Shrink a grape, and you get a raisin. Shrink the grape genetic tree, and you get a looming disaster for oenophiles. That’s according to scientists who discovered that our cultivated wine grapes are more closely related than previously thought.
Sean Myles, a researcher at Stanford University, created a gene chip for common grape cultivars using genomes from the Department of Agriculture. In his study, published in the Proceedings of the National Academy of Sciences, he reveals that 75 percent of our 583 kinds of cultivated grapes are either parents, children, or siblings of each other.
“Previously people thought there were several different families of grape,” Dr. Myles said. “Now we’ve found that all those families are interconnected and in essence there’s just one large family.” [New York Times]
In this grape-world equivalent of the Jerry Springer Show, wines like merlot, pinot noir, and chardonnay are all interrelated in one big incestuous mash-up. And it’s the cultivators who are partly to blame.
The reason is obvious in retrospect. Vines can be propagated by breaking off a shoot and sticking it in the ground, or onto existing rootstock. The method gives uniform crops, and most growers have evidently used it for thousands of years…. The result is that cultivated grapes remain closely related to wild grapes, apart from a few improvements in berry size and sugar content, and a bunch of new colors favored by plant breeders. [New York Times]
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Talk about early intervention. One day, a fetus with a genetic disease may be able to get treatment before it even leaves the womb–and that treatment will come in the form of an extra gift from mom. While this scenario will only come to pass if new mouse research can be translated to humans, the finding are exciting.
The new work solves a medical mystery. When researchers realized they could diagnose a fetus with certain genetic illnesses as early as the first trimester, they plunged into the search for in utero treatments. Ailments like sickle cell anemia and some immune disorders might be treatable with blood stem cells taken from a donor’s bone marrow, researchers thought: the transplanted cells would multiply and populate the fetus’s bone marrow with healthy blood-forming cells, and the fetus’s immature immune system wouldn’t reject the foreign entities. But when researchers tried such transplants, they didn’t work.
“The fact that fetal stem cell transplantation has not been very successful has been puzzling, especially given the widely accepted dogma that the immature fetal immune system can adapt to tolerate foreign substances,” said co-senior author Qizhi Tang…. “The surprising finding in our study is that the mother’s immune system is to blame.” [press release]
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Though the swine flu scare of 2009 may have bumped the avian variety of flu from of the popular imagination, biomedical researchers certainly haven’t forgotten the potential danger it poses. But researchers are constantly forced to play catch-up by following bird flu’s path through the avian population and trying to track its shifting genetics.
The way to finally get the jump on bird flu would be to create a weapon that works against the whole family of avian flu viruses, whatever their slight genetic quirks. And researchers led by Laurence Tiley say in Science this week that they might have found that kind of comprehensive trick: a genetic modification that seems to prevent flu from spreading in chickens.
It’s a decoy.
The birds carry a genetic tweak that diverts an enzyme crucial for transmitting the H5N1 strain. Although they die of the disease within days, the molecular decoy somehow impedes the virus from infecting others. [Nature]
Specifically, this genetic tweak allows the birds to create an RNA impostor. It matches up to the polymerase enzyme the flu virus would use to replicate its genetic material, so that enzyme is attracted to the decoy, which throws off viral replication. Though the modified chickens that were infected with avian flu died, the fact that they didn’t spread the virus is a potentially huge find—once avian flu enters a chicken population it typically spreads like wildfire.
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However far-fetched some of their science has been, the barrage of forensic science TV shows during the last decade has ingrained into people the idea that even the most cautious criminals (we’re looking at you here, Dexter) leave something of themselves behind at the scene of the crime. And thanks to the march of genetic science and sequencing, those bits of someone can tell more and more about them. Even their hair.
In a study coming soon to the journal Human Genetics, Manfred Kayser and colleagues identify genetic markers that can predict a person’s hair color.
