News this Week

Science  17 Jul 2009:
Vol. 325, Issue 5938, pp. 250

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  1. Nominations

    White House Taps Former Genome Chief Francis Collins as NIH Director

    1. Jocelyn Kaiser

    President Barack Obama's announcement last week that he had chosen Francis Collins to lead the National Institutes of Health (NIH) did not come as a big surprise. But it ended months of speculation and ignited a volley of flattering remarks from researchers and biomedical groups. “Francis is one of the most accomplished scientists and scientific leaders of his generation. … Having worked with him for many years, I am sure that he will rise to the unique challenges of this job,” said Elias Zerhouni, who resigned as NIH director last fall.

    Collins is known as a skilled administrator and excellent communicator. Over 15 years, he built a new center at NIH into one of the most visible and innovative institutes. When he stepped down as leader of the National Human Genome Research Institute (NHGRI) last year, he was already considered a leading candidate to run NIH, the $30 billion parent agency.

    Although few would disagree with a White House press notice saying that Collins's work “has changed the very ways we consider our health and examine disease,” Collins does have critics. Some question his support of “big biology” in the genome project portfolio—with timetables and planned targets—and some are concerned about his outspoken Christian faith. He raised eyebrows, for example, when he recently launched a Web site, BioLogos, expanding on his 2006 book explaining how he reconciles his faith with the science of evolution (see sidebar).

    Back to Bethesda.

    Francis Collins appears to be a shoo-in for NIH director.


    Biomedical scientists are pleased, however, to have a permanent leader at NIH, which has been run by an acting director, Raynard Kington, since October. The agency is staggering under an unprecedented number of grant applications seeking to share in NIH's $10 billion windfall from the economic stimulus package. When that money runs out in 2011, it's unclear what will happen to stimulus-funded scientists. If it comes to a crunch, they could benefit from having an internationally renowned genome scientist as a spokesperson.

    Collins, 59, grew up home-schooled during his early years on a farm in rural Virginia and later earned a Ph.D. in physical chemistry and an M.D. At the University of Michigan, his team made early gene-hunting discoveries, finding genes for Huntington's disease and cystic fibrosis. In 1993, he joined the human genome center, taking over from DNA structure co-discoverer James Watson.

    Collins steered the ramp-up of the Human Genome Project, crafting pioneering agreements that required scientists to share genomic data freely. He led a sequencing race against a private effort headed by J. Craig Venter that culminated in a tie to finish a rough draft of the human genome in 2000. Since then, Collins has steered follow-on efforts, including the HapMap, which has fueled the search for genetic risk markers for common diseases.

    Throughout his career, Collins has charmed Congress and the public. He helped push a law through Congress last year that bars discrimination based on genetics. When he resigned from government in 2008, he said he wanted to write a book about personalized medicine but soon thereafter penned an op-ed piece endorsing Obama. He later joined the president's transition team and this year tried to help religious groups come to terms with Obama's order easing limits on the use of federal funds to study human embryonic stem cells.

    Even Collins's biggest fans say that their star will need to carve out a larger role. Collins did “a fabulous job as NHGRI director,” says geneticist Aravinda Chakravarti of Johns Hopkins University in Baltimore, Maryland. But now, Chakravarti says, “he will need to understand, feel, and anticipate the interests of a much broader constituency,” including small-lab investigators in fields such as infectious diseases and cell biology who have felt threatened by the big projects that Collins has championed.

    Collins will also face concerns that the payoff from the Human Genome Project has been oversold. So far, the search for risk markers for common diseases arguably has found little that could be applied to patients. “I do think one of Francis's tasks will be to set high hopes for genomics but also to manage expectations,” especially to convey realistic time frames, says Robert Cook-Deegan, a medical ethicist at Duke University in Durham, North Carolina, and former NHGRI staffer. Collins has had his own DNA “SNP-chipped” for genomic markers but has said that so far these markers seem most useful for finding new drug targets, not predicting risks. In his new book, due out in 2010, Collins is expected to maintain that the payoff of molecular genetics is coming.

    Collins's plate is loaded with controversial issues. Among others, the next NIH chief must craft new conflict-of-interest regulations for grantees and look at a possible restructuring of the entire NIH operation. The “obvious acute issue,” says molecular biologist Keith Yamamoto of the University of California, San Francisco, “is the stimulus money and concern about the 2011 cliff.” Yamamoto has been involved for many years in reforming peer review and was interviewed for the NIH director position.

    Obama has sent Collins's nomination to the Senate for review by the Health, Education, Labor, and Pensions Committee. Collins isn't commenting to the press, but supporters say they hope he can be confirmed before the Senate breaks for recess on 7 August.

  2. Nominations

    Questions About the Language of God

    1. Jocelyn Kaiser

    Although many scientists say geneticist Francis Collins will make a superb director of the National Institutes of Health (NIH), not everyone is celebrating. A discussion about whether Collins's very public religious views will influence his leadership of NIH played out on blogs early this spring and again in the past week. There seems to be little evidence for such worries, but they persist.

    Collins has written that his beliefs played a role in the 2000 White House press conference to announce the draft sequence of the human genome, when President Bill Clinton called the human DNA sequence “the language in which God created life.” In 2006, Collins wrote a book, The Language of God: A Scientist Presents Evidence for Belief, that describes his religious conversion at the age of 27 and how he reconciles this with the science of evolution. Richard Dawkins, the biologist and prominent antireligionist, feuded with Collins for mixing science and faith.

    This spring, Collins raised hackles again when he and several other scientists launched a foundation and Web site, BioLogos, which claims that it “emphasizes the compatibility of Christian faith with scientific discoveries about the origins of the universe and life.” Funded by the Templeton Foundation, which supports projects at the intersection of science and religion (including at AAAS, Science's publisher), BioLogos answers faith-related questions and links to a blog by its founders.

    As weeks passed with Collins the rumored nominee to head NIH but no announcement, some speculated that BioLogos might be an obstacle. One prominent critic, Paul Z. Myers, a biologist at the University of Minnesota, Morris, who runs the anticreationist blog Pharyngula, faults Collins for suggesting that altruism cannot be explained by evolution and instead came from God. “Collins has got some big gaps in his understanding of the field of evolutionary biology,” Myers says. In comments this spring on Pharyngula, others fretted that Collins's beliefs could influence his decisions on topics such as stem cells and sex research.

    But others have pointed out that Collins's record as director of the genome institute doesn't support such fears. And some scientists active in the anticreationist movement approve of his attempts to reach out to the faithful. Evolutionary geneticist Wyatt Anderson of the University of Georgia in Athens says he read Collins's book, and “I get the picture of a very rational scientist.” Josh Rosenau, public information project director of the National Center for Science Education in Oakland, California, says: “It's very useful to have scientists out there like Francis Collins to talk about their beliefs and why they don't see them as in conflict with science.”

    As of last week, Collins is now only “minimally involved” with BioLogos, says his wife, Diane Baker, a BioLogos board member. She says he plans to step down from the foundation once the Senate has confirmed his nomination and that he will decline any speaking engagements or efforts to promote BioLogos.

  3. Obama Nominee

    Geophysicist McNutt Named to Lead U.S. Geological Survey

    1. Richard A. Kerr

    Even before she was officially nominated last week to be the next director of the U.S. Geological Survey (USGS), Marcia McNutt was already angling for broader responsibilities. After her prospective boss, Interior Secretary Ken Salazar, told her that he hoped to elevate science throughout the department, McNutt replied: “Then why don't you make the director of the Geological Survey your science adviser?”

    When Salazar said yes, he put the 57-year-old geophysicist in line to make history twice—as the first woman to lead the 130-year-old survey and as the department's first science adviser. “Now science advice is going to have a more direct way to be communicated to the other agencies,” she says, adding quickly that nothing will happen unless the U.S. Senate confirms her appointment.

    New duties.

    USGS nominee Marcia McNutt would also act as science adviser to the Interior's Ken Salazar.


