Don’t be alarmed, but on a remote island in Scotland the sheep are shrinking.
Instead of gradually increasing in size as expected due to evolution, the average weight of the wild sheep has decreased as average temperatures heat up. The discovery shows that a species’ response to global warming can be unpredictable, and can be based on multiple factors. According to a study published in Science, warmer and wetter winters have made it easier for smaller sheep to survive the hard months and go on to bear offspring, thus passing these “small” genes onto the next generation of sheep.
Since 1985, the average weight of the wild Soay sheep living on the island of Hirta has decreased by about 5 percent. Due to global warming, the winters on the Scottish isles are becoming becoming shorter and milder. That makes food more abundant and allows some of the smaller, more vulnerable and younger sheep to survive. Then they go on to have offspring that tend to be small themselves — and have a better chance of survival because of the increasingly mild winters. “The environmental and evolutionary processes are intertwined. There’s still natural selection, but it’s not leaving as big a signature as it used to. There’s still a disadvantage to being small, but not as much” [Time], says lead researcher Tim Coulson.
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For six years, psychiatrists thought they had found a genetic clue as to what makes some people more prone to depression when they’re hit with an emotional blow: a single gene. A 2003 study created a sensation among scientists and the public because it offered the first specific, plausible explanation of why some people bounce back after a stressful life event while others plunge into lasting despair [The New York Times]. But now a broader analysis of 14 studies has found no link between the gene and the risk of depression, and researchers argue that the 2003 findings were prematurely heralded as a breakthrough. “I think what happened is that people who’d been working in this field for so long were desperate to have any solid finding” [The New York Times], says Kathleen R. Merikangas, one of the authors of the new study.
The so-called “depression gene” that researchers focused on in the 2003 study helps regulate levels of serotonin, a brain chemical that plays a major role in depression and is a key target of antidepressant drugs. Researchers … found from a long-term study of 847 people in New Zealand that those with a short version, or allele, of the serotonin transporter gene were more likely to become depressed by adverse life events than were those with only long alleles [ScienceNOW Daily News].
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How life evolved from a mix of chemicals on the young planet Earth is one of science’s most enduring mysteries, which biochemists are attempting to solve by recreating the earliest building blocks of life in the laboratory.
Earth’s biology is based on DNA, which carries all an organism’s genetic information in a molecule that takes the shape of a spiraling ladder. RNA, the molecule that facilitates protein manufacturing, has a simpler shape–it’s a single strand, as opposed to DNA’s double strand–leading some biologists to propose the RNA world hypothesis in which RNA evolved first and eventually gave rise to DNA. But trying to imagine the assembly of RNA from its chemical components poses its own problems. How could RNA, which encodes proteins, first form, when proteins are needed for [its] synthesis? Now, scientists report that they’ve cooked up molecular hybrids of proteins and nucleic acids that skirt the dreaded paradox [ScienceNOW Daily News].
The hybrids they created could resemble the precursors to RNA, researchers report in Science. “It’s the pre-RNA world. There’s a hypothesis that says RNA is so complicated, it couldn’t have arisen de novo” — from scratch — “on early Earth,” said study co-author Luke Leman…. “So you need some more primitive genetic system that nature fiddled around with and finally decided to evolve into RNA” [Wired.com].
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In some lizard species, it’s not just genetics that determines whether males or females will clamber out of hatching eggs. Some species are also governed by nest temperature, like the the three-lined skink lizard: Seven years ago, Australian biologist Rick Shine showed that low nest temperatures could overrule genetics, and cause embryos to develop into males. Now, Shine and his colleagues have taken their skink research a step farther, showing that the size of an egg’s yolk also plays a mysterious role in the ultimate sex of the offspring.
Physiologist Rachel Bowden, who was not involved in this research, says the study “muddies the water” for everything researchers thought they knew about sex determination in lizards…. “It’s clear that they have sex chromosomes. But it’s also clear that those sex chromosomes can readily be overridden by some other factors. So, the process that leads to sex determination might be fairly plastic” [The Scientist].
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It was only a few years ago that scientists figured out how to reprogram adult cells to make them act like multipurpose stem cells, but the next discoveries are coming fast and furious. Researchers had previously transformed human skin cells into so-called induced pluripotent stem (iPS) cells that can grow into any type of tissue; now, a new study reports that the same feat has been accomplished with pig cells. The achievement raises the possibility that genetically engineered pigs could be reared as organ donors, researchers say.
The created iPS cells could be genetically altered, and then cloned to produce pigs with certain traits. By adding or deleting certain genes, for example, researchers could produce pigs whose organs can be transplanted into patients without them being recognised and rejected. Efforts to do such xenotransplants have already been under way for at least a decade, but iPS cells are easier to genetically engineer and grow in the lab than pig embryos, opening up new possibilities for xenotransplantation [New Scientist]. Pigs are considered potential organ donors because their organs are already similar to those of humans in size and function.