The researchers studied DNA and hair colour information from hundreds of Europeans. They investigated genes previously known to influence the differences in hair colour. “We identified 13 ‘DNA markers’ from 11 genes that are informative to predict a person’s hair colour,” said Professor Kayser. [BBC News]
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In a remarkable medical feat, researchers used a blood sample from a pregnant woman to work out the entire genome of her unborn fetus. The technique, published in the journal Science Translational Medicine, could provide a safer and less invasive way to check a fetus for fatal genetic mutations.
Currently, determining a fetus’s genome requires either amniocentesis, in which a needle is inserted through the mother’s abdomen into the amniotic sac, or chorionic villus sampling, in which a piece of placenta is removed. But both techniques carry a small risk to the baby, and are reserved for cases when there is an increased risk of genetic defects.
“The major advantage of the technique in this paper is that there’s no risk of miscarriage,” said Dr. Diana W. Bianchi, a reproductive geneticist at Tufts University who called the work a “technological tour de force.” Amniocentesis and CVS testing carry about a 1% risk of miscarriage, she said. [LA Times]
The new technique sequences the fetal genome from fragments present in the mother’s blood. In the late 1990s researchers discovered that fragments of fetal DNA are present in maternal plasma, presumably because the DNA gets broken down and crosses over the placental barrier.
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This week in bizarre new forms of mammal reproduction: mice who have genetic material from two fathers but nary a mother, the next step in a progression of scientific efforts to get more creative with sex and reproduction.
“It has been a weird project, but we wanted to see if it could be done” in mice, says Richard Behringer, lead author of the study and a developmental geneticist at M.D. Anderson in Houston. [Wall Street Journal]
Weird, and also complex: The process requires several generations and some creative genetic trickery. To make it happen, Behringer’s team started with a single male mouse. Let’s call him Fred. Scientists took cells from Fred and transformed them into a line of induced pluripotent stem cells, which can grow into any kind of cell in the body. Normally, of course, a male’s sex chromosomes are X and Y. But when the researchers created these stem cells, some of them—about 1 percent—lost the Y chromosome through ordinary mistakes that happen in cell division.
Thus, the scientists had a batch of Fred-derived stem cells that had no Y, and thus were labeled XO cells. The next step was to take ordinary mice blastocysts—early stage embryos that had been conceived in the traditional fashion—and inject the XO cells into them. When this XO-injected embryo was implanted into a normal female mouse, she gave birth to offspring called chimera—what we call animals with two or more genetically distinct populations of cells. In this case the mouse possessed, in addition to the normal cells from its mother and father, some XO cells derived from Fred.
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First came the extraterrestrial speculation. Then came the actual answer. Then came the backlash.
NASA’s big astrobiology news last week had nothing to do with E.T., of course—the team behind a study in Science announced the find of a kind of bacteria that appear to thrive in arsenic and can even use it in place of phosphorus in the backbone of its DNA double helix. But after the big announcement finally happened and squelched the more imaginative rumors, scientists started asking some hard questions about the study online.
Over at Slate, DISCOVER blogger Carl Zimmer rounded up expert critiques from biologists, and many didn’t hold back.
Almost unanimously, they think the NASA scientists have failed to make their case. “It would be really cool if such a bug existed,” said San Diego State University’s Forest Rohwer, a microbiologist who looks for new species of bacteria and viruses in coral reefs. But, he added, “none of the arguments are very convincing on their own.” That was about as positive as the critics could get. “This paper should not have been published,” said Shelley Copley of the University of Colorado. [Slate]
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The science world is abuzz with news of a strange new life form found in California’s Mono Lake: Researchers report that they’ve discovered a bacterium that can not only thrive in an arsenic-rich environment, it can actually use that arsenic to build its DNA. If the researchers, who published their findings in Science, are correct, then they’ve found a form of life unlike anything we’ve ever seen before.
As you might expect, DISCOVER’s blogs offered plenty of coverage of this exciting news.
