A $53 million effort drawing on the work of over 300 researchers has, after six years, produced something of great value to evolutionary biologists and farmers alike: the complete cow genome, which researchers say holds clues to the cow’s evolutionary history, as well as instructions on how to breed better cattle for milk and meat production. One research group sequenced the complete genome of a female Hereford cow, and researchers say that hidden in her roughly 22,000 genes are hints of how natural selection sculpted the bovine body and personality over the past 60 million years, and how man greatly enhanced the job over the past 10,000 [Washington Post]. Another spinoff research project studied the genetic variants between different breeds, and revealed some of the genetic keys to high-quality milk and beef.
Traits carried by bulls are important in determining how much milk a cow produces. Because bulls don’t make milk, however, a bull’s “performance profile” has to be sketched by observing the milk production of his daughters — a process that takes about six years and costs $25,000 to $50,000. Now, male calves can be tested at birth for milk-enhancing traits using gene-chip technology [Washington Post]. Early versions of these gene chips are already in use, ranchers say, but the new information may allow a new level of precision. Researchers also suggested that the genetic information could be used to breed cows that burp up less methane, a greenhouse gas that contributes to global warming.
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“People ordered genomes for Christmas” [The New York Times], says the chief executive of the personal gene-sequencing company Knome, commenting on the recent increased demand for his company’s services. Now, Knome is partnering with the non-profit X Prize Foundation to auction its complete genome scan service on eBay. Bidding will open at $68,000—far below Knome’s current price of $99,000. The auction starts Friday and will continue for 10 days. The highest bidder will walk away with a full readout of their gene map, along with a complete interpretation of their genetic details [CNN].
The auction is essentially a publicity stunt [The New York Times] for the company, and is set to begin Friday in order to coincide with DNA Day, the anniversary of the discovery of the double helix structure. Proceeds will benefit the X Prize Foundation, an educational institute offering a $10 million prize for the sequencing of 100 genomes in 10 days for less than $10,000 per genome. Knome and other personal genetics companies claim that besides identifying risk of diseases, sequencing can also determine an individual’s potential reaction to certain drugs and pick out those that may be ineffective or even toxic…. Genomics plays a critical role in the move towards personalized medicine [CNN].
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Cardiologist and author John Sotos has a theory about why Abraham Lincoln was so tall, why he appeared to have lumps on his lips and even why he had gastrointestinal problems. The 16th president, he contends, had a rare genetic disorder — one that would likely have left him dead of cancer within a year had he not been assassinated [Time]. But for Sotos to prove his case, he needs a snip from a historical relic: a piece of the bloodstained pillowcase on which the dying Lincoln rested his head after he was shot at Ford’s Theater on April 14, 1865.
The piece of cloth is displayed under glass at the Grand Army of the Republic Civil War Museum and Library in Philadelphia. Sotos has asked the museum’s board for a sample of the pillowcase, which is stained with both blood and brain matter. But the board is fiercely debating whether to concede to his request. “This is the Shroud of Turin of Civil War history,” said Andy Waskie, a board member…. “We are guardians in trusteeship of this extraordinarily important artifact. On the basis of pure science, the testing is of interest. We have not eliminated it as an option . . . but we want more information” [The Philadelphia Inquirer].
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Young adults with a genetic variant that increases their chance of developing Alzheimer’s later in life also have increased activity in the section of their brain devoted to memory, a new study has found. Researchers say the results suggest that the memory portion of the brain, the hippocampus, may eventually get worn out from a lifetime of overuse.
Researchers conducted fMRI brain scans of 36 volunteers, half of whom had at least one copy of the gene, known as APOE4. “We were surprised to see that even when the volunteers carrying APOE4 weren’t being asked to do anything, you could see the memory part of the brain working harder than it was in the other volunteers,” [study coauthor Christian] Beckmann said…. “Not all APOE4 carriers go on to develop Alzheimer’s, but it would make sense if in some people, the memory part of the brain effectively becomes exhausted from overwork and this contributes to the disease” [Reuters].
