What’s the News: It turns out that humans aren’t too different from blue-footed boobies, at least when it comes to age and fertility. Researchers have recently discovered that the sperm of blue-footed boobies declines with age. And unlike humans, the blue feet of the boobies also fade with age, revealing that one reason why female boobies tend to mate with brighter-footed males is to ensure the robustness of the sperm and the health of their offspring. “The study provides us with a new way of looking at what lies behind sexual signals,” lead author Alberto Velando told TIME, “pointing to the importance of sexual selection in eliminating genetic mutations.” (more…)

Selfish genes could help destroy mosquitoes’ ability to carry malaria.

What’s the News: Many scientists have played with the idea of creating a genetically modified mosquito that won’t transmit malaria, which kills about 850,000 people a year, and releasing it into the wild. But in the face of the millions of mosquitoes out there that do ferry malaria around, how would the trait spread fast enough to make a difference?

Now, scientists have developed a way to cause a “selfish” gene to spread to more than half of a mosquito population over just a few generations, suggesting a method to quickly and broadly disrupt genes required for carrying malaria.

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What’s the News: Test-tube evolution just went viral: a new study shows how to use viruses’ knack for natural selection to create tailored proteins. Researchers at Harvard say their new technique is a hundred times faster than the usual methods, churning through 200 generations of proteins in 8 days, and, crucially, requires no attention from researchers after it’s set up: a crock pot for evolution. Though a godsend primarily for researchers, in the future it could accelerate the growth of customized proteins for new drugs.

Scientists have harnessed the power of viruses in a method for evolving customized proteins.

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What’s the News: DARPA wants to fund research into technologies that could be built into the genome of microorganisms and keep track of any changes made to the organism’s genes, according a call for proposals the agency made earlier this month. In other words, DARPA wants to “turn on Track Changes” in certain viruses and bacteria.

What’s the Context:

• This genetic surveillance technology would help safeguard intellectual property, DARPA says. (See this PDF for the full description of the request.) Patenting genes has proven controversial enough on its own, so high-tech policing of these patents is unlikely to go down easy.
• Second, this technology could be used for “providing secure access” to dangerous pathogens or “proprietary microorganisms.” In other words, they want it to password-protect bugs, for reasons of health and/or commerce.
• DARPA isn’t shy about asking for proposals that are more than a bit off the wall: how to make a cannon that can fire people onto a tall roof, for instance, or a Jestons-esque flying car.

How the Heck: No idea. And, judging by its description, DARPA isn’t too sure either. The agency is asking for “multidisciplinary research proposals” and gives a nod to “possibly utilizing a cryptographical or complex mathematical approach.”

Image: Wellcome Images / Peter Artymiuk

What’s the News: The reproductive life of a cuckoo is both easy—it lays its eggs in others birds’ nests, and lets them feed the young—and difficult: cuckoos are involved in an “evolutionary arms race” with other birds, finds a new study. Even as cuckoos improve their counterfeiting skills—producing eggs that look more like others birds’—the host birds get better and better at identifying the forged eggs.

How the Heck:

• Knowing that birds have four types of color-sensitive cone cells in their eyes, allowing them to see ultraviolet wavelengths, researchers used a spectroscope to measure the amount of light reflected from hundreds of cuckoo and host-bird eggs. They then fed this data into models to produce images showing how birds see the different types of eggs.
• They discovered that while cuckoo and redstart eggs have a high degree of color overlap, cuckoo eggs targeted for dunnock nests did not.
• Here’s the kicker: Redstarts and dunnocks don’t spot forgeries equally. Redstarts are more discerning of foreign eggs and readily kick out cuckoo forgeries, while the dumb dunnocks accept even the most mismatched eggs. So these findings suggest that cuckoos targeting redstarts evolved the ability to create better forgeries because the redstart has such a good eye. With dunnocks, that evolutionary force wasn’t at play because the birds are so accepting of forgeries; why bother?

What’s the Context:

• What sets this research apart from previous work is how the researchers used UV-sensing equipment to mimic bird vision. (Past research relied merely on human inspection.)
• Not Exactly Rocket Science covers a lot of cuckoo news, from how some host birds have an evolutionary advantage to take care of cuckoo eggs to how grown cuckoos actually mimic hawks to fool small birds.
• Carl Zimmer in The Loom touches on how humans are like cuckoos.

The Future Holds: Scientists still aren’t sure why some hosts, like the dunnock, are so accepting of cuckoo eggs. Some scientists argue that this is because the risk in mistakenly rejecting a real egg outweighs the cost of raising a cuckoo egg. The jury’s still out.