At The Loom, Carl Zimmer writes: “Scientists have found a form of life that they claim bends the rules for life as we know it. But they didn’t need to go to another planet to find it. They just had to go to California.”
At Bad Astronomy, Phil Plait explains exactly how the bacteria can make use of arsenic to build their DNA. A few days ago, Phil also took NASA to task for its press release promising news of “an astrobiology finding that will impact the search for evidence of extraterrestrial life,” which fueled wild speculation on whether NASA had found little green men in the solar system.
At Not Exactly Rocket Science, Ed Yong debunks a few of the more breathless accounts. The bacteria do not “belong to a second branch of life on Earth…. They aren’t a parallel branch of life; they’re very much part of the same tree that the rest of us belong to. That doesn’t, however, make them any less extraordinary.”
At Gene Expression, Razib Khan has more thoughts on the wild speculation that preceded the announcement–which he compares to the hype surrounding the unveiling of the Segway.
Related Content:
80beats: Life Found in the Deepest, Unexplored Layer of the Earth’s Crust
80beats: Do Asphalt-Loving Microbes Point the Way to Life on Titan?
80beats: Arsenic-Eating Bacteria May Resemble Early Life on Primordial Earth
DISCOVER: Renewed Hope for Life on the Red Planet
In the rigid social universe of Revenge of the Nerds-style 1980s movies, jocks beget jocks beget jocks, and the bespectacled geeks they push around beget generations of the same. But could being a victim of social bullying actually be inherited? A new study of DISCOVER’s favorite rodent, the marmot, shows that at least in the animal kingdom, the answer can be yes.
Daniel Blumstein and colleagues tracked yellow-bellied marmots that make their home in the Colorado Rockies for a five year period, from 2003 to 2008. For their study out in the Proceedings of the National Academy of Sciences, the team tracked the family relationships of the individual marmots, as well as who antagonized whom.
Marmots don’t have Facebook yet, but animals living among clusters of burrows in Colorado do interact enough for observers to plot networks with each marmot as a node. An exchange might be friendly, such as a marmot grooming a neighbor or settling down tranquilly nearby. Or a social interaction might go sour, with one marmot nipping or chasing another. “Marmots are grumpy with each other,” Blumstein says, but rarely cause serious injuries. [Science News]
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Researchers have identified 30 genes that play a role in the onset of menstruation in girls. Some of these puberty genes have previously been linked to body weight and fat metabolism, strengthening the connection between the obesity epidemic and the early onset of puberty in industrialized nations.
For the study, published in Nature Genetics, researchers analyzed 32 genome-wide association studies that included more than 87,000 women from the United States, Europe and Australia, and then replicated the results in a further 14,000 women. Of the 30 genes that they found play a role in the timing of women’s first periods, four genes are linked to body mass index, three play a role in metabolism, and three are involved in hormone regulation.
Study co-author, Dr Enda Byrne of the Queensland Institute of Medical Research says the results from this study show that many of the genes that increase risk for weight gain and obesity in adulthood, also influence the onset of puberty. “This supports the idea that the body launches into puberty once it reaches a certain level of nutrient stores and therefore children who are overweight are more likely to undergo early puberty,” says Byrne. [Australian Broadcasting Corporation]
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From Ed Yong:
The vast majority of people who are infected with HIV go on to develop AIDS. Their bodies become riddled with the virus, their immune systems falter, and they are besieged by life-threatening infections. But not everyone shares the same fate. Around 1 in every 300 people infected with HIV carry genetic trump cards that allow them to resist and control the virus. These “HIV controllers” can live with the virus for years. They never develop AIDS and they live long, healthy lives, even if they never take any medication. Their genetic secrets are slowly being revealed.
