal University, told The Siberian Times that because the evolutionary paths of the mammoth and the elephant diverged so long ago, cloning will be challenging. However, the samples will allow geneticists to completely decode the DNA of the mammoth.

The Russian woolly mammoth was between 50 and 60 years old when she died. Though the upper part of her carcass has been devoured by animals, the lower part (the legs and a detached trunk) was “astonishingly, very well preserved,” Viktoria Egorova, chief of the research and clinical diagnostic laboratory of the medical clinic of North-Eastern Federal University told The Siberian Times. The mammoth, which may have met her demise by falling through a hole in the ice, lay in the permafrost of Maly Lyakhovskiy Island until it was found last May.
The mammoth as a species disappeared from Siberia at the end of the Pleistocene era about 10,000 years ago, with warming climate and hunting by humans thought to be contributing factors. An isolated population of woolly mammoths persisted on Wrangel Island in the Arctic Ocean, between the Chukchi and East Siberian Seas, until around 4,000 years ago.

‘We have dissected the soft tissues of the mammoth, and I must say that we didn’t expect such results,” Dr. Egorova told The Siberian Times. The necropsy revealed well-preserved muscle and adipose tissues (loose connective tissues which store fat), and “blood vessels with strong walls,” and within intact blood vessels themselves, for the first time ever in an ancient carcass of an extinct animal, erythrocytes, or red blood cells that contain the oxygen-carrying molecule hemoglobin, Egorova told The Siberian Times.

Biologists have been able to discern cells within the woolly mammoth’s blood that had been in the process of migration (involved in growth and healing) within the lymphoid tissue when the woolly mammoth died, a finding Egorova termed “another great discovery.” The intestines contained remains of the vegetation eaten by the mammoth; its multi-chambered stomach was preserved, as was a kidney, which contained fragments Egorova suspects are kidney stones.

One of the Canadian scientists looking foward to anayzing blood samples from the woolly mammoth is Kevin Campbell, a University of Manitoba professor of environmental and evolutionary physiology who has rearched and written on the subject of hemoglobin in woolly mammoths. In 2010, Campbell wrote a letter in the journal Nature Genetics describing how he had genetically resurrected and analyzed woolly mammoth hemoglobin “to reveal for the first time…the structural underpinnings of a key adaptive physiochemical trait in an extinct species.” He discovered that whereas the efficiency of hemoglobin in elephants to offload oxygen to respiring cells is hampered at low temperatures, mammoth hemoglobin has amino acid substitutions that “provide a unique solution to this problem and thereby minimize energetically costly heat loss.” Since then, Campbell has recreated the hemoglobin of woolly mammoths.

Campbell, who described himself as “bitterly disappointed” that he couldn’t make the necropsy of the woolly mammoth in Russia, said he would be doing the next best thing next week; joining one of his collaborators, Roy E. Weber at Aarhus University, Denmark who will be returning from Russia with some muscle and blood samples extracted from the woolly mammoth. If nothing else, the blood samples may allow Campbell to verify the presence of cold-tolerant hemoglobin in woolly mammoths. “It’s one thing to synthesize mammoth hemoglobin in bacteria: It’s quite another story to study the real thing from a 43,000 year-old specimen,” Campbell told the International Science Times. “No other specimen has ever been so well preserved that we could potentially obtain hemoglobin oxygen-binding data from it. This specimen offers the unique opportunity to collect precisely the same kind of physiologically relevant information from an extinct species as I could from those that are still alive.”

Climate change (as destructive a force as it is for the planet) has proven to be a boon for evolutionary physiologists interested in examining extinct animals. “One of the dirty little secrets of this field is that the increased melting of the North affords the finding of many, many more specimens,” Campbell said. “I don’t want to encourage further global warming, but it is a benefit from permafrost melting and so much being exposed, that they are finding woolly rhinos, bison, a crazy number of ancient horses and specimens in the Canadian and Russian Arctic.” Gold mining and industrial development has also unearthed more prehistoric animals than ever before in human history.