However, the researchers note that they’re far from proving this hypothesis, and say that it’s impossible to tell whether the extra activity contributes to Alzheimer’s symptoms later on or is just a sign of inefficient brain circuitry in the hippocampus [New Scientist].
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People with a family history of depression have an altered brain anatomy, a new study says, even if they themselves have never experienced clinical depression. Brain scans showed a 28-percent thinning in the right cortex — the outer layer of the brain — in people who had a family history of depression compared with people who did not. “The difference was so great that at first we almost didn’t believe it. But we checked and re-checked all of our data, and we looked for all possible alternative explanations, and still the difference was there” [Reuters], said study coauthor Bradley Peterson.
Researchers scanned the brains of 131 individuals ranging in age from 6 to 54, about half of whom came from families with a history of depression. The team was looking specifically for abnormalities in the brain that could signal a predisposition to depression, rather than changes that may be caused by the disease [Reuters]. The cortical thinning seems to fit the definition as a warning flag. Says Peterson: “That’s what is so extraordinary. You’re seeing it two generations later, and you’re seeing it in both children and adults…. And it’s present even if those offspring themselves have not yet become ill” [The New York Times].
The cerebral cortex is largely responsible for reasoning, planning, and mood, and researchers suggest that its thinning may interfere with a person’s ability to interpret social and emotional cues from others. Interestingly, not all of the subjects with depressed family members showed thinning on both sides of their cortices; it was primarily those with thinning in the left hemisphere who had actually developed depression.
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Playing true to form, Google cofounder Sergey Brin is launching an ambitious, expensive effort using unorthodox tactics, but this time he’s taking on Parkinson’s research. In cooperation with the personal genetics testing company 23andMe, which was cofounded by Brin’s wife, Anne Wojcicki, Brin is hoping to get 10,000 Parkinson’s patients to fill out online questionnaires and get their genomes scanned. To encourage participation, 23andMe will provide the DNA scan for $25, a fraction of the normal $399 price. Brin, who says he has an elevated risk of Parkinson’s, will contribute the bulk of the money for the study, although he declined to disclose the total costs.
Wojcicki says that getting full genetic information for so many patients could reveal genetic patterns to the disease, which has already been linked to a handful of genes. “We want to try and find out if there are other genetic variations that are associated with Parkinson’s or with rapid progression or slow progression,” said Wojcicki, in a telephone interview yesterday. “Also, why some people respond well to therapy, some people don’t, and some develop resistance faster” [Bloomberg].
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The controversy surrounding stem cell research might soon be moot, with new research showing that ordinary skin cells can be transformed into an equivalent of embryonic stem cells, which have been the focus of research because of their ability to become any kind of cell in the human body. This is known as a pluripotent state, and the new research, published in two articles in Nature, marks the first time that scientists have turned skin cells into induced pluripotent stem cells or iPS cells—which look and act like embryonic stem cells—without having to use viruses in the process [Reuters].
Scientists have been able to make stem cells from adult cells for more than a year, but relied on the injection of a virus to trigger the transformation of the cell into the embryonic state. These cells could not be used on patients, however, because of the risk they presented of developing cancer. Now, researchers in Britain and Canada have produced the cells by using strands of genetic material, instead of potentially dangerous genetically engineered viruses, to coax skin cells into a state that appears biologically identical to embryonic stem cells [Washington Post].
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A new study shows that teenage boy developed cancerous tumors because of the stem cell therapy he received years ago for a rare genetic condition. The boy, now 17, suffered from ataxia telangiectasia, or AT, a neurodegenerative disease that interferes with the part of the brain that controls movement and speech. AT patients do not usually live past their teens or 20s, and the Israeli boy, whose identity was not publicly revealed, was taken to Russia for experimental treatment. The first neural stem cells, taken from fetuses, were first injected into his brain and spinal cord when he was nine, and he received further injections at ages 10 and 12.