Reference: “AVIAN VISION AND THE EVOLUTION OF EGG COLOR MIMICRY IN THE COMMON CUCKOO” Mary Caswell Stoddard and Martin Stevens. DOI: 10.1111/j.1558-5646.2011.01262.x

Image: NHM

Back in the 1980s, gene therapy was one of science’s greatest hopes and hypes, and researchers predicted the technique would be used to cure a huge range of illnesses. During the 90s, many early gene therapy trials were effective or downright dangerous, some causing cancer or even death. But more recently, scientists who stuck with gene therapy have started to see positive results, with promising treatments for malformed hemoglobin, color blindness, and depression. (See the DISCOVER magazine feature “The Second Coming of Gene Therapy” for more.) Now, researchers have announced that they’ve successfully treated the symptoms of Parkinson’s disease in a small group of people—a far cry from a cure, but still a step in the right direction.

I Once Was Blind but Now I See

The theory behind gene therapy is simple: A healthy gene hitches a ride into the patient’s genome on a virus, replacing the genes responsible for some genetic disease or disorder. Actually doing this is more difficult, because humans have a little thing called an immune system that’s remarkably efficient at finding and destroying foreign bodies. After the first U.S. death from gene therapy in 1999, and leukemia cases in France the same year, many started to think that gene therapy was more of a problem than an answer.

The early and awful failures forced all of the researchers in the field to retreat and reconsider the staggering complexity that challenged them. They could not just replace a bad gene with a good gene, as some early pundits had hoped—they also had to orchestrate the nuanced and elaborate dance between the gene products (proteins) and the patient’s immune system, which could recognize a foreign body and viciously attack it. After that was settled, gene therapists still had to find a suitable virus, or vector, to carry replacement genes into human cells without inciting a damaging or deadly immune response…. It was this new perspective more than anything else that turned gene therapy from a simple but failed and frustrated hope into, once again, medicine’s next big thing—a stunning spectacle of hubris, ignominy, and redemption on the scientific stage. [DISCOVER]

New: Gene Therapy and Parkinson’s Disease

While there’s no cure for Parkinson’s as of yet, doctors have an arsenal of methods, ranging from drugs, brain stimulation, and (now) gene therapy that help reduce the disease’s symptoms. Hopes for using gene therapy to alleviate Parkinson’s effects aren’t new. What is new is that scientists have successfully completed the first randomized, controlled, double-blind trial of treating Parkison’s patients with gene therapy—and they found that it significantly improved debilitating symptoms such as tremors, motor skill problems, and rigidity. (more…)

Brown rice. White rice. Sushi. Rice pudding. Rice in all its wonderful forms is the main food source of over three billion people, which makes this statistic all the more ominous: Right now, droughts and floods threaten over 25% of Earth’s rice harvests. But that doesn’t faze one group of scientists who have discovered that rice evolved to to resist floods also resist droughts.

The gene Sub1A, which is found in a few strains of rice, is responsible for this dual flood-drought protection. The researchers who discovered it in 1996 feared that a gene that protects a plant against flooding might make it especially sensitive to drought. So UC–Riverside researcher Julia Bailey-Serres and her colleagues were all the more surprised that the Sub1A gene actually makes rice better at coping with water shortage. This welcome trait became apparent after the water-starved plants grew fresh shoots after the researchers subjected the plants to a mock drought in the lab.

So how does a single gene work against both floods and droughts? The gene triggers a stressed plant to go dormant (whether that stress is an overabundance or lack of water) until the environment recovers from that stress. This may seem like an ability of limited use out in the world, but it’s actually important for some plants. After water levels go down at the end of a flood, a rice plant that had grown accustomed to soaking in water becomes dehydrated, as if it were suffering through a drought. As strange as it sounds, drought is a natural process in the flooding cycle, and it’s this fact that tricks the Sub1A gene into allowing rice plants to become dormant during both floods and droughts, conserving energy for up to two weeks, before reawakening after the waters recede or rain finally returns.

This gene for flood tolerance only naturally occurs in certain low-yielding rices in India and Sri Lanka, but scientists have already genetically engineered some high-yielding rice to exhibit this trait—which means that some farmers have also unknowingly been protecting their crops from droughts as well.

