Dear reader: You’re a mutant. But take comfort—it’s not just you. According to recent research, every person on Earth introduces between 100 and 200 new genetic mutations into the human genome.
BBC News reports:
[Researchers] looked at thousands of genes in the Y chromosomes of two Chinese men. They knew the men were distantly related, having shared a common ancestor who was born in 1805.
By looking at the number of differences between the two men, and the size of the human genome, they were able to come up with an estimate of between 100 and 200 new mutations per person.
This number of mutations is small compared to the size of the full human genome, so finding them was apparently quite a feat. Such a feat, in fact, that one of the scientists reportedly said that “finding this tiny number of mutations was more difficult than finding an ant’s egg in an emperor’s rice store.”
Some mutations can give rise to health conditions like cancer, so being able to identify new genetic variations not only could teach us about our own evolution, but could even help prevent disease-causing alterations in our DNA.
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Image: flickr / ghutchis
Could milk from mice be the next key ingredient in infant formula? Perhaps…if researchers can find an efficient way to milk them, that is.
Apparently, getting the tiny rodents to produce lactoferrin, a protein found in human breast milk, wasn’t a problem, once the Russian scientists added a few human genes to the mice’s genome.
Mouse milk naturally has a higher concentration of proteins than the human stuff, so when the mice began producing human milk protein, they made a lot of it. In fact, the fuzzy creatures produced up to six ounces of lactoferrin per quart of milk, as opposed to the measly four to five grams per quart pumped out by humans. The lactoferrin in breast milk is important because it shields babies from infection as their immune systems form.
Mass production of human milk protein could allow the substance to be used in synthetic infant formula. Today, formula is largely made up of protein from soybeans or cow’s milk, and although the subject remains controversial, some experts say it does not provide babies with the same health benefits of human milk.
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No, he’s not Supercat, but apparently a fuzzy feline in the southwest Chinese city of Chongqing began sprouting triangular, fur-covered “wings” out of his back when he was about a year old.
Some speculate the strange growths are the result of a mutation caused by chemicals the cat’s mother was exposed to before giving birth. It’s certainly possible, since the heavily industrialized city of Chongqing is packed with chemical, metal, and automobile factories pumping out acid rain and air pollution. In fact, as of 2004 the city was the second most polluted worldwide. And it’s taking its toll: Environmental authorities suspect chemical contaminations were behind the deaths of thousands of fish in the Fujiang River in Chongqing a few months ago.
Others say the so-called wings are actually growths from an embryo that never completely separated from the cat before birth – in other words, the cat’s, er, Siamese twin.
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If you can drink your friends under the table, you may have your genes to thank. Researchers at the University of California, San Francisco, have for the first time pinpointed a genetic mutation that determines your tolerance for booze. Specifically, those who have the so-called “happy hour” mutation produce a protein called epidermal growth factor, or EGF, which allows them to imbibe more alcohol than their peers before feeling its effects, such as falling asleep or getting just plain sloppy.
Of course, the “happy hour” gene comes at a cost: Experts say a high tolerance for booze predisposes a person to alcoholism. As such, scientists say that they might be able to both decrease alcohol tolerance and help treat alcoholism by deactivating the gene.
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We blame genes for obesity, mental illness, and a host of other issues. But can they determine when we lose our virginity? Researchers are now saying yes, they can—or, at least, that’s what media reports are saying researchers are saying.
Here’s the real deal: According to a study out of California State University, our genes may play a (minor, debated) role in the age at which people first have sex.
CSU psychologist Nancy Segal looked at 48 pairs of twins who were separated at birth to see how genes influenced their sexual maturity. To compare the twins’ sexual histories, Segal had each of them take a “sexual life history interview” composed of a “sexual meaning survey, a sexual life history timeline, and a sexual behavior questionnaire.” The researchers found that most twins lost their virginity at around 19 years of age. New Scientist calls the findings “modest” at best—the genes “explain a third of the differences in the participant’s age of first intercourse.”
Of course, despite screaming headlines to the contrary, exactly how genes are linked to the loss of virginity is still thoroughly “speculative,” as Segal told DISCOVER. Other groups have pinpointed a gene—DRD4— that has been linked to age of loss of virginity.