His condition deteriorated and he was using a wheelchair by age 13, when he also began to complain of headaches. Tests showed two growths, one pushing on his brain stem and the other on his spinal cord. The tumors were removed in 2006 and his health has since remained stable. But scientists at Tel Aviv University who wanted to determine the origin of the cancer have been in the lab ever since, and their findings have just been published in PLoS Medicine. The team found that the tumor could not have arisen from the boy, because he [has two disease-causing versions of the gene] that causes AT, while the DNA from the tumor cells carried only the normal version [The Scientist].
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A cure for the common cold may eventually be within reach, now that scientists have sequenced the genetic code of 99 strains of the common cold virus.
The research team, whose findings are published in Science, found that the strains are organized in about 15 family groups, each with its own ancestral path, which may explain why no one anti-viral drug works against all of them [Medical News Today]. By mapping a family tree of the common cold virus, or human rhinovirus, the researchers say they can identify the similarities and differences among all the strains. That family tree shows that some regions of the rhinovirus genome are changing all the time but that others never change. The … unchanging regions … are therefore ideal targets for drugs because, in principle, any of the 99 strains would succumb to the same drug [The New York Times].
The study also found something not thought possible in that type of virus: they recombine to form new strains…. which may account for the speed with which new strains emerge within one season [Medical News Today].
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For the first time, scientists have derived and cultured embryonic stem (ES) cells from rats, paving the way for genetically engineered rats that would more accurately model some human diseases than the currently available genetically engineered mice. Two collaborating teams developed a new approach to derive the ES cells, using a new cocktail of molecules to protect their precious pluripotency, the ability to differentiate into any type of cell. “This is a major development in stem cell research because we know that rats are much more closely related to humans than mice in many aspects of biology. The research direction of many labs around the world will change because of the availability of rat ES cells,” says Qilong Ying [Xinhua], who led one of the teams.
ES cells from mice have been available since 1981, and different researchers have created hundreds of different strains of “knock-out” mice—ones raised from ES cells in which certain genes are silenced to make apparent the genes’ functions. With mice, ES cells were grown with a mixture of growth signals to make them divide without differentiating. But transferring the same technique to rats and other mammals proved surprisingly difficult. To the great frustration of researchers, stem cells isolated from rat embryos and cultured with growth signals would quickly lose their pluripotency. The new strategy, reported in two studies in Cell [subscription required], involves growing the ES cells in a mixture of three key molecules that block the signals that normally induce differentiation. “Our discovery was that if you want to maintain cells in the undifferentiated state, you must block signals, not activate them,” says Ying… By repressing differentiation, the researchers could hold the cells in what they call a “ground state,” a blank slate ready to turn into any tissue in the body [Science News].
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In the western world, marriage between first cousins is labeled incest or inbreeding, and in the United States the practice is banned or restricted in 31 states. But a new essay argues that such laws are based on an outdated notion of the genetic risks involved in cousins marrying and reproducing. [T]hose laws “seem ill-advised” and “should be repealed,” a geneticist and medical historian write…. “Neither the scientific nor social assumptions that informed them are any longer defensible” [Scientific American].
First cousins share about an eighth of their genes, and are therefore more likely to receive two copies of some recessive gene that poses health problems. Scientists had assumed that the children of first cousins would therefore be more likely to be born with birth defects. But coauthor Hamish Spencer writes that the risk of congenital defects is about 2 per cent higher than average for babies born to first-cousin marriages – with the infant mortality about 4.4 per cent higher – which is on a par with the risk to babies born to women over 40. “Women over the age of 40 have a similar risk of having children with birth defects and no one is suggesting they should be prevented from reproducing,” said Professor Spencer [The Independent].