The researchers who peformed the autopsy on the woolly mammoth will hold a conference in Greece in May to announce the results.

http://www.isciencetimes.com/articles/6946/20140313/woolly-mammoth-dna-cloning-elephant-clone.htm

China is cloning on an industrial scale

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By David Shukman

You hear the squeals of the pigs long before reaching a set of long buildings set in rolling hills in southern China.

Feeding time produces a frenzy as the animals strain against the railings around their pens. But this is no ordinary farm.

Run by a fast-growing company called BGI, this facility has become the world’s largest centre for the cloning of pigs.

The technology involved is not particularly novel – but what is new is the application of mass production.

The first shed contains 90 animals in two long rows. They look perfectly normal, as one would expect, but each of them is carrying cloned embryos. Many are clones themselves.

This place produces an astonishing 500 cloned pigs a year: China is exploiting science on an industrial scale.

To my surprise, we’re taken to see how the work is done. A room next to the pens serves as a surgery and a sow is under anaesthetic, lying on her back on an operating table. An oxygen mask is fitted over her snout and she’s breathing steadily. Blue plastic bags cover her trotters.

Two technicians have inserted a fibre-optic probe to locate the sow’s uterus. A third retrieves a small test-tube from a fridge: these are the blastocysts, early stage embryos prepared in a lab. In a moment, they will be implanted.

The room is not air-conditioned; nor is it particularly clean. Flies buzz around the pig’s head.

My first thought is that the operation is being conducted with an air of total routine. Even the presence of a foreign television crew seems to make little difference. The animal is comfortable but there’s no sensitivity about how we might react, let alone what animal rights campaigners might make of it all.

I check the figures: the team can do two implantations a day. The success rate is about 70-80%.

Dusk is falling as we’re shown into another shed where new-born piglets are lying close to their mothers to suckle. Heat lamps keep the room warm. Some of the animals are clones of clones. Most have been genetically modified.

The point of the work is to use pigs to test out new medicines. Because they are so similar genetically to humans, pigs can serve as useful “models”. So modifying their genes to give them traits can aid that process.

One batch of particularly small pigs has had a growth gene removed – they stopped growing at the age of one. Others have had their DNA tinkered with to try to make them more susceptible to Alzheimer’s.

Back at the company headquarters, a line of technicians is hunched over microscopes. This is a BGI innovation: replacing expensive machines with people. It’s called “handmade cloning” and is designed to make everything quicker and easier.

The scientist in charge, Dr Yutao Du, explains the technique in a way that leaves me reeling.

“We can do cloning on a very large scale,” she tells me, “30-50 people together doing cloning so that we can make a cloning factory here.”

A cloning factory – an incredible notion borrowed straight from science fiction. But here in Shenzhen, in what was an old shoe factory, this rising power is creating a new industry.

The scale of ambition is staggering. BGI is not only the world’s largest centre for cloning pigs – it’s also the world’s largest centre for gene sequencing.

In neighbouring buildings, there are rows of gene sequencers – machines the size of fridges operating 24 hours a day crunching through the codes for life.

To illustrate the scale of this operation, Europe’s largest gene sequencing centre is the Wellcome Trust Sanger Institute near Cambridge. It has 30 machines. BGI has 156 and has even bought an American company that makes them.

BGI’s chief executive, Wang Jun, tells me how they need the technology to develop ever faster and cheaper ways of reading genes.

Again, a comparison for scale: a recently-launched UK project seeks to sequence 10,000 human genomes. BGI has ambitions to sequence the genomes of a million people, a million animals and a million plants.

Wang Jun is keen to stress that all this work must be relevant to ordinary people through better healthcare or tastier food. The BGI canteen is used as a testbed for some of the products from the labs: everything from grouper twice the normal size, to pigs, to yoghurt.

I ask Wang Jun how he chooses what to sequence. After the shock of hearing the phrase “cloning factory”, out comes another bombshell:

“If it tastes good you should sequence it,” he tells me. “You should know what’s in the genes of that species.”

Species that taste good is one criterion. Another he cites is that of industrial use – raising yields, for example, or benefits for healthcare.

