Some like it hot. The bacteria Francisella tularensis is among them. It likes to live at the temperatures present inside human bodies, and give us the disease tularaemia. But Barry Duplantis figured out a way to make the body an unattractive destination for the bacteria: He injected it with the genes of a cold-lover.

In a study in this week’s Proceedings of the National Academy of Sciences, Duplantis brought in Colwellia psycherythraea, a bacteria that can survive in the icy temperatures of the Arctic, but would die at a temperature like the nearly 100 degrees inside our bodies. By transferring genes responsible for that temperature sensitivity into F. tularensis, he created versions of that bacteria with lower heat tolerances.

When he injected these microbes into mice, they couldn’t migrate to warm areas like the lungs and do damage. Plus, the presence of the incapacitated bacteria acted as a sort of vaccine, putting the animals’ immune systems at the ready. When the researchers later gave the mice large exposures to unaltered F. tularensis, they didn’t get as sick as control mice.

For plenty more on this study, check out Ed Yong’s post at Not Exactly Rocket Science.

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Image: Richard Finkelstein

Los Angeles police say that Lonnie Franklin Jr. may be the “grim sleeper” serial killer they have sought for more than 20 years. And if indeed they do have their man, they have his son to thank—for getting arrested himself.

Franklin is one of the first major suspects nabbed by police using familial DNA. With this controversial method, investigators look for partial matches between DNA left at a crime scene and DNA profiles that are stored in police databases; a partial match may indicate that the person is related to the target individual sought by the cops.

The trail began to heat up when the DNA of Franklin’s son was entered in a state database after he was convicted in a weapons case, authorities said. The son’s DNA was similar to genetic material found on the victims, and authorities soon began following around Franklin to get his DNA and see if he was the suspected killer [AP].

The cops posed as waiters at a restaurant where the elder Franklin ate, which is how they obtained a complete DNA sample from him–they grabbed a plate and napkin he tossed after eating a slice of pizza. The investigators say that when they found the match to the samples in their evidence, it eased 25 years of frustration at not being able to track him down.

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Geneticists have found a way to alter the sexual preference of lab mice. When they bred mice that had one gene deleted, the females declined male companions and preferred instead to court other females, according to a study published yesterday in BMC Genetics. But whether these results have any implications for humans is still far from clear.

Chankyu Park and his team at the Korea Advanced Institute of Science and Technology deleted the female’s fucose mutarotase gene and, as a result, changed the brain’s exposure to enzymes that control brain development.

The gene, fucose mutarotase (FucM), is responsible for the release of an enzyme by the same name, and seems to cause developmental changes in brain regions that control reproductive behaviors. The mice without the enzyme would refuse to let males mount them, and instead tried to copulate with other females. [AOL News]

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We can predict your chances of living exceptionally long, with 77 percent accuracy, by looking at 150 tiny genetic variants. That’s what researchers claimed in a Science paper that we described last week. Those predictive powers have left some feeling a little uneasy–and not just about what futures are buried in their genomes. Where the paper‘s authors saw correlations, some experts are now seeing errors from DNA testing chips.

No DNA chip is perfect; it can get things wrong as it sorts through hundreds of thousands of genetic variants. In fact, certain chips might even make the same error repeatedly. That could cause problems, because what looks like a genetic variant common to a group of people could instead just be an echoed flaw in one chip’s testing capabilities.

Newsweek, which broke this story, reports that the Boston University researchers who led the study did, in fact, use different chips, but not enough different chips to rule out this potential error. They used two different types of DNA chips to test the centenarian group (about 1,000 people whose ages ranged from 95 to 119): a 370 chip that examines 370,000 genetic variants and a 610-Quad that examines 610,000 variants. The control group (of about 1,200 younger people) was tested with those two chips and a few others, thus possibly hiding any shared errors.

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Clearly, the people of Tibet must have evolved quickly to tolerate a life spent living at the top of the world. How quickly? A study out in this week’s Science, which compared Tibetans to Han Chinese to see the differences in their DNA, says that the two groups may have diverged no more than 3,000 years ago. If natural selection has changed Tibetans in such a short time, it would be the fastest known example of human evolution. But not everybody is buying this time line.

As DISCOVER noted when a similar study by another team came out in May, natives of the Tibetan plateau seem to survive the altitude because their bodies make less hemoglobin. It’s somewhat counter-intuitive:

In theory higher levels of haemoglobin would be beneficial, because this would improve oxygen transport. But high levels could make the blood thicker and less efficient at carrying oxygen, says Jay Storz of the University of Nebraska-Lincoln [New Scientist]. (Storz writes the accompanying commentary in Science.)

Looking at the differences in genes that regulate that, the team found vast differences between the Han and the Tibetans, with one version appearing in 87 percent of Tibetans studied but only 9 percent of Chinese. However, the assertion by the scientists at the Beijing Genome Institute—that their findings mean the two group broke apart just three millennia ago—has ruffled archaeologists who believe that the Tibetan plateau has been continuously occupied for much, much longer: more like 7,000 to 21,000 years.

For more about all of this, check out Razib Khan’s post at Gene Expression.