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The fishing boats that relentlessly sweep the northern Atlantic Ocean looking for cod may be changing the genetics of the species, researchers say, in a case of “fisheries-induced evolution.” Commercial fishing techniques used to harvest the valuable fish are wiping out the cod that swim at shallower depths, which have a genetic variant that’s not seen in cod that stick to deeper water. If overfishing of cod continues, the research team believes the genetic variant will be lost all together. “Man the hunter has become a mechanised techno-beast,” the team writes. “Modern fisheries are uncontrolled experiments in evolution” [New Scientist].
Evolutionary biologist Einar Árnason and his colleagues studied the changing population of the cod fishery around Iceland; it’s one of the largest in the world, yielding roughly 200,000 metric tons a year. The stocks are in far better shape than the collapsed fisheries in the western Atlantic [ScienceNOW Daily News]. In the new study, published in the journal PLoS ONE, the researchers examined how the genotypes of Icelandic cod have changed between 1994 and 2003.
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Scientists have taken another step in cellular reprogramming that points the way towards the use of a patient’s own cells to treat genetic diseases. In a proof of concept study, researchers took skin cells from patients with a rare condition, Fanconi anemia, which causes skeletal problems and bone-marrow failure, and raises sufferers’ risk of cancer [Technology Review]. In the skin cells, the researchers fixed the genetic defects that caused the disease, and then reprogrammed the cells to act like stem cells capable of growing into any type of tissue.
The corrected stem cells could be grown into blood precursor cells for therapy. As these would carry a patient’s own DNA, except for the mutation responsible for the illness, they could be transplanted without risk of rejection by the body’s immune system [Times Online]. However, the patched up cells were not used to treat patients in this study, because it isn’t yet clear whether such cells are safe. Comments molecular geneticist Chris Mathew: “In future it may become possible to transfer the corrected stem cells back into the patient, but much work remains to be done before this can be transferred from the lab bench to the bedside” [The Scientist].
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Researchers have endowed lab mice with the human version of a gene involved in language, and while the mice didn’t exactly sit up and start reciting poetry about cheese, they did show some intriguing differences in both their vocal patterns and brain structure.
Mice have their own form of the gene, called FOXP2, but they and all other animals lack key changes found only in humans and our evolutionary cousins, Neanderthals. Some researchers speculate that these differences may help explain why humans are the only animal able to communicate with complex languages, and not simple grunts, barks or songs [New Scientist]. By tweaking the gene in mice and changing it to the human form, researchers hoped to get a clue as to how our early hominid ancestors were changed by the new form of the gene.
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Five small monkeys that glow green under ultraviolet light are providing a beacon for medical research. Researchers introduced a jellyfish gene that codes for a fluorescent protein into the embryos of marmosets, and found that the resulting monkeys expressed the gene in all the cells of their body, including their egg and sperm cells–which means the genetically engineered primates can naturally pass on the foreign trait to their offspring. While creating a family of glowing monkeys doesn’t have obvious benefits for medical science, researchers say the study was really just a proof of concept.
Researchers have added genes to rhesus macaques before, but the new work with marmosets is the first to document that monkeys can pass an inserted gene along to future generations. That’s important because it opens the door to creating colonies of such “transgenic” monkeys by breeding, which would be far simpler than the cumbersome process of making each animal from scratch by inserting genes into embryos [AP]. Now that researchers have mastered the technique, they hope to create transgenic monkeys that carry genes associated with such diseases as Parkinson’s and Lou Gehrig’s disease.
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All’s fair in the fight against the AIDS virus–including medical sneak attacks. Researchers have devised a novel strategy to attack HIV by completely bypassing the immune system and instead tricking the muscles into producing virus-fighting proteins.
The quest for an HIV vaccine has been given a bad prognosis recently, due to increasing agreement that the human immune system isn’t clever enough to outsmart the ever-changing surface of the virus [Technology Review]. But using the new technique, researchers were able to protect monkeys from infection by the simian immunodeficiency virus (SIV), the animal virus most closely related to HIV. While lead researcher Philip Johnson cautions that there’s no guarantee that the vaccination process will work in humans, he’s eagerly looking forward to human trials in a few years.
Most efforts at blocking AIDS have sought to stimulate the body’s immune system to produce antibodies that fight the disease. This model has worked for diseases such as measles and smallpox. It hasn’t done as well with HIV/AIDS; test vaccines have failed to produce a protective reaction. So Johnson decided to try something different. “We used a leapfrog strategy, bypassing the natural immune system response that was the target of all previous HIV and SIV vaccine candidates,” Johnson said [AP].
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A major new lawsuit is challenging the notion that human genes can be patented just like the latest mousetrap built by a basement inventor. The case focuses on two genes, BRCA1 and BRCA2, that are linked to a higher risk of breast and ovarian cancer, and which were patented by the company Myriad Genetics more than 10 years ago. Now, the ACLU has organized a lawsuit backed by organizations representing more than 100,000 doctors and geneticists, and will argue that the information contained in each person’s DNA should not be private property.