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A hormone produced in the gut appears to limit bone formation, scientists report in Cell [subscription required]. The hormone, serotonin, is the same one produced by the brain to regulate mood, learning, and sleep, but the new study finds that serotonin produced by the gut has an entirely separate function. Mice engineered to produce extra serotonin formed weak bones, while mice engineered to produce less serotonin developed extra-strong bones. The research, though still basic, suggests new avenues of osteoporosis research in humans. “It’s what you’d call a landmark study,” Bjorn Olsen [a Harvard cell biologist who was not involved with the study] says. “It opens new doors” [Science News].
Although serotonin produced by the gut makes up 95 percent of the body’s serotonin, its function had not been well understood. The connection between serotonin and bone formation revealed itself through two types of rare human diseases, both involving the gene Lrp5. People with one mutation produced less Lrp5 protein, developing fragile bones and blindness, while people with another mutation produced extra Lrp5 protein, developing unusually dense bones and resistance to osteoporosis. However, when the authors of the new study looked into the gene further, they were surprised to find that it acted not in bone cells but in cells of the gut. “We, as bone [researchers], thought of the skeleton as functioning independent of everything else,” said [Cliff Rosen, a bone biologist]. This group “asked the question, ‘could there be other regulators outside the skeleton that are regulating bone?’ and found the answer to be ‘yes.’” [The Scientist].
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Injury to nerve cells in the brain and spinal cord, once considered permanent, may be reversible after all. A pair of new studies demonstrate how to override two biological mechanisms that prevent damaged cells of the central nervous system from regrowing. The first obstacle are genes that prevent nerve growth and the second are chemical signals that repress nerve growth.
In the first study, published in Science [subscription required], Harvard researchers identified a gene, PETN, that inhibits the major growth pathway in nerve cells. They created genetically modified “knock-out” mice that lacked the gene. Normally, axons in the optic nerve of adult mice do not regenerate when crushed—and worse yet, about 80% of the neurons with severed axons die. But in mice lacking PTEN, 50% of neurons survived and about 10% of axons in the optic nerve regrew—as far as 4 millimeters in 28 days. “To have any manipulation that can make these axons grow from where they were severed near the retina all the way down the optic nerve is just amazing,” [ScienceNOW Daily News] commented neurobiologist Ben Barres.
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Ten intrepid genetic explorers have volunteered to have their genetic information posted on the Internet for anyone’s perusal, along with photographs, their disease histories, allergies, medications, ethnic backgrounds and a trove of other traits, called phenotypes, from food preferences to television viewing habits [The New York Times]. The 10 volunteers are the first participants in the Personal Genomics Project, an endeavor run by Harvard Medical School that hopes to offer free genetic testing to 100,000 people in exchange for their privacy.
The project aims to advance genome research by tapping volunteers who have a Facebook-mentality sense of privacy–minimal–and enough excitement about genomic science that they are willing to lay out their genetic and medical information so any researcher can sift through it for links between genes and traits. “There’s a hope that by making these data public, you can harness crowd-sourcing power in the same way that Wikipedia and YouTube and Google and Linux all emerged from cooperative, distributed efforts” [Boston Globe], said Harvard psychology professor Steven Pinker, who is one of the 10 pioneers.
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In a counterintuitive new study, researchers have found that obese women get less pleasure from drinking a chocolate milkshake than average-weight women, and suggest that obese women are therefore more likely to overeat in an attempt to get that high. Researchers used a fMRI brain scanner to record women’s levels of the pleasure-providing brain chemical dopamine while they were sipping milkshakes, and found that obese women had a muted pleasure response.
They also studied a dopamine-regulating gene variant that has previously been linked to obesity, and showed that women with this variant had the lowest dopamine levels and were also very likely to gain weight over the ensuing year. Dopamine expert Nora Volkow says this furthers the research on the genetic component of obesity: “It takes the gene associated with greater vulnerability for obesity and asks the question why. What is it doing to the way the brain is functioning that would make a person more vulnerable to compulsively eat food and become obese?” [AP]
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