Given all the hoopla, it’s worth asking, are these studies really linking genes and virginity at all? DRD4 is known as the “risk taking” gene? People who are risk takers also abuse alcohol and drugs or engage in delinquent behavior—virginity is only one risk-taking measure, and an arguable one at that.
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Remember the guy from Super Size Me who ate about 23,000 Bic Macs and never got fat? Ever wonder how he did it? Turns out he may have been born without the “fat enzyme.”
The enzyme MGAT2 is found in the intestines and determines the fate of our food by regulating how it is metabolized: It either makes fat go straight to your waistline, or converts it into energy. Scientists in California have discovered that when mice are missing the gene for MGAT2, they can eat whatever they want and never have to worry about getting fat.
The University of California at San Francisco knocked out the gene in experimental mice to see how their bodies grew after feeding them different diets. When the normal and experimental mice were fed a diet low in fat, both sets of mice grew the same way. But when the mice were eating a 60 percent fat diet (i.e., a typical American diet), the experimental mice weighed 40 percent less and had 50 percent less fat than the normal mice.
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Is it a “chickenosaurus,” or a “dinochicken?” Famed paleontologist Jack Horner says that if you want to grow a dinosaur, you have to start with a chicken egg. As descendants of dinos, chickens carry some of the same DNA. So if chicken embryos have their genes reversed-engineered for every trait that they share with dinosaurs— like long tails, teeth, and three-fingered hands— you can grow living animals with dinosaur traits.
Previously, paleontologists thought they would be able to extract DNA from amber and then use it to clone dinosaurs, just as Michael Crichton detailed in his novel. But the real life experiments repeatedly failed and the idea appears to be possible only in fiction.
Horner (who was an inspiration for the character Dr. Alan Grant) thinks “the better route is to start with a descendant and work backwards. By taking a bird and manipulating four or five of its genes, you can grow a long tail instead of wings.” Then you can manipulate other traits to produce a complete dinosaur.
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Scientists have discovered two pounds of a dried plant that turned out to be the oldest marijuana in the world. Inside one of the Yanghai Tombs excavated in the Gobi Desert, a team of researchers found the cannabis packed into a wooden bowl resting inside a 2,700-year-old grave. It was placed near the head of a blue-eyed, 45-year-old shaman among other objects like bridles and a harp to be used in afterlife.
At first, the researchers thought the dried weed was coriander. Then they spent 10 months getting the cannabis from the tomb in China to a secret lab in England. Finally, the team put the stash through “microscopic botanical analysis” including carbon dating and genetic analysis, and discovered the stash was really pot.
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This is it. The evolution of Homo sapiens is complete, says British geneticist Steve Jones—not because we’ve reached some pinnacle of perfection, but because we’ve run ourselves into an evolutionary dead end. Jones argues that the structures of contemporary society have jammed the three main drivers of evolution: natural selection, mutations, and random change.
He spoke yesterday at the University College London, delivering a lecture entitled “Human Evolution is Over” (in case you had any doubts as to his hypothesis). Here are his three main points:
1) Fewer early deaths. If everyone lives to reproductive maturity (in the developed world, nearly 98 percent of people survive to the age of 21), natural selection can do little work.
2) Fewer elderly fathers. As a man ages, the likelihood of genetic mutations in his sperm increases dramatically. It used to be common for men to father many children with many different women well into old age, but this is less acceptable in today’s society.
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Break a mirror and you’re stuck with bad luck. Walk under a ladder and you’re tempting fate. Sound ridiculous? Scientists believe such beliefs may be genetic, part of adaptive behaviors passed on to create an evolutionary advantage to surviving impeding danger.
Boiled down, a superstition is the belief that one event caused another event, without any evidence of the link. “All animals will display behaviors that imply a causal relationship that isn’t there,” says Kevin Foster, evolutionary biologist at Harvard University. Foster uses a pigeon as an example: The pigeon will take flight if it hears a hand clap, the same way it would react if it heard a gun shot.
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