    Such directness and initiative could be hallmarks of her tenure at the 8800-employee, $1.1-billion-a-year agency, an amalgam of geologists, biologists, and hydrologists. As science adviser, she'll also be working closely with other scientific branches of the department, such as the National Park Service and the Fish and Wildlife Service.

    McNutt has made a habit of breaking new ground. She was the first female physics major at Colorado College, the first female lifeguard for the city of Minneapolis, and, she guesses, the first woman to train in underwater demolition with Navy SEALs. Her career in tectonophysics has taken her from the ocean island volcanism of French Polynesia to the uplift of the Tibetan Plateau. She began her professional life with 3 years at USGS before joining the Massachusetts Institute of Technology in 1982. Since 1997, she has been president and CEO of the Monterey Bay Aquarium Research Institute, a $40-million-a-year, 200-employee oceanographic research institution in Moss Landing, California, that focuses on the nearshore of Monterey Bay.

    “She brings an incredible skill set to the job,” says geophysicist Mary Lou Zoback of Risk Management Solutions in Newark, California, who was formerly with USGS. “Marcia's nomination clearly affirms that the Geological Survey is a science agency that should be led by a scientist.” Zoback predicts that McNutt will work closely with two other recent Administration appointees, marine ecologist Jane Lubchenco of the National Oceanic and Atmospheric Administration and Secretary of Energy Steven Chu.

  4. Ancient DNA

    Sequencing Neandertal Mitochondrial Genomes by the Half-Dozen

    1. Elizabeth Pennisi
    Across the continent.

    Entire mitochondrial genomes now exist for these four Neandertal bones and two more, suggesting low genetic diversity in this extinct human.


    Fourteen years ago, sequencing just a few hundred bases of mitochondrial DNA from a Neandertal drew applause worldwide. Ancient DNA studies have come a long way since then. On page 318, a team led by Svante Pääbo of the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, describes a new technique the team used to decipher the entire mitochondrial genomes from five of these extinct humans. These genomes show relatively little genetic diversity among Neandertals scattered across Europe and Russia.

    “This is an important step for ancient DNA,” says Eddy Rubin, whose lab at the Lawrence Berkeley National Laboratory in California did some of the first work sequencing Neandertal nuclear DNA. Adds Eske Willerslev, who studies ancient DNA at the University of Copenhagen in Denmark, the new technique “provides a solution to a technical problem: … how to target specific regions of interest.”

    Ancient DNA is difficult to sequence because genetic material degrades over time into small fragments just tens of bases long and errors are often introduced into the aging sequence. Moreover, 99% of fossil DNA tends to be contaminating sequence from microbes and fungi that have infiltrated the decaying bone. Three years ago, researchers began sequencing all of the DNA in Neandertal samples, then separating out what looked like human sequence from the mix. New sequencing technologies made the project affordable enough to go after the entire Neandertal nuclear genome (Science, 17 November 2006, p. 1068), which was announced in February (Science, 13 February, p. 866).

    Some of that project's DNA came from mitochondria, and researchers assembled it into the first entire Neandertal mitochondrial genome in 2008. Sequencing another mitochondrial genome that way would cost as much as $400 million, says Pääbo graduate student Adrian Briggs. That would make comparing multiple Neandertal genomes—the only way to understand the population size and structure of our closest relative—prohibitively expensive. So Briggs came up with a better way. His new cost: about $8000 per mitochondrial genome.

    The approach uses probes that recognize and isolate only Neandertal mitochondrial DNA from all the contaminating DNA in a sample. Thus, Briggs winds up sequencing just the material he's looking for.

    To do this, he first attaches short sequence tags to all the pieces of DNA in his sample, creating a DNA “library” that can be copied to ensure there will be enough ancient DNA for future use. Using the already-sequenced Neandertal mitochondrial genome as a template, Briggs designed 574 probes to cover the entire mitochondrial genome. When a probe links up with its target sequence in a mass of DNA fragments, an enzyme copies the rest of the DNA in that piece many times over. Thus, Briggs was able to isolate the whole mitochondrial genome and sequence it using the latest high-throughput sequencing technologies. Others have used similar approaches, but Briggs tailored his for the short, degraded fragments found in fossils.

    Briggs and his colleagues sequenced 16,565 mitochondrial bases extracted from bones from Spain, Germany, Croatia, and Russia (see map) and analyzed those genomes along with the one sequenced earlier, which comes from a long bone fragment from Croatia. The bones ranged in age from 38,000 to 70,000 years old. The team also compared the ancient DNA with mitochondrial genome data from about 100 modern individuals.

    Briggs and postdoc Jeffrey Good found 55 places out of the 16,565 bases where the mitochondrial genomes varied across the six ancient samples. On average, they found 20 differences between any two samples. In modern humans, about 60 differences exist between any two samples, making Neandertals about one-third as diverse. That isn't unexpected given that humans come from across the globe and that the Neandertals were confined to Europe and Russia, notes John Relethford, a biological anthropologist at the State University of New York College at Oneonta. The results call into question earlier suggestions that Neandertals were divided into separate, regional populations, but more data are needed to be sure, says Briggs.

    By the Max Planck group's calculations, this diversity translates into the equivalent of at most 3500 breeding Neandertal females, or up to 7000 including males, lower than previous rough estimates of about 10,000. This so-called effective population size is far less than the actual population and represents a theoretical attempt, based on the population's genetic diversity, to quantify the number of individuals who are breeding at any given time. For example, Anders Götherström of Uppsala University in Sweden calculates that although the Swedish population numbers 9 million, the effective population size is about 100,000; he estimates that the 3500 might translate very roughly into about 70,000 Neandertals.

    “Low population size may have been a general aspect of Neandertal biology,” says Briggs. With relatively few individuals, the species may have been more vulnerable to extinction from climate change or competition from our ancestors, he adds.

    Such a small number “is not too surprising,” says ancient DNA expert Alan Cooper of the University of Adelaide in Australia, as archaeological evidence had been pointing toward this. Cooper and others caution that analyzing mitochondrial DNA has limits as it is “in effect ‘one gene’ because all its genes are so tightly linked.” Thus, says Cooper, “this is just one view of Neandertal evolutionary history.”

  5. India

    Lunar Survey Spacecraft Develops an Attitude Problem

    1. Pallava Bagla

    NEW DELHI—India's first moon probe, Chandrayaan-1, has suffered a critical malfunction that jeopardizes the remainder of the mission. The spacecraft, which entered lunar orbit last November, can no longer orient itself with high precision. “Its pointing accuracy has been compromised,” says a mission engineer who asked for anonymity.

    Chandrayaan-1 achieved all of its mission objectives before the malfunction was detected in May, says G. Madhavan Nair, chair of the Indian Space Research Organization (ISRO) in Bangalore. It was a “dream run” until then, Nair told Science. Some foreign scientists with instruments aboard Chandrayaan-1 concur that the probe performed well. “The data … are unique and reveal a new moon,” says Stas Barabash of the Swedish Institute of Space Physics in Kiruna, whose Sub keV Atom Reflecting Analyser is investigating the interaction of the solar wind with the lunar surface. The spacecraft is continuing a search for water ice, gathering data for a three-dimensional lunar atlas, and mapping minerals.

    Stunning images.

    Chandrayaan-1 has returned excellent data despite a glitch, says G. Madhavan Nair.


    The first inkling of something amiss came on 19 May, when the satellite was raised from a lunar orbit 100 kilometers above the surface to a 200-kilometer orbit—allowing for greater stability and easier maneuvering. ISRO did not disclose the pointing failure; instead, it announced that “after successful completion of all major mission objectives,” the higher altitude would enable further studies on gravity anomalies and imaging a wider swath of the lunar surface. Nair denies that ISRO sought to hide the problem with the $100 million robotic mission, saying there was no need to go public since there was “no degradation or deterioration in the mission.”

    The broken instrument is a star sensor, which orients the probe. Its failure is “disheartening,” says George Joseph, director of the Center for Space Science and Technology Education in Asia and the Pacific in Dehradun. “The precision with which the spacecraft was maneuvered into the moon orbit was in itself a fantastic achievement,” says Joseph, who helped design the mission.