The plantiffs also include individual cancer patients like Genae Girard, who was diagnosed with breast cancer, and took Myriad’s genetic test to see if her genes also put her at increased risk for ovarian cancer, which might require the removal of her ovaries. The test came back positive, so she wanted a second opinion from another test. But there can be no second opinion [The New York Times]. Since Myriad owns the patent to both the two genes and the test that looks for them, no other company can develop a competing test.
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The swine flu virus that has infected almost 6,500 people in 33 countries is not the product of a lab accident, World Health Organization officials declared yesterday.
The health officials were arguing against a hypothesis that emerged earlier this week. An Australian researcher named Adrian Gibbs who was has been involved in the development of antiviral flu drugs issued a report suggesting the new strain may have accidentally evolved in eggs scientists use to grow viruses and drugmakers use to make vaccines. Gibbs said he came to his conclusion as part of an effort to trace the virus’s origins by analyzing its genetic blueprint. “One of the simplest explanations is that it’s a laboratory escape,” Gibbs said…. “But there are lots of others” [Bloomberg]. Gibbs said this new virus had evolved faster than other flu viruses found in pigs, which he said suggested that it combined with other viruses being used in a lab. He argued that the virus could have then escaped into the general population.
But at a press conference, WHO official Keiji Fukuda announced that the hypothesis had been investigated and rejected. “Based on that evaluation by all of the laboratories, the conclusion is that this group of scientists feels that the hypothesis does not really stand up to scrutiny,” Dr. Fukuda said. “The evidence suggests that this is a naturally occurring virus and not a laboratory-derived virus” [MedScape]. He did not go into specifics of the investigation, but did say that the virus’s mutation rate was typical.
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In a masterful work of “DNA origami,” researchers have created a nanoscale DNA “box” which can be opened with DNA “keys”. One day, such structures could be filled with drugs, injected into the blood, and then unlocked when and where the drugs are required [New Scientist]. Researchers say the boxes could also be used as minuscule environmental sensors that open or close in response to a stimulus, or as the logic gates of a DNA-based computer.
To accomplish this feat, described in a paper in Nature, researchers exploited the fact that complementary DNA bases–the fundamental building blocks of DNA’s double helix–attach to each other. To design the box, the researchers developed a computer program to generate a continuous single-stranded DNA sequence that, along with smaller DNA fragments that act as staples, would self-assemble into the desired shape. The sequence was devised with many complementary regions so that it would automatically fold into six roughly square accordion-like sheets–the sides of the box–based on DNA’s natural tendency to pair into double strands. The DNA staples, also driven by the pairing of complementary sequences, stitched the sheets’ edges together to form a hollow cube with a hinged lid [Technology Review]. The final product was a box that measured 42 by 36 by 36 nanometers, and had a cavity big enough to hold enzymes or virus particles.
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Researchers have found good evidence that the troubling sleep disorder narcolepsy is an autoimmune disease, in which the body’s own immune system attacks healthy brain cells. A new study published in Nature Genetics links narcolepsy to mutations of two genes involved in critical roles in protecting the body from disease. These two variations, they say, are likely conspirators against [cells that produce] hypocretin, a hormone that promotes wakefulness, and that narcoleptics have been found to lack [HealthDay News].
Narcolepsy is a disruptive disorder that can trigger “sleep attacks” without any warning during any normal activity. In addition, some people can experience “cataplexy”, where strong emotions such as anger, surprise, or laughter can trigger an instant loss of muscle strength, which, in some cases, can cause collapse [BBC News]. There is currently no cure for narcolepsy, although the symptoms can be largely controlled with a mix of stimulants and sleep-suppressing medications.
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One week ago the world suddenly took note of swine flu, as a growing death toll in Mexico and the first rumors of cases in other countries raised the possibility of a pandemic. Now, after a fearful week of public paranoia and near hysterical reactions from some governments, researchers have taken their first hard look at the genetics of the virus. While the Centers for Disease Control still says it’s premature to say anything about the virulence compared with other strains of influenza based on genetic analysis [Technology Review], some researchers are arguing that the virus may be no more dangerous than the seasonal flu that hits every winter. But at this point, it is impossible to predict with any accuracy how the virus will continue to evolve [BBC News].
The H1N1 virus that is currently infecting humans is a blend of two viruses, a Eurasian swine flu and a North American swine flu, explains Raul Rabadan, a researcher who has analyzed the new virus. Influenza viruses mutate constantly and they also swap genetic material with one another promiscuously, especially if an animal or person is infected with two strains at once. Rabadan’s team said this particular strain looked partly like another hybrid, or what scientists call a reassortant, virus [Reuters]. The North American virus appears to contain genes from human and bird flu viruses as well, left over from previous genetic shufflings.
Flu researcher Wendy Barclay, who has also studied the virus’s genetic makeup, says that what she has seen thus far raises few red flags. When a flu virus binds to the upper respiratory tract, it tends to cause mild illness but can be easily spread as people cough and sneeze, Professor Barclay explains. If a virus binds further down in the lungs, it tends to cause much more severe illness, as in the case of the H5N1 avian flu virus which has caused concern in recent years [BBC News]. This swine flu virus appears to bind to the upper respiratory tract, Barclay says.
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