Related Content:
DISCOVER: #49: Plant Migration Tied to Climate Change
80beats: Worsening Drought Threatens Australia’s “Food Bowl”
80beats: Global Warming May Make Half the World Hungry by 2100
80beats: More Floods, Droughts, and Hurricanes Predicted for a Warmer World

Image: flickr / matsuyuki

Swine flu is not gone, and it is not stagnant. Though the public health scare about the 2009 swine flu pandemic subsided, the virus—like avian flu—remains in pockets of animals, shuffling its genes while hidden from the watchful eyes of virus experts. Virologists call this genetic switcheroo “reassortment,” and it’s how new and dangerous strains of flu snuck up on humankind in the past—and how they could do it again. This time, though, virologist Jinhua Liu and colleagues are trying to get a jump on the viruses.

For a new study in the Proceedings of the National Academy of Sciences today, this team of Chinese researchers simulated what could be a dire situation for humans: swine flu (H1N1) and avian flu (H9N2) together in one animal. When these flu strains are together they can exchange genetic material. So to test what that mixing might produce, Liu’s team swapped genes between the two and created 127 hybrid viruses, testing each on mice.

Eight of these hybrid strains turned out to be more virulent and dangerous in the mice than their parent strains of swine flu and bird flu. [National Geographic]

According to Dutch virologist Ab Osterhaus, we can’t be sure that these eight nasty strains are the ones that would hit humans hardest—animal studies aren’t perfect.

“Mice mirror, to a certain extent, what happens in humans,” he says, but they are not perfect model animals. Liu agrees. He plans to investigate how contagious his new viral blends are in guinea pigs and ferrets—animals whose respiratory system better reflects our own feverish battle with flu. [ScienceNOW]

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They’re about three and a half feet tall and their origins are mysterious, but an isolated group of Ecuadorians with a genetic mutation causing dwarfism are making news for another reason: They hardly ever get cancer or diabetes. Medical researchers say the villagers’ genetic protection from these diseases could lead to preventative treatments for the general population–and could therefore increase human longevity.

The villagers’ condition is called Laron syndrome, which is caused by an insensitivity to growth hormone.

Laron syndrome results from a mutation in the gene that codes for growth hormone receptor (GHR), a protein that binds with the human growth hormone and ultimately results in the production of the insulin-like growth factor 1 (IGF1), causing cells to grow and divide. When a person has two of these mutated and non-working genes, they can develop the disease. [LiveScience]

Jaime Guevara-Aguirre, the leader of the study about the Ecuadorians appearing in Science Translational Medicine, has been looking into their condition and extraordinary resistance to age-related diseases for more than two decades, since his serendipitous discovery of the people while riding horseback in Ecuador.

“I discovered the population in 1987,” Dr. Guevara-Aguirre said in an interview from Ecuador. “In 1994, I noticed these patients were not having cancer, compared with their relatives. People told me they are too few people to make any assumption. People said, ‘You have to wait 10 years,’ so I waited. No one believed me until I got to Valter Longo in 2005.” [The New York Times]

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It was a stroke of serendipity that may one day help those who hide under comb overs or wear wigs: scientists studying how mice bowels react to a stress-reducing chemical have inadvertently discovered a cure to baldness. But unfortunately, it looks like this cure won’t apply to genetic baldness, which is by far the main cause of most hairless pates. Still, researchers hope the lucky find will eventually be used to battle at least some of the bare heads of humans.

The story begins with mice that were genetically modified to produce too much corticotrophin-releasing factor, or CRF–a type of stress hormone. Normally, as these stressed-out rodents age, their backs lose hair. But a group of researchers from the Veterans Administration and the University of California at Los Angeles didn’t care about hair, they just wanted to study the effects of a chemical on the modified mice.

Researchers at the Salk Institute developed a peptide called “astressin-B”, which blocks the action of CRF, and the teams injected the peptide into the bald mice. They weren’t thinking about baldness at all — they wanted to test whether the astressin had any impact on the mice’s gastrointestinal tracts. The first injection did nothing, so the team gave the mice additional injections over five days, and then measured the effects on the newly de-stressed mice’s colons. [Popular Science]

With most of the experiment done, the researchers forgot about the mice for three months. Then they returned for some follow-up tests:

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As more hospitals have begun using DNA testing to analyze babies with birth defects, doctors have occasionally discovered that a family’s little bundle of joy is also a product of incest. Since this is a new dilemma brought on by the spread of technology, doctors are now debating how to handle these incest surprises.

Geneticist Arthur Beaudet at Baylor College of Medicine addressed the issue yesterday in an article in the medical journal The Lancet. The genetic test, the single nucleotide polymorphism-based array, helps doctors identify missing genes (and can therefore help explain a child’s birth defect or disability)–but it also identifies swaths of identical DNA that a child may have inherited from two closely related parents.