“A third category is if it looks cute – anything that looks cute: panda, polar bear, penguin, you should really sequence it – it’s like digitalising all the wonderful species,” he explains.

I wonder how he feels about acquiring such power to take control of nature but he immediately contradicts me.

“No, we’re following Nature – there are lots of people dying from hunger and protein supply so we have to think about ways of dealing with that, for example exploring the potential of rice as a species,” the BGI chief counters.

China is on a trajectory that will see it emerging as a giant of science: it has a robotic rover on the Moon, it holds the honour of having the world’s fastest supercomputer and BGI offers a glimpse of what industrial scale could bring to the future of biology.

Read more: http://www.bbc.co.uk/news/science-environment-25576718

Thanks to Kebmodee for bringing this to the attenion of the It’s Interesting community.

‘Jumping Genes’ Linked to Schizophrenia

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Roaming bits of DNA that can relocate and proliferate throughout the genome, called “jumping genes,” may contribute to schizophrenia, a new study suggests. These rogue genetic elements pepper the brain tissue of deceased people with the disorder and multiply in response to stressful events, such as infection during pregnancy, which increase the risk of the disease. The study could help explain how genes and environment work together to produce the complex disorder and may even point to ways of lowering the risk of the disease, researchers say.

Schizophrenia causes hallucinations, delusions, and a host of other cognitive problems, and afflicts roughly 1% of all people. It runs in families—a person whose twin sibling has the disorder, for example, has a roughly 50-50 chance of developing it. Scientists have struggled to define which genes are most important to developing the disease, however; each individual gene associated with the disorder confers only modest risk. Environmental factors such as viral infections before birth have also been shown to increase risk of developing schizophrenia, but how and whether these exposures work together with genes to skew brain development and produce the disease is still unclear, says Tadafumi Kato, a neuroscientist at the RIKEN Brain Science Institute in Wako City, Japan and co-author of the new study.

Over the past several years, a new mechanism for genetic mutation has attracted considerable interest from researchers studying neurological disorders, Kato says. Informally called jumping genes, these bits of DNA can replicate and insert themselves into other regions of the genome, where they either lie silent, doing nothing; start churning out their own genetic products; or alter the activity of their neighboring genes. If that sounds potentially dangerous, it is: Such genes are often the culprits behind tumor-causing mutations and have been implicated in several neurological diseases. However, jumping genes also make up nearly half the current human genome, suggesting that humans owe much of our identity to their audacious leaps.

Recent research by neuroscientist Fred Gage and colleagues at the University of California (UC), San Diego, has shown that one of the most common types of jumping gene in people, called L1, is particularly abundant in human stem cells in the brain that ultimately differentiate into neurons and plays an important role in regulating neuronal development and proliferation. Although Gage and colleagues have found that increased L1 is associated with mental disorders such as Rett syndrome, a form of autism, and a neurological motor disease called Louis-Bar syndrome, “no one had looked very carefully” to see if the gene might also contribute to schizophrenia, he says.

To investigate that question, principal investigator Kazuya Iwamoto, a neuroscientist; Kato; and their team at RIKEN extracted brain tissue of deceased people who had been diagnosed with schizophrenia as well as several other mental disorders, extracted DNA from their neurons, and compared it with that of healthy people. Compared with controls, there was a 1.1-fold increase in L1 in the tissue of people with schizophrenia, as well as slightly less elevated levels in people with other mental disorders such as major depression, the team reports today in Neuron.

Next, the scientists tested whether environmental factors associated with schizophrenia could trigger a comparable increase in L1. They injected pregnant mice with a chemical that simulates viral infection and found that their offspring did, indeed, show higher levels of the gene in their brain tissue. An additional study in infant macaques, which mimicked exposure to a hormone also associated with increased schizophrenia risk, produced similar results. Finally, the group examined human neural stem cells extracted from people with schizophrenia and found that these, too, showed higher levels of L1.

The fact that it is possible to increase the number of copies of L1 in the mouse and macaque brains using established environmental triggers for schizophrenia shows that such genetic mutations in the brain may be preventable if such exposures can be avoided, Kato says. He says he hopes that the “new view” that environmental factors can trigger or deter genetic changes involved in the disease will help remove some of the disorder’s stigma.