    Mission scientists say Chandrayaan-1 hit most of its scientific milestones. “Visually arresting” images from NASA's Mini-SAR radar of craters in permanent shadow “will be extremely useful in unraveling the complex geological history of the moon,” says principal investigator Paul D. Spudis of the Lunar and Planetary Institute in Houston, Texas. “Chandrayaan's achievements are quite remarkable,” adds Carlé Pieters of Brown University, principal investigator of the Moon Mineralogy Mapper. The higher orbit will require the team to “replan” operations, Pieters says, “but overall the tradeoffs will probably result in an equally strong science product.”

    The payload that will suffer most is India's Lunar Laser Ranging Instrument, designed to measure altitude variations within a 5-meter accuracy. It was designed to operate at a 100-km orbit; at 200 km, the return signal may be too weak, says a mission specialist. Also unclear is whether projects tied to x-ray and near-infrared spectrometers will be completed, says Christian Erd of the European Space Agency in Noordwijk, Netherlands.

    “There is nothing to be worried or alarmed about,” insists Nair. “The mission is almost over.” Indeed, the global scientific team will meet in late August or early September in India to decide whether to keep Chandrayaan-1 going or guide it to a controlled crash before it completes its nominal life of 2 years.


    From Science's Online Daily News Site


    Cat Purrs Evoke Baby Cries There may be more to a cat's purr than meets the ear. A new study reports that our feline friends modify their signature sound when seeking food, adding a higher-frequency element that exploits our sensitivity to infant wails—and thus making it harder to ignore.

    Don't Blame Birds for 1918 Flu It has become almost common wisdom that the virus that caused the 1918 flu pandemic was an avian strain introduced into the human population shortly before the pandemic erupted. But a new study disputes that hypothesis, arguing instead that genes of the 1918 virus had circulated in mammalian hosts, most likely pigs and humans, for several years before 1918. Multiple gene-swapping events brought them together in a single killer strain, say the researchers; improving surveillance in humans and in swine could, in the future, give scientists an early alert to such events.

    Swearing Eases the Pain You just stubbed your toe, hard, on the corner of that stupid table again. What's the first thing out of your mouth? If it's something you wouldn't see printed in a family newspaper, you may actually be doing yourself a favor. Foul language may be decreasing your pain, according to a new study.

    Flexible Fibers Act Like Cameras Picture a wall that stares back at you. Or a uniform that shows a soldier a 360-degree view of a battlefield. Both scenarios are possible courtesy of a new generation of flexible, translucent fibers developed by researchers at the Massachusetts Institute of Technology in Cambridge. These so-called multimaterial fibers can turn incoming light waves into images without the need for a camera lens. And unlike fiber-optic cables, they can transmit images that have been captured across their entire length.

    Read the full postings, comments, and more on

  7. Archaeology

    Roundup of Utah Collectors Stirs a Debate on Enforcement

    1. Keith Kloor*

    BLANDING, UTAH—Last month, after 16 residents from this town in southern Utah were arrested and accused of stealing prehistoric Indian artifacts from public and tribal lands, nobody was more surprised than Teri Paul, director of the state's Edge of the Cedars State Park Museum, which features archaeological exhibits on the area's Native American cultures. “I guess I just got it into my head that locals weren't doing this anymore.”

    After the bust.

    Interior Secretary Ken Salazar (left) announces the arrest of Utah residents for taking artifacts from federal and Native American lands.


    The town was the center of a similar raid back in the mid-1980s. Old traditions die hard, though. Blanding, like numerous other communities in the Four Corners region, has a long-standing tradition of digging up Native American ruins for recreation and profit. The habit took hold during American archaeology's embryonic period between the 1800s and 1920s—ironically, a time when the Smithsonian Institution and others sponsored expeditions to the Southwest and paid locals to find artifacts. Federal laws now make it a crime to take such trophies from public lands and Indian reservations, but the practice of “pothunting” continues, fueled by a lucrative black market in antiquities.

    This latest crackdown is the culmination of a 2.5-year-old undercover investigation by the Federal Bureau of Investigation (FBI) and the Department of the Interior that netted 24 alleged looters in the archaeology-rich region. It is renowned for Chaco Canyon's Great Houses and Mesa Verde's cliff dwellings, both grand vestiges of the Anasazi, a farming civilization that flourished from 500 C.E. to 1300 C.E. The dragnet on 10 June, Science has learned, extended to art dealers and collectors in a dozen cities from Tucson, Arizona, to Santa Fe, New Mexico. Agents searched homes and businesses and seized personal files and computers. Two members of a family in Blanding accused of looting last week pleaded to charges and surrendered a collection of artifacts.

    The case has aroused strong passions among Southwestern archaeologists, prompting many to take sides on how best to cure pothunters of their destructive urge. Some strongly support the federal action; others take a jaundiced view of the heavy-handed police tactics and argue that such an approach will not deter determined looters, especially those who come from communities where a sub-culture of pothunting stubbornly persists.

    No context.

    The polychrome bowl (right) is classed as having an unknown origin, as many recovered artifacts will be.


    Government archaeologists involved in the investigation paint an emerging picture that is as lurid as it is far-reaching. “We're talking widespread, systemic destruction of archaeological sites,” says Emily Palus, a Bureau of Land Management (BLM) archaeologist based in Washington, D.C. Many of the items were dug out from Indian burials, such as a turkey-feather blanket, a copper bracelet, and a pair of ancient sandals associated with the Anasazi.

    Scientists say looting of these sites is akin to tearing pages out of a history book. “If you rip out enough pages, pretty soon the book doesn't make sense,” says Jerry Spangler, executive director of the Colorado Plateau Archaeological Alliance, a Utah-based antiquity preservation group.

    Enforcement of antitheft laws has been lax in the past, according to many Southwestern archaeologists. But Spangler believes the recent sweeps finally demonstrate “that federal authorities do consider pothunting as a serious crime.” The message of the raids is unmistakable, particularly in the way they were carried out, with FBI SWAT teams descending on homes with guns drawn and placing arrested suspects in handcuffs and leg irons, says Richard Wilshusen, an archaeologist who teaches at Colorado College in Colorado Springs: “It's the OK Corral. It's the Clanton Gang finally being taken on.”

    Among the Blanding citizens swept up in the 10 June raid was James Redd, the town's prominent physician, who killed himself the next day. (Another suspect from Durango also took his own life a week later.) Redd's death has since triggered an angry backlash against the federal raids, with both of Utah's Republican senators calling the investigation “overkill” and demanding that Congress initiate a probe into FBI's antipothunting operation. The backlash may feed a growing debate among experts over the use of punishment—rather than education—as a means of changing public attitudes.

    Canyons of riches

    The biggest challenge, many archaeologists say, is conveying the importance of archaeological protection for scientific purposes. That's difficult enough when Indiana Jones and a treasure-hunting aura popularly define the field. The challenge is made even harder in a place like Four Corners, which is believed to contain the highest density of archaeological sites in the country, if not the world. For example, after news spread of the raids in Blanding, one resident (whose in-laws were among those arrested) told The Salt Lake Tribune: “It's just something everyone does in Blanding. There are artifacts everywhere.”

    Overall, a history dating back at least 10,000 years can still be widely found across the landscape, from rock-art panels and arrowheads to collapsed pueblos (above-ground dwellings) and rock shelters. In San Juan County alone, where Blanding is located, more than 25,000 archaeological sites have been inventoried. The Edge of the Cedars museum was built directly adjacent to the stone walls and kivas of a 1000-year-old Anasazi village. Paul, noting that 92% of the county is federal land, much of it rugged wilderness, says, “In any given canyon, you'll find site after site.”

    But even many of these sites are being “vacuumed” of surface artifacts, such as potsherds and arrowheads, says Paul. That eliminates vital clues to possible dwellings and other larger sites nearby, which are often buried underground. Experienced pothunters, using shovels or, worse, a back-hoe, take the damage to another, incalculable level. “Digging and removing artifacts destroys their context, and it limits the information that can be obtained from a site about previous cultures,” says Laird Naylor, a BLM archaeologist in the Monticello Field office, whose jurisdiction covers San Juan County, Utah.