Researchers studying thousands of people with HIV, some with the controllers and some without, found something surprising:
Amazingly, every single one of these variants sits within a specific part of our sixth chromosome, among a set of genes called class I HLA genes. The proteins they produce form part of the internal security checks that defend us from infections. They grab small pieces of other proteins from inside our cells and display them on the outside, waving them under the noses of passing T-cells. If the T-cells recognise these pieces as parts of bacteria, viruses or other foreign invaders, they tell the infected cell to self-destruct and set the immune system on red alert.
Check out the rest of this post at DISCOVER blog Not Exactly Rocket Science.
Related Content:
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80beats: Good News: Anti-Microbial Gel Cuts HIV Infection Rates for Women
80beats: New HIV Hope? Researchers Find Natural Antibodies That Thwart the Virus
80beats: Gene Therapy Hope for HIV: Engineered Stem Cells Hold Promise
80beats: Did the Eradication of Smallpox Accidentally Help the Spread of HIV?
Image: Wikimedia / HIV Budding
Rosalind Franklin would probably not have appreciated her posthumous reputation. First there was the colossal insult of being denied due credit for her role in the discovery of DNA’s double helix shape, a breakthrough that revealed not only the form of our genetic material, but also how it functioned. James Watson and Francis Crick received the lion’s share of the glory for that finding, and for decades Franklin was a historical footnote.
But it seems likely that this no-nonsense scientist wouldn’t have appreciated being reduced to a feminist cartoon either–more recently, she’s been held up as an example of a woman crushed by the good old boys network.
That’s why a new play at New York’s Ensemble Studio Theatre is so necessary, and so right on the money. The play, called Photograph 51, honors Franklin’s achievements and rues her relative obscurity, but it also returns to her the ambiguities and complexities that a real human being deserves.
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Three times the plague has appeared in deadly force. And all three times, scientists have found, the disease-bearing bacteria originated in China and spread across the world through different routes.
The plague’s most famous appearance came as the Black Death in 14th century Europe, when it wiped out nearly a third of the population. But it also struck as the Justinian Plague in the Byzantine Empire of the 6th century, and a less severe outbreak spread around the world and reached the American mainland in 1900 (see map above). This week in the journal Nature Genetics, Mark Achtman and colleagues rebuilt the evolutionary history of the bacterium Yersinia pestis, the cause of bubonic plague, and traced all three major waves of plague back to a starting point in China.
By looking at genetic variations in living strains of Yersinia pestis, Dr. Achtman’s team has reconstructed a family tree of the bacterium. By counting the number of genetic changes, which clock up at a generally steady rate, they have dated the branch points of the tree, which enables the major branches to be correlated with historical events. [The New York Times]
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Scientists knew that overweight mothers tend to have more overweight children. But is the same true for fathers? This week in Nature, Margaret Morris and her team demonstrated this effect in male rats, the first time it’s been shown to work in males. The findings are another example of how non-genetic factors, like how much a parent eats, can have a biological impact on offspring.
The researchers put one of their two groups of male rats on a high-fat diet, the other on a normal one. Unsurprisingly, the high-fat rats put on a lot of weight and began to show symptoms of type II diabetes, like insulin resistance and struggles with metabolizing glucose. And then there were their kids:
The real surprise came when Morris’s team went on to examine the obese rats’ female offspring. These too had problems regulating insulin and glucose levels. The healthy fathers, however, had correspondingly healthy daughters. Whether similar defects emerge in sons remains to be seen. [Nature News]
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Next time you’re at the pub with friends, take it easy on the lightweights—the ones who are getting a little silly after just a couple of drinks. That might be a blessing in disguise, according to a new study, because the 10 to 20 percent of people whose genetics make them especially sensitive to booze might also be at greatly reduced risk to develop alcoholism.
In the journal Alcoholism: Clinical and Experimental Research, Kirk Wilhelmsen and colleagues identified a particular gene associated with the easily intoxicated. The gene in question encodes an enzyme called CYP2E1, responsible for metabolizing not just alcohol in the brain, but also other substances like acetaminophen (Tylenol).
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