Combined with previous studies on other disorders, the new study suggests that L1 genes are indeed more active in the brain of patients with neuropsychiatric diseases, Gage says. He cautions, however, that no one yet knows whether they are actually causing the disease. “Now that we have multiple confirmations of this occurring in humans with different diseases, the next step is to determine if possible what role, if any, they play.”

One tantalizing possibility is that as these restless bits of DNA drift throughout the genomes of human brain cells, they help create the vibrant cognitive diversity that helps humans as a species respond to changing environmental conditions, and produces extraordinary “outliers,” including innovators and geniuses such as Picasso, says UC San Diego neuroscientist Alysson Muotri. The price of such rich diversity may be that mutations contributing to mental disorders such as schizophrenia sometimes emerge. Figuring out what these jumping genes truly do in the human brain is the “next frontier” for understanding complex mental disorders, he says. “This is only the tip of the iceberg.”

Thanks to Dr. Rajadhyaksha for bringing this to the attention of the It’s Interesting community.

http://news.sciencemag.org/biology/2014/01/jumping-genes-linked-schizophrenia

Study reveals gene expression changes with meditation

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With evidence growing that meditation can have beneficial health effects, scientists have sought to understand how these practices physically affect the body.

A new study by researchers in Wisconsin, Spain, and France reports the first evidence of specific molecular changes in the body following a period of mindfulness meditation.

The study investigated the effects of a day of intensive mindfulness practice in a group of experienced meditators, compared to a group of untrained control subjects who engaged in quiet non-meditative activities. After eight hours of mindfulness practice, the meditators showed a range of genetic and molecular differences, including altered levels of gene-regulating machinery and reduced levels of pro-inflammatory genes, which in turn correlated with faster physical recovery from a stressful situation.

“To the best of our knowledge, this is the first paper that shows rapid alterations in gene expression within subjects associated with mindfulness meditation practice,” says study author Richard J. Davidson, founder of the Center for Investigating Healthy Minds and the William James and Vilas Professor of Psychology and Psychiatry at the University of Wisconsin-Madison.

“Most interestingly, the changes were observed in genes that are the current targets of anti-inflammatory and analgesic drugs,” says Perla Kaliman, first author of the article and a researcher at the Institute of Biomedical Research of Barcelona, Spain (IIBB-CSIC-IDIBAPS), where the molecular analyses were conducted.

The study was published in the journal Psychoneuroendocrinology.

Mindfulness-based trainings have shown beneficial effects on inflammatory disorders in prior clinical studies and are endorsed by the American Heart Association as a preventative intervention. The new results provide a possible biological mechanism for therapeutic effects.

The results show a down-regulation of genes that have been implicated in inflammation. The affected genes include the pro-inflammatory genes RIPK2 and COX2 as well as several histone deacetylase (HDAC) genes, which regulate the activity of other genes epigenetically by removing a type of chemical tag. What’s more, the extent to which some of those genes were downregulated was associated with faster cortisol recovery to a social stress test involving an impromptu speech and tasks requiring mental calculations performed in front of an audience and video camera.

Perhaps surprisingly, the researchers say, there was no difference in the tested genes between the two groups of people at the start of the study. The observed effects were seen only in the meditators following mindfulness practice. In addition, several other DNA-modifying genes showed no differences between groups, suggesting that the mindfulness practice specifically affected certain regulatory pathways.

However, it is important to note that the study was not designed to distinguish any effects of long-term meditation training from those of a single day of practice. Instead, the key result is that meditators experienced genetic changes following mindfulness practice that were not seen in the non-meditating group after other quiet activities — an outcome providing proof of principle that mindfulness practice can lead to epigenetic alterations of the genome.

Previous studies in rodents and in people have shown dynamic epigenetic responses to physical stimuli such as stress, diet, or exercise within just a few hours.

“Our genes are quite dynamic in their expression and these results suggest that the calmness of our mind can actually have a potential influence on their expression,” Davidson says.