    Spangler points out that preservation is also important because methods and science are always improving. “You want to be able to save these sites for the archaeologists that come after us 20 and 50 years from now, because they're going to be so much more advanced than us.”

    Archaeologists admit that the reasons for site protection are poorly conveyed to the general public. That's why Jonathan Till, a contract archaeologist with Abajo Archaeology in Bluff, Utah, argues that getting pothunters to change their ways will happen through education, not prosecution. He says BLM is failing miserably because it lacks resources and labor power. Till notes that BLM oversees 800,000 hectares of public land in San Juan County and has only two archaeologists and one ranger. “That's just absurd,” he says. “Those people are stretched way too thin to be able to do their jobs effectively and to be able to act as educators. They just cannot do that.”

    Brian Quigley, acting manager for BLM's Monticello field office, agrees that it would be nice to have more boots on the ground: “We do the best we can with the resources we have,” he says. The situation is similar in BLM offices across the state of Utah. For example, just north, in the Price field office, an area also chock-full of archaeological sites, including the world-famous Nine-Mile Canyon under BLM's watch, Blaine Miller is the sole archaeologist. “I've been the only one here for the past 25 years,” he says.

    Given this shortage of labor power, archaeologists are divided over the best way to stamp out pothunting. Winston Hurst, a respected independent archaeologist who consults on academic and industry projects and lives in Blanding, criticizes the federal raids as “bizarre theater” in which “the symbolism of the way it was carried out ends up trumping the substance of why they're doing it in the first place.” Hurst says the only way to conquer archaeological looting is through “intelligent discourse, and by treating people with respect.” But if “you're going to punch people in the nose, there's absolutely no open-mindedness, nothing but a fight, and once it's a fight, they're going to retrench in opposition to you.”

    Looted sites.

    Culminating a 2.5-year investigation, a coordinated sweep seized objects at many locations around Blanding, Utah.

    Other Southwestern archaeologists are also inclined to take a softer approach. “No archaeologist likes looting, but it seems like so much overkill to do this to normal people,” says Catherine Cameron, a professor of archaeology at the University of Colorado, Boulder. “They surrounded houses early in the morning, like it was a drug bust. These are not bad people. You don't need to do that to people like they are dangerous criminals.”

    But Kevin Jones, Utah's state archaeologist, has little sympathy for the Blanding residents who were implicated in robbing graves. “Maybe upstanding citizens are not used to being arrested that way; maybe now they will think twice about committing that kind of crime.”

    • * Keith Kloor is a writer in New York City.

  8. ScienceInsider

    From the Science Policy Blog

    Congressional spending panels last week looked favorably on basic research programs at the Department of Energy (DOE) but were skeptical about innovations proposed for 2010 by the Obama Administration. House of Representatives and Senate appropriators came very close to the president's $4.94 billion request for the Office of Science. But they showed little enthusiasm for Energy Secretary Steven Chu's plan to fund eight large energy research centers, with the House approving $35 million of the $280 million request and the Senate suggesting a way to spend $44 million.

    At a meeting at the U.S. National Academy of Sciences last week, NASA Associate Administrator Edward Weiler warned that the shrinkage of NASA's planetary budget from $3 billion to $1.5 billion in the past 4 years means that “we no longer have a viable Mars program.” Weiler announced an unprecedented agreement with the European Space Agency to conduct a joint program of Mars missions.

    The University of California released a plan last week that will shave $184 million from the university's projected $813 million short-fall in state funding over the next 2 years. It calls for furloughs to be scaled according to pay grade—from 11 days, equivalent to a 4% cut, for those making less than $40,000 a year to 26 days, or a 10% cut for those making more than $240,000. Employees funded entirely from nonstate sources would be exempt.

    Maria Leptin, the new director of the European Molecular Biology Organization, wants to review how to balance EMBO's reliance on its journals for revenue with the scientific community's desire to make the journals open-access.

    Health care workers should be first in line for inoculation when vaccines against the swine flu virus are ready and approved, an expert panel at the World Health Organization concluded in a meeting last week.

    For a full Q&A with Leptin and other science policy news, go to

  9. Insulin Resistance

    Prosperity's Plague

    1. Gary Taubes

    Researchers have linked a growing number of chronic diseases to the metabolic disorder known as insulin resistance; two general theories have emerged about its mechanism.


    Type 2 diabetes, a disorder of insulin resistance, is on the rise.

    Welcome to the age of insulin resistance. This condition is the thread that runs through many chronic afflictions of modern times—obesity, heart disease, and, most conspicuously, type 2 diabetes. All are entangled with diet, and all are linked causally to a dysfunctional response to insulin, the hormone that orchestrates the body's use and storage of nutrients.

    Insulin resistance is the fundamental defect in type 2 diabetes, a disease that afflicts 6% of adult Americans, up from 3% in the early 1970s. Most type 2 diabetics are obese, a condition that's so closely associated with insulin resistance that many researchers assume that it is a cause. The prevalence of obesity has increased in the United States almost 2.5-fold since the early 1970s, from 14% to 34%, according to the most recent national surveys.

    Metabolic syndrome is another insulin-resistant condition. By some estimates, it afflicts 50 million Americans. It's defined by a cluster of abnormalities—including abdominal obesity, hypertension, and high blood sugar—that precede both coronary heart disease and type 2 diabetes. Stroke, nonalcoholic fatty liver disease, polycystic ovary syndrome, asthma, some cancers, and even Alzheimer's disease have also been associated with insulin resistance.

    Once it takes hold, insulin resistance sets up a vicious cycle: As tissues become unresponsive to insulin, the pancreas compensates by secreting ever more insulin, and gradually the tissues grow more resistant.

    Elucidating the causes of this destructive cycle is one of the most critical endeavors in modern medicine. Researchers have made progress identifying events that lead to type 2 diabetes and other insulin-involved diseases. But working back up the chain of causality has been a challenge. Unambiguous evidence on the initial stages of disease is missing, making it an excruciatingly difficult task to pin down the causes at the cellular and molecular level.

    “The field is in a funny stage right now,” says Mitchell Lazar, director of the Institute for Diabetes, Obesity and Metabolism at the University of Pennsylvania. “It's gone from having too few candidate explanations [for insulin resistance] to having too many.” Now when someone comes along with yet another possibility, Lazar says, “you go, ‘Okay, get in line, buddy.’ There are a lot of things that have to be figured out.”

    Several candidate mechanisms have emerged in the past decade, and two competing theories have gained wide support. One is that cells essentially become poisoned by fat. This lipotoxicity or lipid overload hypothesis holds that normal processes break down when fat (adipose) tissue cannot store excess fat, and fat accumulates inappropriately in muscle and liver cells.

    The main rival to this idea, the inflammation hypothesis, is that as fat cells increase in size with the accumulation of fat, they release inflammatory cytokines and molecules known as adipokines. It's these molecules, so this theory goes, that cause insulin resistance elsewhere in the body. Researchers are now confident that these inflammatory mechanisms play some role in insulin resistance. But they still can't say for sure whether those roles are causal.

    Tangled pathways

    What makes insulin resistance such an extraordinarily difficult problem to study is that it constitutes “the ultimate systems biology question,” says endocrinologist C. Ronald Kahn of the Joslin Diabetes Center in Boston, which is affiliated with Harvard Medical School.

    Insulin is the primary regulator of fat, carbohydrate, and protein metabolism; it regulates the synthesis of glycogen, the form in which glucose is stored in muscle tissue and the liver, and it inhibits the synthesis of glucose by the liver. It stimulates the synthesis and storage of fats in fat depots and in the liver, and it inhibits the release of that fat. Insulin also stimulates the synthesis of proteins and of molecules involved in the function, repair, and growth of cells, and it functions as a signaling molecule conveying information on fuel availability from the periphery to the brain and central nervous system.