Related Content:
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Gene Expression: Tibet & Tibetans, Not Coterminus
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Image: Wikimedia Commons

UPDATE: Some experts are questioning the validity of this study, and are suggesting that technical errors skewed the results. Full coverage here.

If you want to know how to get old, it’s best to ask the experts. That’s what Paola Sebastiani, a researcher at Boston University School of Public Health, did;  She decided to look at the genes of 1,055 people, many who had already seen their 100th birthday.

As described in a paper published in Science today, Sebastiani’s team found that they could predict a person’s  “exceptional longevity” with 77 percent accuracy.

The researchers looked at small variants called single-nucleotide polymorphisms (or SNPs) on the centenarians’ genomes;  Sebastiani found she could use 150 SNPs to predict who would live to such exceptional ages.

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Investigators are now swabbing dog cheeks. A dog DNA database–similar to the one the FBI keeps for criminals–may help to deter dog-fighting.

Dog-fighting is a federal crime and a felony offense in every U.S. state, but it’s difficult to detect and stop. Officers rarely catch fighters in the act, and the industry, as a multimillion-dollar business, makes money not only from gambling on the violent and often fatal matches, but also from breeding and selling champion dogs.

The New York Times reports that some dogs sell for as high as $50,000 dollars. The American Society for the Prevention of Cruelty to Animals estimates that there could be tens of thousands of people involved in dog fighting in the United States.

So where does the genetics come in?

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What struck down ancient Egypt’s King Tutankhamen at the tender age of 19?

Just this winter, Egyptian researchers seemed to think they had a definitive answer. After years of genetic tests and CT scans, they concluded that royal incest had produced a sickly boy with a bone disorder, and argued that a malaria-bearing parasite finished him off. But now a team of German researchers is arguing that the observations actually point to death from the inherited blood disorder sickle cell disease (SCD).

People with SCD carry a mutation in the gene for haemoglobin which causes their red blood cells to become rigid and sickle-shaped. A single copy of the sickle-cell gene confers increased immunity to malaria, so it tends to be common in areas where the infection is endemic – such as ancient Egypt. People with two copies of the gene suffer severe anaemia and often die young. [New Scientist]

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Happy Birthday, human genome. On June 26, 2000 a group of scientists at the White House announced that they had a working draft of our genetic blueprints. They hadn’t sequenced all our genes; the Human Genome Project and its private-sector competitor Celera Genomics still had some gaps to fill in. Still, scientists believed this data might hold clues to the causes of certain diseases and could lead to new treatments.

Even before the project’s start, some scientists were skeptical: Was mapping our genome a waste of money and time? Even among public hoopla and presidential speeches, scientists cautioned that applying the results would take time. Now, ten years later, many are asking: What have we learned? Here we round up some opinions about the impact of the project.

The Bad?

Some see fewer medical treatments than advertised. Instead of simple relationships between common variants and specific diseases, sequencing uncovered sheer complexity. Researchers now think that intricate relationships between rare variants may cause many diseases.

The difficulties were made clear in articles by Nicholas Wade and Andrew Pollack in The Times this month. One recent study found that some 100 genetic variants that had been statistically linked to heart disease had no value in predicting who would get the disease among 19,000 women who had been followed for 12 years. The old-fashioned method of taking a family history was a better guide. Meanwhile, the drug industry has yet to find the cornucopia of new drugs once predicted and is bogged down in a surfeit of information about potential targets for their medicines. [The New York Times]

As genetic sequencing goes, what once took years and millions of dollars can now take months and thousands. Still, some worry that the drive to sequence more, faster has led to techniques that make reading results increasingly hard.

The advances in speed … have come at a cost. Only short stretches of DNA can be sequenced at a time, so the pieces have to be joined together by looking for overlaps between them. While early instruments sequenced pieces up to 900 base pairs long, most high-speed machines produce “reads” of less than 100 base pairs. That means the overlaps are much shorter, making it far harder to join the pieces together, so assemblers use existing genomes as a guide — which can lead to mistakes. [New Scientist]

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It doesn’t take much to be a vile, bloodsucking pest. You, human, have three billion base pairs in your genome, but the body louse—which has been a typhus-spreading scourge of humanity for millennia—carries just 108 million. That’s what scientists say today in a study in the Proceedings of the National Sciences that describes how they sequenced the body louse genome.

Because the body louse (a separate creature from the head or pubic louse) lives entirely on humans, hatching in our clothes and eating our blood, its genome can get away with being so streamlined, study author Barry Pittendrigh says:

“Most of the genes that are responsible for sensing or responding to the environment are very much reduced,” Pittendrigh said. The body louse was found to have “significantly fewer genes” for smell and taste, as well as minimal genes responsible for a “simple visual system,” the study authors wrote. They found just 10 genes to code for odor receptors [Scientific American].

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Behold La conversione di San Paolo (The Conversion of St. Paul), one of the masterworks of Caravaggio. The Italian artist of the Baroque era was famous for the chiaroscuro shading—dramatic contrasts of light and dark—evident in this conversion scene. But he was also renowned for living hard and dying young. Four centuries after his death, Italian researchers say they’ve found his bones, and they might know what actually killed him: the lead in his paints.