“The regulation of HDACs and inflammatory pathways may represent some of the mechanisms underlying the therapeutic potential of mindfulness-based interventions,” Kaliman says. “Our findings set the foundation for future studies to further assess meditation strategies for the treatment of chronic inflammatory conditions.”

Study funding came from National Center for Complementary and Alternative Medicine (grant number P01-AT004952) and grants from the Fetzer Institute, the John Templeton Foundation, and an anonymous donor to Davidson. The study was conducted at the Center for Investigating Healthy Minds at the UW-Madison Waisman Center.

http://www.news.wisc.edu/22370

Thanks to Dr. D for bringing this to the attention of the It’s Interesting community.

How the Whale Became the Whale

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About 54 million years ago, a semiaquatic deerlike creature headed into the water for good, giving rise to whales and their relatives. The newly sequenced genome of the minke whale, a baleen whale found worldwide, tells the story of how stressful this move to live underwater was. An international team has decoded the genomes of four minke whales, a fin whale, a bottlenose dolphin, and a finless porpoise, comparing these cetaceans’ genes to the equivalent genes in other mammals. It found whale-specific mutations in genes important for the regulation of salt and of blood pressure and for antioxidants that get rid of charged oxygen molecules that can harm cells. These molecules increase in number as the whale uses up its oxygen supply during dives. Whales also had larger numbers of related genes, called gene families, for dealing with sustained dives, the team reports online today in Nature Genetics. Overall, 1156 gene families had expanded, and several increased the number of enzymes that help the whale cope with low-to-no oxygen conditions. A few of those expanded families are also expanded in naked mole rats, which live underground where oxygen is scarce. But the numbers of genes for body hair and for taste and smell had decreased. And of course, there were genes and gene families that help explain why whales look the way they do.

http://news.sciencemag.org/biology/2013/11/scienceshot-how-whale-became-whale

Thanks to Dr. Rajadhyaksha for bringing this to the attention of the It’s Interesting community.

R.I.P. Frederick Sanger, Two-Time Nobel-Winning Scientist, died yesterday at age of 95

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By DENISE GELLENE

Frederick Sanger, a British biochemist whose discoveries about the chemistry of life led to the decoding of the human genome and to the development of new drugs like human growth hormone and earned him two Nobel Prizes, a distinction held by only three other scientists, died on Tuesday in Cambridge, England. He was 95.

His death was confirmed by Adrian Penrose, communications manager at the Medical Research Council in Cambridge. Dr. Sanger, who died at Addenbrooke’s Hospital in Cambridge, had lived in a nearby village called Swaffham Bulbeck.

Dr. Sanger won his first Nobel Prize, in chemistry, in 1958 for showing how amino acids link together to form insulin, a discovery that gave scientists the tools to analyze any protein in the body.

In 1980 he received his second Nobel, also in chemistry, for inventing a method of “reading” the molecular letters that make up the genetic code. This discovery was crucial to the development of biotechnology drugs and provided the basic tool kit for decoding the entire human genome two decades later.

Dr. Sanger spent his entire career working in a laboratory, which is unusual for someone of his stature. Long after receiving his first Nobel, he continued to perform many experiments himself instead of assigning them to a junior researcher, as is typical in modern science labs. But Dr. Sanger said he was not particularly adept at coming up with experiments for others to do, and had little aptitude for administration or teaching.

“I was in a position to do more or less what I liked, and that was doing research,” he said.

Frederick Sanger was born on Aug. 3, 1918, in Rendcomb, England, where his father was a physician. He expected to follow his father into medicine, but after studying biochemistry at Cambridge University, he decided to become a scientist. His father, he said in a 1988 interview, “led a scrappy sort of life” in which he was “always going from one patient to another.”

“I felt I would be much more interested in and much better at something where I could really work on a problem,” he said.

He received his bachelor’s degree in 1939. Raised as a Quaker, he was a conscientious objector during World War II and remained at Cambridge to work on his doctorate, which he received in 1943.

However, later in life, lacking hard evidence to support his religious beliefs, he became an agnostic.

“In science, you have to be so careful about truth,” he said. “You are studying truth and have to prove everything. I found that it was difficult to believe all the things associated with religion.”