    “Compared with other hormones,” the late J. Denis McGarry of the University of Texas Southwestern Medical Center wrote in Science in 1992 (30 October 1992, p. 766), “insulin elicits a bewildering array of metabolic responses in target cells. Deciding which of these are dependent or independent events continues to pose a major challenge.” Sixteen years later, that assessment still holds true.

    A fundamental role of insulin is to orchestrate the use of fuels in the body, partitioning them to oxidation or storage. When blood sugar is elevated—during and immediately after a meal, for example—insulin works to store excess calories as fat in the fat tissue and transport glucose into muscle tissue. It also signals the mitochondria to use glucose as the primary fuel source. As insulin and blood sugar levels drop in the hours after a meal, they allow fatty acids to be mobilized from stored fat and signal the mitochondria to oxidize these fatty acids for conversion into energy. This “metabolic flexibility,” or the capacity to switch easily between glucose and fat for fuel, is a key feature of healthy individuals, as endocrinologist David Kelley, now at Merck Research Laboratories in Rahway, New Jersey, has pointed out.

    In insulin resistance, these natural responses break down and become pathological. A “natural system of feedback loops,” as Merck's Luciano Rossetti says, is overwhelmed or degraded and disease is often the response. The operative word, though, is “often.”

    Even among healthy individuals, measurements of insulin-stimulated glucose uptake, insulin sensitivity, and insulin resistance will vary by 600% to 800%. “There's an enormous range,” says endocrinologist Gerald Reaven of Stanford University in Palo Alto, California, who deserves much of the credit for persuading the medical research community to take insulin resistance seriously as a causal factor in heart disease and type 2 diabetes. A quarter of this variation in sensitivity can be explained by variations in physical fitness, and another quarter by weight, a relationship that Reaven says has held up in studies of populations as diverse as the Pima Indians of Southwest Arizona and descendants of Europeans living in Palo Alto. “Clearly, the more obese you are, the more insulin resistant you are,” Reaven says, but the same variation can be found in obese subjects, a third of whom are relatively insulin sensitive.

    Without being able to pinpoint the tissue, organ, and cell type in which insulin resistance first manifests itself, says Stephen O'Rahilly, co-director of the Institute of Metabolic Science at the University of Cambridge in the United Kingdom, it's virtually impossible “to unpick the causal chain.”

    What researchers almost invariably measure, though, is how the entire body responds to insulin, not how the individual tissues and organs do. And how the body responds also changes dramatically over the course of a day, and from day to day, in response to food intake or physical activity. “We're studying a phenomenon that is happening differentially over a 24-hour period,” says O'Rahilly. “But most studies are done when the subject or patient is fasting. Those are essentially looking at insulin's dialog with the liver and how sensitive the liver is to insulin. It tells you very little about how sensitive the skeletal muscle or the adipocyte is.”

    Fuel economy.

    Among insulin's many functions is as partitioner of metabolic fuels—carbohydrates, fats, and protein—for use and storage in tissues.


    Fat overload

    In the mid-1970s, endocrinologists focused on the insulin receptor itself as a likely key to the puzzle. They assumed that resistance was caused either by down-regulation of the insulin receptor—a normal desensitization process—or by a defect in the receptor itself or the binding of insulin to the receptor. By the mid-1980s, Jerrold Olefsky, now at the University of California, San Diego, had demonstrated that the primary defect was downstream in the signaling pathway, not in the receptor itself.

    Since the early 1990s, the observation that insulin resistance is associated with elevated levels of free fatty acids in the bloodstream has led researchers to focus on lipid overload as the precipitating event. Several observations support the hypothesis. The single best predictor for the presence of insulin resistance in young, lean offspring of type 2 diabetics, according to Gerald Shulman, an endocrinologist at Yale University, is the accumulation of fat inside muscle cells. Shulman and his colleagues have also studied sedentary populations of lean, healthy, elderly subjects and obese, insulin-resistant adults and children. In all those cases, he says, “the more fat inside the muscle cells, the more insulin resistant they are.”

    Using nuclear magnetic resonance spectroscopy to do noninvasive measurements of metabolic fluxes—what Shulman calls “basically real-time biochemistry in humans”—Shulman and his colleagues have established that when fat accumulates inside muscle cells, it blocks an intracellular chain of events that normally triggers glucose transport into the cell. The specific culprit, according to Shulman, is the buildup of diacylglycerols (DAGs)—an intermediate product in the formation of triglycerides, the form in which fat is stored in cells. When DAGs accumulate inside muscle cells or liver cells, Shulman has found, they shut down the insulin-signaling pathway. In the muscle cells, they do so by inhibiting the translocation of a protein, glut4, to the cell membrane, where it would normally work to pump glucose into the cell. Insulin-stimulated glucose transport no longer works efficiently, and the cell is insulin resistant.

    Fat as they come.

    Researchers made a mouse that can accumulate huge amounts of fat, as the one on the left does by over-expressing adiponectin. The result: This mouse was insulin sensitive.


    “Over the last decade,” says Shulman, “we've been able to test this hypothesis using the power of mouse genetics. In more than a dozen transgenic gene knockout models, any time we raise intracellular diaclyglycerols, the mice get insulin resistance in the target tissues; any time we lower it, we prevent insulin resistance.” In March, Shulman and his colleagues reported in the journal Cell Metabolism that DAG accumulation can also account for insulin resistance in the liver caused by the consumption of high-fructose diets.

    The way to think about this, says Shulman, is that the concentration of DAG in a cell is balanced between the delivery of fat to the cells (in the form of fatty acids), the oxidation of fat, and the storage of the fat as triglycerides. “Any time you alter that balance to get a net accumulation of DAGs, through more delivery or decreased oxidation, you get insulin resistance. Anything that flips the balance the other way”—by blocking entry of fatty acids into the cell, for instance, promoting fatty acid oxidation, or even promoting the conversion of DAGs into triglycerides—“prevents insulin resistance.” In that sense, the DAGs work as both an intermediate form of a storage molecule and a signaling molecule that tells the cell whether fatty acids are accumulating and whether it's necessary or beneficial to continue pumping in glucose.


    Competing with the lipid overload hypothesis is the theory that inflammation is to blame. The idea was sparked in the mid-1990s, when Gökhan Hotamisligil of the Harvard School of Public Health and Bruce Spiegelman of Harvard Medical School reported that the inflammatory cytokine TNF-α was overexpressed in animal models of obesity. They demonstrated that they could induce insulin resistance in fat cells in vitro by exposing them to TNF-α. They also showed that they could protect obese strains of mice from insulin resistance by knocking out the genes either for TNF-α itself or for TNF-α receptors.

    “If you can't store fat properly, it's going to build up in liver and muscle and cause insulin resistance.”



    The hypothesis began to gain wide acceptance after Steven Shoelson of the Joslin Diabetes Center reported in 2001 that he could make cells insulin resistant by overexpressing IKK-β, a molecule that works in signaling pathways to activate the inflammatory mediator NF-κB. Among the compounds that inhibit IKK-β are salicylates, aspirin-like compounds that are used at high doses to treat rheumatoid arthritis and rheumatic fever, both inflammatory conditions. “That struck a chord with me,” says Shoelson, because “among the list of things that can cause low blood sugar are salicylates.” One obvious implication, he says, is that “inflammation is a potential pathogenic mediator of both insulin resistance and type 2 diabetes.”

    Since then, Shoelson has demonstrated in a series of studies through 2005 that insulin resistance can be induced in lean strains of mice by overexpressing NF-κB in their fat or liver cells and that obese mice can be protected from insulin resistance by inhibiting NF-κB expression. Last year, Shoelson and his colleagues published the results of a pilot study in Diabetes Care demonstrating that salicylate therapy could indeed both control blood sugar and reduce inflammatory mediators in obese subjects. Meanwhile, Hotamisligil has linked yet another molecule involved in inflammation, JNK, to obesity and insulin resistance. JNK plays a “predominant role” in the regulation of insulin sensitivity, Hotamisligil wrote on 5 September 2008 in PloS ONE: It is over-expressed in animal models of obesity, and knocking it out in these animals both decreases their adiposity and protects them from insulin resistance.