First, the researchers had to find his remains. Caravaggio died in 1610 in the Tuscan town of Porto Ercole, but his remains were whereabouts unknown until a researcher claimed to turn up a death certificate in 2001 pointing to the crypts there. The bones the scientists found there matched a man aged 38 to 40 (Caravaggio’s age range at his death) and dated to his era. And the DNA matched combinations found in people from the painter’s hometown and sharing his original surname, Merisi or Merisio.

“There can’t be the scientific certainty because when one works on ancient DNA, it is degraded,” Giorgio Gruppioni, an anthropologist on the team, told The Associated Press. “But only in one set of bones did we find all the elements necessary for it to be Caravaggio’s — age, period in which he died, gender, height.” The group says there is an 85 percent probability they are right, though team leader Silvano Vinceti says that is conservative. “We are being cautious,” he said. “As a historian I can say we have found the remains… All evidence concurs” [AP].

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The Food and Drug Administration has a message for the personal genomics revolution: slow down.

Personal DNA tests have been available for years now from companies like 23andMe and Pathway Genomics, and the direct-to-consumer tests have sold briskly even while the companies tried to sort out whether or how their systems would be regulated by the FDA. Then last month, Pathway took the next big step, offering to sell their tests over the counter in the nation’s largest drugstore chain, Walgreens.

For the FDA, that was one step too far, and it began to make noise about regulation. Now the agency’s leader in this field, Alberto Gutierrez, has sent official letters to all the major personal DNA-testing companies saying it intends to regulate the tests as medical devices, and that the companies must provide evidence of their scientific validity.

The letters, posted on the F.D.A. Web site on Friday, say the companies must apply for approval or discuss with the agency why certain test claims do not require such approval. But the letters stop short of saying the tests must be taken off the market until they are approved. Dr. Gutierrez said in an interview that it would be unfair to remove the tests from the market because the agency had not clearly told the companies that the devices needed approval [The New York Times].

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Researchers have published the largest-existing study on the genetic causes of autism, comparing 996 autistic individuals to 1,287 people without the condition. Their results, which appear today in Nature, may provide unexplored avenues for treatment research, but also show in new detail the disorder’s sheer genetic complexity. For example, they have found “private mutations” not shared between people with autism and not inherited from their parents.

According to The Centers for Disease Control and Prevention, one in 110 children in the United States has autism spectrum disorder, and that the prevalence of autism among eight-year-olds has increased 57 percent from 2002 to 2006. There is no known cure, although intensive behavioral therapy helps some kids.

Hilary Coon, Ph.D., a lead author on the study and research professor of psychiatry at the University of Utah School of Medicine, said while research shows scientists are making progress in understanding the causes of autism, it is increasingly clear that autism is a multifaceted disorder with both genetic and environmental causes. “We are whittling away at it,” Coon said. “But a brain-related disorder, such as autism, is amazingly complex. It’s not really one entity.” [University of Utah press release]

For this study, researchers at the international Autism Genome Project wanted a closer, more detailed picture of the over 100 genes commonly linked to autism. They looked for rare variants–small deletions or additions to the DNA sequences that make up these genes. They found that people with autism had a higher number of these variants than those without the disorder, and that some of these DNA differences were not inherited. That means these DNA changes occurred either in the egg cell, sperm, or in the developing embryo.

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Just how connected are the Jews, genetically speaking? Despite the fact that pockets of Jewish people are spread around the globe, the new genetic analysis by Harry Ostrer and his team says that they share genetic markers that go back thousands of years.

In the study in the American Journal of Human Genetics, Ostrer investigated Jewish people from all over the world:

Historians divide the world’s 13 million living Jews into three groups: Middle Eastern, or Oriental, Jews; Sephardic Jews from Spain and Portugal; and Ashkenazi Jews from Europe [ScienceNOW].

Taking nuclear DNA samples from 237 Jews—some from each group—the team compared them to samples from more than 400 non-Jewish people who lived in the same regions.

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Here in the United States, people are all atwitter about Craig Venter’s announcement last week of a new “synthetic cell,” and whether it constitutes creating life or simply a nifty new step in genetic engineering. Across the pond in the U.K., however, there are increasing rumblings of a more practical matter: Whether the patents that Venter is seeking to protect his work will bring a chill to genetic engineering research elsewhere.

Dr Venter’s [team] has applied for patents on the methods it used to create the new organism, nicknamed Synthia, by transferring a bacterial genome built from scratch into the shell of another bacterium. Synthia’s genetic code contains four DNA “watermarks”, including famous quotations and the names of the scientists behind the research, that could be used to detect cases of unauthorised copying [The Times].

Nobel winner John Sulston is the main man sounding the alarm (pdf); he argues that Venter is trying to obtain a “monopoly” on a range of genetic engineering techniques, which would prevent other researchers from freely experimenting with those methods. He’s also a familiar adversary to Venter. The two butted heads a decade ago when scientists were rushing to sequence the human genome.

Craig Venter led a private sector effort which was to have seen charges for access to the information. John Sulston was part of a government and charity-backed effort to make the genome freely available to all scientists [BBC News].

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