Dr. Sanger stayed on at Cambridge and soon became immersed in the study of proteins. When he started his work, scientists knew that proteins were chains of amino acids, fitted together like a child’s colorful snap-bead toy. But there are 22 different amino acids, and scientists had no way of determining the sequence of these amino acid “beads” along the chains.
In 1962, Dr. Sanger moved to the British Medical Research Council Laboratory of Molecular Biology, where he was surrounded by scientists studying deoxyribonucleic acid, or DNA, the master chemical of heredity.

Scientists knew that DNA, like proteins, had a chainlike structure. The challenge was to determine the order of adenine, thymine, guanine and cytosine — the chemical bases from which DNA is made. These bases, which are represented by the letters A, T, G and C, spell out the genetic code for all living things.

Dr. Sanger decided to study insulin, a protein that was readily available in a purified form since it is used to treat diabetes. His choice of insulin turned out to be a lucky one — with 51 amino acids, insulin has a relatively simple structure. Nonetheless, it took him 10 years to unlock its chemical sequence.

His approach, which he called the “jigsaw puzzle method,” involved breaking insulin into manageable chunks for analysis and then using his knowledge of chemical bonds to fit the pieces back together. Using this technique, scientists went on to determine the sequences of other proteins. Dr. Sanger received the Nobel just four years after he published his results in 1954.

Dr. Sanger quickly discovered that his jigsaw method was too cumbersome for large pieces of DNA, which contain many thousands of letters. “For a while I didn’t see any hope of doing it, though I knew it was an important problem,” he said.

But he persisted, developing a more efficient approach that allowed stretches of 500 to 800 letters to be read at a time. His technique, known as the Sanger method, increased by a thousand times the rate at which scientists could sequence DNA.

In 1977, Dr. Sanger decoded the complete genome of a virus that had more than 5,000 letters. It was the first time the DNA of an entire organism had been sequenced. He went on to decode the 16,000 letters of mitochondria, the energy factories in cells.

Because the Sanger method lends itself to computer automation, it has allowed scientists to unravel ever more complicated genomes — including, in 2003, the three billion letters of the human genetic code, giving scientists greater ability to distinguish between normal and abnormal genes.

In addition, Dr. Sanger’s discoveries were critical to the development of biotechnology drugs, like human growth hormone and clotting factors for hemophilia, which are produced by tiny, genetically modified organisms.

Dr. Sanger shared the 1980 chemistry Nobel with two other scientists: Paul Berg, who determined how to transfer genetic material from one organism to another, and Walter Gilbert, who, independently of Dr. Sanger, also developed a technique to sequence DNA. Because of its relative simplicity, the Sanger method became the dominant approach.

Other scientists who have received two Nobels are John Bardeen for physics (1956 and 1972), Marie Curie for physics (1903) and chemistry (1911), and Linus Pauling for chemistry (1954) and peace (1962).

Dr. Sanger received the Albert Lasker Basic Medical Research Award, often a forerunner to the Nobel, in 1979 for his work on DNA. He retired from the British Medical Research Council in 1983.

Survivors include two sons, Robin and Peter, and a daughter, Sally.

In a 2001 interview, Dr. Sanger spoke about the challenge of winning two Nobel Prizes.

“It’s much more difficult to get the first prize than to get the second one,” he said, “because if you’ve already got a prize, then you can get facilities for work and you can get collaborators, and everything is much easier.”

New research on adult neurogenesis shows that about 1,400 new brain cells are born every day, and about 80% of human brain cells in the dentate gyrus of the hippocampus undergo renewal in adulthood

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by Leonie Welberg

The question of whether adult neurogenesis occurs in the human hippocampus has been a hotly debated topic in neuroscience. In a study published in Cell, Frisén and colleagues now settle the debate by providing evidence that around 1,400 dentate gyrus cells are born in the human brain every day.