    Hotamisligil now believes that the primary cause of JNK activation is stress in the cell's endoplasmic reticulum, which functions to synthesize and fold proteins. In fat tissue, it works to package complex lipids such as cholesterol and triglycerides. Stress in the endoplasmic reticulum will activate JNK, says Hotamisligil, and it's easy to imagine that the demands put on the endoplasmic reticulum by an expanding fat cell are the source of the stress.

    The picture that's coming together is that obesity is a low-grade inflammatory state. Excess fat or at least large, overstuffed fat cells activate the immune system, promoting “elevated levels of inflammatory cytokines—IL6, TNF-α, JNK, all kinds of stuff,” says Guenther Boden of Temple University in Philadelphia.

    A primary source of these inflammatory signals is now believed to be macrophages trapped in the adipose tissue, a discovery first made in 2002 by Anthony Ferrante and his colleagues at Columbia University and, independently, by Hong Chen and colleagues at Millennium Pharmaceuticals. In lean humans or animals, says Ferrante, 5% of the cells in adipose tissue will be macrophages, compared with upward of 50% in obese humans or animals. What recruits the macrophages into the adipose tissue is still an open question. Nonetheless, says Hotamisligil, “it's pretty clear that if there are inflammatory cytokines or stress signals around, the insulin receptor does not function very well.”

    Main contenders.

    Two explanations for the mechanism of insulin resistance have emerged: inflammation (left) and lipid overload (right). In the inflammation hypothesis, enlarged fat cells attract macrophages and excrete inflammatory signals that work in the muscle cell, via the kinase JNK, to block an insulin receptor substrate (IRS-1) and shut down the insulin-signaling pathway. In the lipid-overload hypothesis, enlarged fat cells leak fatty acids, causing diacylglycerols (DAGS) to accumulate in muscle cells. These inhibit insulin signaling through nPKCs and then block the insulin receptor substrate IRS-1.


    Focusing on fat tissue

    When researchers discuss their favored hypotheses of insulin resistance, the metaphor that often comes to mind is a Russian nesting doll. Elucidate one mechanism of causation, and it immediately implies the existence of yet another mechanism further down the causal pathway that might be still more fundamental. The end point in this progression, however, invariably seems to be the fat tissue itself.

    This has been a consistent theme in insulin-resistance research going back to the early days. Consider, for instance, that impaired glucose uptake by skeletal muscle has traditionally been perceived as the major contributor to insulin resistance. But one reason blood sugar is elevated in type 2 diabetes after a meal, and the primary reason it remains elevated during fasting conditions, is because the liver continues to synthesize glucose and pump it out into the bloodstream even when that glucose is no longer needed.

    Insulin was always thought to suppress this process directly, and researchers believed that its failure to do so was a direct manifestation of insulin resistance by liver cells. But Richard Bergman of the University of Southern California in Los Angeles and his colleagues demonstrated in the mid-1990s that this failure to inhibit glucose production in the liver is actually an indirect effect of insulin resistance, and that the real location of the insulin resistance is at the fat tissue. What happens, says Bergman, is that the fat cells become resistant to insulin, which then fails to efficiently suppress, as it should, the release of fatty acids from these cells. It's those liberated fatty acids that in turn stimulate the inappropriate production of glucose by the liver. “We believe most of the effect of insulin on the liver is indirect,” Bergman says, “and it's mediated by free fatty acids” released from the fat tissue. (Complicating matters further, some of the apparent failure of insulin to suppress glucose production in the liver, as Rossetti and collaborators have demonstrated, also appears to be mediated by insulin resistance in the brain.)

    Most researchers now believe that both inflammation and DAG accumulation are causal factors in insulin resistance, but this raises the obvious question of what causes the inflammation, and what causes the DAGs to accumulate in muscle and liver cells in the first place. One likely possibility, says Shulman, is that people simply eat too much for their level of physical activity. The excess nutrients, in this scenario, then overwhelm the fat tissue, causing the fat cells to expand and secrete inflammatory molecules, or they spill out of the fat tissue and instead accumulate where they don't belong. But that doesn't explain why some obese individuals—often very obese—remain resolutely insulin sensitive. This suggests that something about the fat tissue itself, and maybe its ability to absorb and retain fatty acids and do so in a manner that doesn't induce inflammation, is the fundamental defect, the critical factor determining whether fatty acids will accumulate as triglycerides in healthy fat depots or as DAGs in liver and muscle cells.

    A telling piece of evidence, suggests Shulman, is that insulin resistance is also common in rare genetic disorders known as lipodystrophies, which are characterized by a deficiency or complete absence of fat cells. Lipodystrophic individuals have little or no place to temporarily store the calories they consume before they use them for fuel, and they are extremely insulin resistant. Researchers have also created lipodystrophic mouse models, genetically manipulated to have no fat cells, and these are also extremely insulin resistant. The fact that insulin resistance occurs in mice and humans lacking the fat cells necessary to store excess nutrients, says Shulman, “suggests that if you can't store fat properly, it's going to build up in liver and muscle and cause insulin resistance.”

    So what does it mean to store fat properly? The key, some researchers say, is the ability to expand adipose tissue in a specific way. When fat tissue can generate new adipocytes, these researchers believe, it creates fresh storage capacity instead of shunting excess fat into existing, over-stuffed fat cells. According to this hypothesis, insulin resistance develops when fat cells are overstuffed, stressing the endoplasmic reticulum and attracting macrophages, releasing inflammatory mediators, or leaking fatty acids out into the circulation—or any combination of these.

    Among the evidence supporting this hypothesis is a transgenic mouse created by Philipp Scherer of the University of Texas Southwestern Medical Center at Dallas and his colleagues in 2007. It happens to be, as Scherer says, “probably the fattest mouse ever made.” It's also extremely insulin sensitive. This particular mouse overexpresses a molecule called adiponectin, discovered by Scherer in 1995, that appears to stimulate the formation of new fat cells. Scherer says his transgenic mouse continues to generate new small fat cells which can “deposit all these calories taken in into an expandable healthy fat pad.” The liver stays in pristine shape, he says: “There's no lipid accumulation [even in muscle cells], … and there's improved insulin sensitivity.”

    Another line of evidence supporting this hypothesis comes from experience with insulin-sensitizing drugs, known as thiazolidinediones, used to treat type 2 diabetics. These drugs target a receptor on cells, called PPARγ, that also works in the subcutaneous fat tissue to differentiate new adipocytes. The diabetic patient gets fatter, but the excess is stored in new small fat cells rather than in overstuffed old ones. The patient gains insulin sensitivity as a tradeoff for the extra fat. “You redistribute fat out of the muscle, liver, and beta cells into subcutaneous fat,” says Ralph DeFronzo, chief of the diabetes division at the University of Texas Health Science Center at San Antonio. “As long as the fat is in subcutaneous adipocytes, it can't hurt you.”

    “It's pretty clear that if there are inflammatory cytokines or stress signals around, the insulin receptor does not function very well.”



    Good and bad fat cells?

    While researchers have made considerable progress elucidating these mechanistic connections, every insight seems to come with unanswered questions or observations that remain stubbornly controversial.

    Take the critical observation that fatty acid levels are elevated in obesity, and the idea that this leads to DAG accumulation in liver and muscle cells. At least some researchers—Keith Frayn, for instance, who studies adipose tissue metabolism at the University of Oxford in the United Kingdom—question whether this is true. “Every review of insulin resistance talks about an increase in free fatty acids” with obesity, Frayn says. “We have been looking at a collection of 1200 normal healthy individuals, and we see no correlation in that collection between body mass index and free fatty acids in plasma.”

    The evidence that large, overstuffed fat cells are the problem has also recently been challenged. Reaven and Sam Cushman, a fat metabolism researcher at the U.S. National Institute of Diabetes and Digestive and Kidney Diseases in Bethesda, Maryland, reported in August 2007 that when they look at subjects with the same level of moderate obesity but different degrees of insulin sensitivity, they find that the insulin-resistant subjects actually have fat cells that tend to be smaller, rather than larger.