In the few months that Baylor has been performing these detailed genetic tests, there have been fewer than 10 cases of consanguinity — the phenomenon of inheriting the same gene variations from two closely related people, said Dr. Arthur L. Beaudet, chairman of Baylor’s department of molecular and human genetics. However, wider use of such testing in children with disabilities is expected to identify additional cases of incestuous parentage. [ABC News]

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Scientists are devising cleverer and cleverer means to see inside the brain—and creating some amazing pictures along the way.

These psychedelic images come from one of two studies in the journal Nature Methods, which present similar but slightly different ways to color the connections between neurons in a fruit fly. The projects build upon similar research from 2007 that achieved this “brainbow” effect in mice, and they could allow for new ways to track the formation and purpose of brain cells.

The researchers gave the insects genes for a red, a green, and a blue fluorescent protein. The genetic control system they devised spurs each cell to make a different amount of each of the three proteins. Like the red, blue, and green pixels on a TV screen, the combination of the three proteins causes each cell to glow a unique color. [ScienceNOW]

The inserted genes come from naturally glowing jellyfish. They allow not just individual cells to be seen, but also connections:

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Considering the huge numbers of species that have had their DNA sequenced in the wake of the genomics revolution, it might be surprising that scientists are so excited about a tiny freshwater crustacean. But this one is special: The genome of the water flea contains a staggering 30,907 genes—the most ever seen in an animal, and about 8,000 more than humans have.

Daphnia has a large number of never-before seen genes…. “More than one-third of Daphnia‘s genes are undocumented in any other organism — in other words, they are completely new to science,” said Don Gilbert, coauthor and Department of Biology scientist at IU Bloomington. [Discovery News]

According John Colbourne, coauthor of the study in Science, those never-before-seen genes are not dead weight, but rather some of the most important in the crustacean’s genome for responding to changes in its environment.

Not all of the crustacean’s genes are active at any given time. Rather, a large portion of them are switched on or off with changes in the flea’s environment. They are “more or less environment-specific,” Colbourne says. Although they are “coding for the same proteins, they’re being expressed differently depending on what environmental stresses you expose the animal to.” [Scientific American]

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What would you do if calcium deposits were building up in your blood vessels and making it hard to walk, and your doctors said they couldn’t help because they had no idea what disease you had, or how to treat it? Before 2008 you wouldn’t have had many options, but thanks to the National Institute of Health (NIH) you now have at least one: visit the Undiagnosed Diseases Program–where medical researchers just cracked their very first case.

Located in Bethesda, Maryland, this program takes on the medical cases that stump other hospitals. The program has received over 1700 referrals since it started, and has accepted only 330 of them. The results of their first case were published this week in The New England Journal of Medicine, but it all started with dumbfounded doctors and some confusing x-rays:

In 2009, the program received a referral from a Kentucky doctor for two sisters, Paula Allen and Louise Benge, who suffered from joint pain and showed calcium buildup in their arteries in x-rays…. The images “astounded us,” [program director William] Gahl said. The team obtained DNA samples from the sisters and other family members (three of Allen and Benge’s siblings had the same recessive disease) and scanned the DNA for markers called single nucleotide polymorphisms that the researchers used to narrow the location of the disease gene. By also examining this genetic region in two other families with similar disorders, the researchers were able to pinpoint a mutation in a specific gene, NT5E, which is involved in breaking down calcification in the arteries. [ScienceInsider]

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Welcome to the family of critters with sequenced genomes, orangutans. In Nature this week, scientists unveil the draft DNA sequencing of our great ape cousins—the only great apes that live exclusively in Asia.

The researchers assembled the draft genome of the female Sumatran orangutan (Pongo abelii) using a whole-genome “shotgun” strategy, an old-fashioned approach that cost about $20 million. In addition, the researchers gathered sequence data from five wild Sumatran orangutans and five Bornean orangutans (Pongo pygmaeus) using a faster and thousandfold cheaper next-generation platform. [LiveScience]

What did scientists find in there? For one thing, orangutans share about 97 percent of the their genome with humans, compared to the 99 percent we famously share with chimpanzees. The two orangutan species—inhabiting the Indonesian islands of Borneo and Sumatra—diverged about 400,000 years ago, lead author Devin Locke says. That’s much more recently than scientists had thought.

They also discovered that over the last 15 million years, orangutan DNA changed at a different rate than either ours or chimps’. Orangutans have undergone fewer mutations of the DNA, have a lower gene turnover rate, and have fewer duplicated DNA segments.

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