The authors made use of a birth-dating method that is based on the principle that 14C in the atmosphere is taken up by plants and — because humans eat plants and animals that eat plants — eventually also by humans. As 14C is incorporated into DNA during cell division, the 14C content of a cell is thought to reflect 14C levels in the atmosphere at the time of the birth of the cell. Importantly, atomic bomb testing in the 1950s and 1960s resulted in a spike in atmospheric 14C levels, and levels declined after 1963; this means that the level of 14C in cellular DNA can be used as a relatively precise marker of a cell’s birth date.

The authors applied the 14C birth-dating method to whole hippocampi dissected from post-mortem brains donated by individuals who were born in different years in the twentieth century. They separated neurons from non-neuronal hippocampal cells, purified the neuronal DNA and determined 14C levels. Neuronal 14C levels did not match atmospheric 14C levels in the individual’s birth year but were either higher (for people born before 1950) or lower (for people born after 1963), suggesting that at least some of the hippocampal cells were born after the year in which an individual was born.

Computer modelling of the data revealed that the best-fit model was one in which 35% of hippocampal cells showed such turnover, whereas the majority did not (that is, they were born during development). Assuming that, in humans, adult neurogenesis would take place in the dentate gyrus rather than in other hippocampal areas (as it does in rodents), and as the dentate gyrus contains about 44% of all hippocampal neurons, this model suggests that about 80% of human dentate gyrus cells undergo renewal in adulthood. This is in striking contrast to the scenario in mice, in which only ~10% of adult dentate gyrus neurons undergo renewal. The study further showed that there is very little decline in the level of hippocampal neurogenesis with ageing in humans, which is again in contrast to rodents.

It is now well established that adult-born neurons have a functional role in the mouse and rat dentate gyrus and olfactory bulb. A previous study using the same neuronal birth-dating method established that no adult neurogenesis takes place in the olfactory bulb and cortex in humans, but the new study has elegantly shown that the situation is different in the dentate gyrus. Whether the adult-born neurons have functional implications in humans remains a topic for future investigation.

http://www.nature.com/nrn/journal/v14/n8/full/nrn3548.html?WT.ec_id=NRN-201308

Thanks to Kebmodee for bringing this to the attention of the It’s Interesting community.

Litterbugs Beware: Turning Found DNA Into Portraits

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Heather Dewey-Hagborg was sitting in a therapy session a while ago and noticed a painting on the wall. The glass on the frame was cracked, and lodged in the crack was a single hair. She couldn’t take her eyes off it. “I just became obsessed with thinking about whose hair that was, and what they might look like, and what they might be like,” she says.

On the subway ride home, she noticed all of the insignificant things people left behind — a dropped cigarette butt, a chewed-up piece of gum. Like the hair stuck in the frame, she wondered how much genetic material might have been tossed away with the trash. So Dewey-Hagborg started collecting these forgotten “artifacts,” as she calls them, and bringing them back to a lab to analyze their embedded genetic material.

Yet it might seem Dewey-Hagborg would be more comfortable in a studio than a laboratory. She’s an artist; a doctoral student in Information Art at Rensselaer Polytechnic Institute in Troy, N.Y. For her most recent project, though, much of the creative process takes place in front of a centrifuge, wearing latex gloves, deep in the map of the human genome.

In short, Dewey-Hagborg extracts DNA from these samples of trash and turns that information from code into life-sized 3-D facial portraits resembling the person who left the sample behind. She can code for eye color, eye and nose width, skin tone, hair color and more. She starts by cutting up her sample, sometimes the end of a cigarette, thin slices of a chewed wad of gum, sometimes hair, and incubates the sample with chemicals to distill it into pure DNA. She then takes that DNA, and matches the code with different traits on the genome related to the way human faces look.

“That’s a very tiny subset of all of the things that we know about the entire mapping of the human genome, ” she says.

Next, she sends the DNA to a sequencing company that sends her back a text file full of A, C, Ts and Gs — the four nucleic acid bases that DNA is made out of. She then reads that information in a program she designed herself, translating the code into traits, then using those traits to build a 3-D model of a face. Dewey-Hagborg can determine ethnicity, gender, even a tendency to be overweight.