    “The conventional wisdom has been that the obese have these very big fat cells, and these secrete all these terrible things [inflammatory cytokines in particular], and these terrible things make you insulin resistant,” says Reaven. “What we found is that if you looked at the ratio of small fat cells to large, insulin-resistant people had the higher proportion of small cells.” To Reaven, this suggests that the underlying problem in insulin resistance isn't the large fat cells themselves but a relative inability to expand smaller fat cells into larger ones as needed. “If you can't make good fat cells to store fat,” he says, “then the fat may end up in ectopic places where it does more harm than good.”

    One observation that seems indisputable is that when individuals lose weight, they become more insulin sensitive. If nothing else, this has given researchers the confidence to assume that excess body fat—particularly in the abdomen and around the internal organs—is a fundamental cause of insulin resistance. But that still avoids the question of what causes insulin resistance in lean individuals. This is something few researchers will even address, although one possibility is that they, too, simply can't store fat safely in subcutaneous pads.

    “The biggest question in the whole field of insulin resistance is still this direction of causality,” says O'Rahilly. “Does obesity make you insulin resistant? Or does underlying factor x cause both obesity and insulin resistance?”

  10. U.S. Space Program

    Can Bolden Banish NASA Blues?

    1. Andrew Lawler*
    Looking ahead.

    The Senate is expected to approve Charles Bolden and Lori Garver to lead NASA.


    Next week marks 40 years since NASA first put men on the moon. But trepidation about the space agency's future is dampening celebration of that milestone achievement. “NASA is not what it was,” declared the chair of the Senate Commerce, Science, and Transportation committee during last week's confirmation hearing for Charles Bolden Jr., President Barack Obama's choice to lead the agency.

    Rather than inspiring the nation with wondrous feats of science and exploration, said Senator Jay Rockefeller (D–WV), NASA is adrift. The agency's biggest fan on Capitol Hill agrees. “That magic is gone,” bemoaned Senator Bill Nelson (D–FL), who once flew on the soon-to-be-retired shuttle. Even Bolden, a 62-year-old retired Marine general and astronaut, joined the chorus of gloom during a hearing in which legislators lauded his fitness for the job.

    But some remedies to this midlife crisis are emerging. The day before Bolden testified, the National Academies' National Research Council (NRC) released a report urging the space agency to link its efforts to broader national goals. Both the report and Bolden suggest that NASA support more basic research, as it once did, and take the lead in monitoring the environment. Both thrusts will require greater cooperation with other nations, they add.

    The biggest question facing NASA is whether the 2004 vision of President George W. Bush to return humans to the moon by 2020 and then on to Mars is still alive. During the presidential campaign, Obama promised to build a large new rocket that can put humans back on the lunar surface, and Bolden told senators that is still in the cards. “We will go on to the moon,” he said. But he avoided mention of any timeline and left up in the air the second phase of Bush's vision. “I want to go to Mars,” Bolden declared, before noting that this would be at least a 20-year venture.

    Next month, a blue-ribbon panel chaired by retired aerospace executive Norman Augustine will lay out options for the replacement of the shuttle and whether it will be designed with a lunar base and a Mars mission in mind. But the more salient issue is how the White House will react.

    The academies' report makes some suggestions. America's Future in Space: Aligning the Civil Space Program with National Needs argues that NASA needs shaking up so that “a disciplined space program can serve larger national imperatives.” Toward that end, the panel recommends that NASA create a nimble research shop modeled on the Defense Department's Defense Advanced Research Projects Agency.

    Of Related Interest

    Apollo 11 anniversary

    In celebration of the 40th anniversary of the first lunar landing, Science is making available, free with site registration, the complete contents of its 30 January 1970 issue, in which much of the science from the Apollo 11 mission was first reported.

    [Image credit: NASA]

    In his Senate testimony, Bolden strongly backed a renewed emphasis on basic science and engineering, particularly aeronautics. His nominated deputy, Lori Garver, told legislators that she foresees “a great future in utilizing the space station for biomedical research” once the orbiting facility is completed. She said the research would focus on human diseases, an area largely ignored by the Bush Administration, and on preparing astronauts for long stints in space.

    The academy report and Bolden also agree that NASA must revitalize its Earth-observation system and work with other countries to gather data on the planet's environmental health. Strengthening international ties is essential on other fronts, too, NASA science chief Edward Weiler warned researchers meeting last week in Washington, D.C.: “On our own, we can't do what people would like us to.”

    Mars is a case in point. “We no longer have a viable Mars program,” Weiler confessed to a planetary science decadal study group. To help build one, NASA and the European Space Agency tentatively agreed early this month at a meeting in Plymouth, U.K., on a cooperative Mars robotic exploration effort. Although details from that meeting have yet to be made public, one NASA official said that finding life on the Red Planet is high on the list.

    The NRC study also urged NASA to expand its roster of partners in human exploration beyond Europe, Japan, Canada, and Russia. Neither Bolden nor the White House has spoken publicly about this idea, but several Washington officials predicted that Obama's efforts to strengthen relationships with other countries, notably China and India, will eventually include space cooperation.

    The former shuttle pilot also expects help from the private sector. “The government cannot fund everything we want to do,” he said, calling for entrepreneurs to take a larger role.

    Bolden, who grew up in South Carolina during segregation and who would be the first African American to lead NASA, faced no tough questions during the hearing. Nelson, who accompanied Bolden on a 1985 shuttle mission, called him an “overcomer” of personal, racial, and professional barriers. Concerns about his role as an aerospace consultant appear to have dissipated.

    The Senate is expected to confirm Bolden easily although not necessarily before it goes on holiday in August. Once he takes the helm, Bolden's biggest challenge will be to win support from the White House for a new approach to space exploration that fires the imagination of Congress and the public. If he fails, the agency may be left celebrating past triumphs rather than working toward future milestones.

    • * With reporting by Richard A. Kerr.

  11. Solar System Evolution

    Shifting Orbits Gave Solar System A Big Shakeup, Model Suggests

    1. Richard A. Kerr

    Dynamicists simulating the solar system's early days are finding that a violent reshuffling of bodies large and small may explain many of today's planetary mysteries.

    Hard times.

    A catastrophic rearrangement of the outer planets may have pummeled Earth's moon with huge impacts.


    Isaac Newton inspired generations with his vision of the planets, their moons, and all the miscellaneous flotsam of the solar system as one huge planetary clock that has kept precise time over the eons. But planetary scientists are finding that the most massive pendulums within the planetary timepiece—the four outermost planets—haven't always been orbiting where they are today. They've moved, some a considerable distance outward.

    The most catastrophic scenario for such planet migration, dubbed the Nice model (after the French city), has been gaining ground of late. It envisions the great reshuffling as a brief, violent affair that not only put the outer planets where they are today but also created the Kuiper belt of small icy bodies beyond Neptune, gave the planets scores of oddly orbiting moons, and bombarded the solar system with a rain of asteroids and comets so fierce that it would have cooked all but the deepest subterranean life on early Earth.

    If such a cataclysmic rearrangement did indeed occur, “almost every nook and cranny of planetary science has been affected by it,” says planetary dynamicist William Bottke of the Southwest Research Institute (SwRI) in Boulder, Colorado. The latest support for the Nice model, a new explanation for primitive-looking asteroids, appears this week in Nature. But the model has more hurdles to clear, such as explaining why the innermost planets—Earth and its neighbors—weren't reshuffled as well.

    A French quartet

    Today, the sun's planets fall tidily into two neighborhoods: the inner solar system, home of small, rocky Mercury, Venus, Earth, and Mars; and the outer solar system, where enormous Jupiter and its smaller (but still huge) gaseous cousins Saturn, Uranus, and Neptune trace out stately decades-long orbits. In between lies a no planet's land of rubble, the asteroid belt.

    About 10 years ago, planetary dynamicists realized that the outer planets had moved over time and that migrating planets could dump small bodies such as comets and asteroids into the inner solar system like salt from a shaker. But there was a problem: The solar system had formed 4.6 billion years ago, but astronomers saw no sign of such a cosmic bombardment until 700 million years later. How could trillions upon trillions of bodies have been kept locked up in the outer solar system for so long, only to be suddenly unleashed?

    Four planetary dynamicists had an idea (Science, 3 December 2004, p. 1676). Harold Levison of SwRI, Rodney Gomes of the National Observatory in Rio de Janeiro, Brazil, and Kleomenis Tsiganis of Aristotle University of Thessaloniki, Greece, had all at one time or another conducted research with astronomer Alessandro Morbidelli at the Observatory of the Côte d'Azur in Nice. They began with a scheme in which the outer planets had formed much closer to the sun than they are now. Immersed in a disk of planet-building debris, however, the planets wouldn't have stayed where they formed. Any time a planet encountered a planetesimal and gravitationally flung it away, the planet would drift an infinitesimal amount in reaction. Massive Jupiter barely budged, but Saturn and the other relative lightweights crept inexorably away from the sun.

    Eventually, Saturn's outward drift would have brought Jupiter and Saturn into their so-called 1:2 resonance, in which Saturn made two orbits in the time it took Jupiter to make one. (Today, the ratio is closer to 1:2.5.) Then Jupiter could repeatedly give Saturn a gravitational nudge at the same point in Saturn's orbit so that the nudges could accumulate, the way repeatedly pushing a swing at the same point in its arc sends it higher.

    The repeated orbital boosts would have stirred the outer solar system into a frenzy. The Nice group ran computer simulations of the gravitational interactions of the planets and planetesimals with the planets starting bunched in close. Once locked in their resonance, the model's Jupiter excites the orbit of Saturn, stretching its orbit until it can gravitationally scatter the much smaller Uranus and Neptune outward into a lingering disk of planetesimals. In all the hubbub, the two outermost planets can even cross orbits and exchange positions.

    The model's Neptune then sends planetesimals every which way. A million billion of them pummel Earth's moon in less than 100 million years; the inner planets fare no better. “This is a very violent event,” Levison said at a workshop last November.* “The solar system rearranges itself, and the inner solar system gets clobbered.”

    In three papers published in 2005, the Nice group reported signs that such a rearrangement and bombardment may have actually happened. The slightly tilted and elongated final orbits of their model's outer planets resemble the planets'actual orbits, they reported. All earlier modeling had left the outer planets with perfectly circular orbits with no tilt.

    Planetary forensics

    Encouraged, the Nice group began looking farther afield for clues to the early solar system's evolution. “It's like a bloody crime scene,” says Levison. “Sometimes the splatters on the wall can tell you more about the crime than the body itself.” First, the Nice group looked at Jupiter's Trojan asteroids, the small bodies that lead and trail the giant planet approximately in its own orbit. According to a leading theory, they got there when Jupiter's growing envelope of gas dragged planetesimals into the planet's orbit, but that theory never explained why some of the Trojans move in steeply inclined orbits.

    In Nice model simulations, when Jupiter and Saturn cross their 1:2 resonance, the Trojans naturally turn up just as they should, the group reported in one of its 2005 papers. The modeled Trojans' range of orbits matches the actual orbits “remarkably” well, they wrote. The final number of Trojans in the model fit the observed number. And the model has them coming from the same reservoir of icy planetesimals as the comets, which would explain the Trojans' cometlike spectral color.

    The Nice group also hypothesized that similar resonances between migrating Uranus and Neptune could produce the Trojans in Neptune's orbit. Planetary dynamicists David Nesvorný of SwRI (and a sometime collaborator of Nice group researchers) and David Vokrouhlický of Charles University in Prague confirmed that prediction this June in The Astronomical Journal.

    Since 2005, Nice group members and colleagues have found more fingerprints of a sudden and violent planetary rearrangement all over the solar system, from the asteroid belt to the solar system's outer limits. The four outer planets have distant moons whose origins and behavior have been hard to explain. These moons wing about every which way, half of them revolving “backward.” Unlike the inner, well-behaved moons, which obviously formed like mini–solar systems from disks of debris, the more distant, irregular satellites must have arrived from elsewhere, but how they managed to get into orbit remained a mystery.

    In a 2007 paper in The Astronomical Journal, Nesvorný, Vokrouhlický, and Morbidelli showed how close encounters of two planets—like those in the Nice model's migration scenarios—can deflect a nearby planetesimal into orbit around a planet. The modeled orbits and the number of captured moons compared well with observations for moons around Saturn, Uranus, and Neptune. “That's another success,” says Levison.

    A big kablooie.

    When the outer planets (colored orbits) rearranged themselves (center), they scattered planetesimals (green dots), including Saturn's 213-kilometer irregular satellite Phoebe (above).


    Beyond the outer planets, Levison and Nice colleagues used their model to try to understand the Kuiper belt, the disk of icy bodies orbiting the sun beyond Neptune. They were “able to explain the basic mysterious aspects of the [Kuiper belt] population,” says Levison—no mean feat in a region where oddities abound. For example, Kuiper belt objects orbit inside the 1:2 resonance with Neptune, as if it presented a barrier. Some belt objects travel in resonance with Neptune, and some do not. Some orbits are inclined, and some are not. And some Kuiper belt bodies are sorted into high- or low-inclination orbits depending on their size and color. In Nice model simulations that Levison and colleagues reported in 2008 in Icarus, seven of these peculiarities appeared naturally in the Kuiper belt. “It looks pretty good,” says Morbidelli. “Most features are explained within one scenario.”

    Levison and colleagues report this week in Nature that the dark, organic-rich residents of the outer asteroid belt could be icy interlopers thrown there by migrating planets. Most theorists have assumed that the outer belt's water-rich D-type asteroids formed where they are now, at relatively low temperatures, whereas the higher temperatures of the inner belt baked out any water and organics, leaving rocky bodies. But in Nice model runs, Jupiter slings icy planetesimals inward where jovian resonances capture them, tame their gyrating orbits, and then move on, leaving the newly arrived “asteroid” orbiting toward the outer parts of the asteroid belt.

    Growing acceptance

    “It's scary,” says Levison. “It's a crazy idea, and it's working remarkably.” He's particularly impressed with the way the Nice model creates gravitational conditions essential to producing different aspects of the solar system, such as the Trojans and irregular satellites. No alternative explanation—such as the slow migration of planets without a resonance crossing—has those essential conditions, Levison says.

    Many other planetary scientists are impressed, too. “The overall model has held up quite well,” says planetary dynamicist Stuart Weidenschilling of the Planetary Science Institute in Tucson, Arizona. “It's pretty much accepted as the paradigm for how the solar system could have evolved.” And researchers in and out of the Nice group are exploring for possible implications elsewhere: the inner and outer Oort cloud of comets far beyond the Kuiper belt; the interiors of Jupiter's large satellites; and the mysterious dark stuff coating some satellites of the outer planets, among other places.

    Although the Nice model may be on a tear, “there's still some more work to be done,” says Weidenschilling, to prove that it really happened that way. For one thing, there's a problem with Earth and its fellow inner planets. “The inner planets are not stable in the Nice model,” notes planetary dynamicist Renu Malhotra of the University of Arizona, Tucson. For example, in the model, Mars might fly out of the solar system as resonances of migrating outer planets sweep through.

    And delaying the heavy bombardment to 3.9 billion years ago is tricky. Even with the 1:2 resonance of Jupiter and Saturn to light the fuse, it requires that material in a belt beyond the newly formed outer planets “delicately hang around for 700 million years, essentially doing nothing,” says Malhotra. “That seems very difficult.” The Nice group is working on both problems and is guardedly optimistic about solving them. “We haven't got much of an alternative,” says Morbidelli. “The only coherent scenario is ours.”

    • * Workshop on the Early Solar System Impact Bombardment, 19–20 November 2008, Houston, Texas.