But even all of that can’t give her the whole picture. Much of the information is still missing, and Dewey-Hagborg has to fill in the gaps. She compares that part of the work to a sketch artist. “This person is more likely to be overweight, to have pale skin, to have freckles, blue eyes, how do I interpret this?”

People often ask her how accurate the portraits are. Of course, she has no way of knowing. After all, she collects these items from anonymous sources. But she did start off with her own portrait based on her own DNA. She exhibited that at an art and technology space in Chelsea.

“Half of the people would say, ‘Wow! It looks just like you!'” she says. “The other half would say, ‘Wow! It looks nothing like you!” The portraits are subjective in a big way, she acknowledges, but says much of the information is solidly based in data.

Though she started this project in part to “open up the conversation about genetic surveillance,” she says, it’s taken on another purpose. Right now she’s working with the Delaware medical examiner’s office to try to identify a woman in a 20-year-old unsolved case by using some of the victim’s remains to build a 3-D portrait of her. She’s six weeks away from finishing the process, when investigators will, for the first time, have some idea of what the victim looked like before her death.

http://www.npr.org/2013/05/12/183363361/litterbugs-beware-turning-found-dna-into-portraits

Thanks to Dr. Lutter for bringing this to the attention of the It’s Interesting community.

Carnivorous Plant Ejects Junk DNA

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The carnivorous humped bladderwort (Utricularia gibba), found on all continents except Antarctica, is a model of ruthless genetic efficiency. Only 3% of this aquatic plant’s DNA is not part of a known gene, new research shows. In contrast, only 2% of human DNA is part of a gene. The bladderwort, named for its water-filled bladders (shown left) that suck in unsuspecting prey, is a relative of the tomato. Since their evolutionary split 87,000 years ago, both plants have experienced episodes of genetic duplication where the plants’ DNA doubled in size. But while the tomato has held onto a lot of those duplicates, the bladderwort has thrown out anything it doesn’t need, and now has a genome only a tenth as long as the tomato’s. The finding, published recently in Nature, overturns the notion that this repetitive, non-coding DNA, popularly called “junk” DNA, is necessary for life.

http://news.sciencemag.org/sciencenow/2013/05/scienceshot-carnivorous-plant-ej.html

Life quite possibly existed before Earth, claim scientists

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Life existed long before Earth came into being, and may have originated outside our solar system, scientists claim.

Researchers say life first appeared about 10 billion years ago – long before Earth, which is believed to be 4.5 billion years old. Geneticists have applied Moore’s Law – observation that computers increase exponentially in complexity, at a rate of about double the transistors per integrated circuit every two years – to the rate at which life on Earth grows in complexity.

Alexei Sharov of the National Institute on Ageing in Baltimore, and Richard Gordon of the Gulf Specimen Marine Laboratory in Florida, replaced the transistors with nucleotides – the building blocks of DNA and RNA – and the circuits with genetic material. Their findings suggest life first appeared about 10 billion years ago, far older than the Earth’s projected age of 4.5 billion years. Like in the 2012 sci-fi movie Prometheus, as our solar system was forming, pre-existing bacteria-like organisms, or even simple nucleotides from an older part of the galaxy, could have reached Earth by hitching an interstellar ride on comets, asteroids or other inorganic space debris.

However, the calculations are not a scientific proof that life predates Earth – there’s no way of knowing for sure that organic complexity increased at a steady rate at any point in the universe’s history.

“There are lots of hypothetical elements to (our argument) … But to make a wider view, you need some hypothetical elements,” Sharov said.

Sharov said that if he had to bet on it, he’d say “it’s 99 per cent true that life started before Earth – but we should leave one per cent for some wild chance that we haven’t accounted for.”

The theory of “life before Earth,” if found true, challenges the long-held science-fiction trope of the scientifically advanced alien species. If genetic complexity progresses at a steady rate, then the social and scientific development of any other alien life form in the Milky Way galaxy would be roughly equivalent to those of humans, the report said.

“Contamination with bacterial spores from space appears the most plausible hypothesis that explains the early appearance of life on Earth,” researchers said.

http://www.phenomenica.com/2013/04/life-did-exist-before-earth-claim-scientists.html