• Published online: 12 April 2007; | doi:10.1038/news070409-10 / http://www.nature.com/news/2007/070409/full/070409-10.html

    First monkey genome sequenced

    New genome has scientists going bananas.

    Erika Check



    The rhesus macaque : 93% like you and me.

    Getty
    In some ways, macaque monkeys are a lot like people: they can reside in cities, eat everything from peanuts to ice cream, and prefer to live in communities. Research published today will help scientists to figure out any genetic reasons behind these similarities - and behind our differences, from the macaques' short size and hairy bodies to their vulnerability to disease.

    Writing in the journal Science today, researchers present the DNA sequence of the rhesus macaque, a species of monkey living all across Asia. Old-world monkeys such as the macaque are thought to have diverged from the primate line that led to humans some 25 million years ago. But an in-depth study of portions in the new sequence reveals that we are still 93% identical in our DNA.

    Knowing the sequence of the macaque genome is important to scientists because captive-bred macaques are often used in tests of experimental drugs and medical treatments. Understanding how they differ from us should help to better predict when a drug will have a different effect on humans than it did in animal tests. But the macaque sequence is also exciting for scientists because it should help them learn more about what makes us human.

    Compare and contrast

    "When you sequence the genome of a non-human primate, you open the door to understanding the biology of an animal that's really closely related to us, and that's very exciting," says George Weinstock of the Baylor College of Medicine in Houston, Texas, a leader of the macaque sequencing effort.

    Scientists sequenced the chimpanzee, a much more recent relative and closer cousin of ours, in 2005, showing that we are 98% identical in DNA. The macaque genome provides a third reference point in comparing these two. So, for instance, if scientists find a DNA difference between humans and chimps, they can check it against the macaque sequence to figure out whether the chimp or the human carries the more ancient version of the DNA.

    By performing such comparisons, scientists hope to be able to home in on regions of the genome that contributed to the evolution of humans. This method will become even more powerful over the next few years, as scientists add other non-human primate genomes to the mix: the gibbon, the marmoset, the orangutan and the gorilla are all on the cards.

    Sweet tooth

    The macaque genome has already provided some insight into evolution.

    One gene group that has massively expanded in the macaque, as compared with the human, is important to sugar digestion. Perhaps this is a genetic adaptation that allowed macaques to start eating a fruit-heavy diet, the researchers speculate.

    The scientists' analysis also points out that many of the types of genes that differ between macaques and humans are found in our immune systems, which orchestrate our bodies' defences against disease. By studying these differences, scientists might be able to fine-tune their use of the macaque as a stand-in for people in medical experiments.

    "Having a macaque genome means they can be used more wisely in research," Weinstock says.

    References
    1. Rhesus Macaque Genome Sequencing and Analysis Consortium. Science, 316 . 222 - 234 (2007).
























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  • Published online: 12 April 2007; | doi:10.1038/news070409-11

    Dinosaur protein sequenced

    Lucky find shows up record-breaking fossil.

    Heidi Ledford



    Digging through the rock in Montana yielded the surprise find.

    Science
    Palaeontologists have sequenced some protein from a 68-million-year-old fossilized Tyrannosaurus rex bone.

    The protein - a key component of bone and connective tissue called collagen - blasts the record for the oldest protein ever sequenced. Before this, the oldest sequenced protein (also collagen) came from a mammoth fossil that was 100,000-300,000 years old. So the new find, reported this week in the journal Science, is quite a surprise.

    Scientists hope that if similar molecular data can be recovered from other fossils, the information can be used to firm up the dinosaur family tree and to better understand their relationship with living animals.

    But evolutionary biologists caution that the information from a single type of protein, such as collagen, is inadequate for building a proper family tree.

    Nor is sequencing a single type of protein going to open the doors to Jurassic Park. Scientists would need DNA - which is much more fragile - in order to get the full genome of an ancient animal.

    "I think it's a really great experiment," says Mark Norell of the American Museum of Natural History in New York. "But is this going to change the way we look at dinosaurs? Well, probably not."

    Hard core protection

    Many paleontologists don't think to check their fossils for protein, says palaeontologist Mary Higby Schweitzer of North Carolina State University in Raleigh, a co-author on the study. It's been known for a long time that dinosaurs exhibit wonderful microstructural preservation," she says. "However, it's always been assumed that preservation does not extend to the cellular or molecular level."

    This particular fossil, which has been shown to contain soft tissues before, was unusually well preserved.

    It was found within 1,000 cubic metres of sandstone in the badlands of eastern Montana. The rock is thought to have kept away damaging groundwater and bacteria. "As the tissues begin to liquefy, the enzymes of decay and degradation are drained away in the sand, whereas in the mud it just sits and stews in its own juices," says Jack Horner, a palaeontologist at the Museum of the Rockies at Montana State University in Bozeman and an author on the study.

    Collagen is very abundant and collagen fibres form a particularly tough, triple helix, with three strands of protein wound together like rope. The collagen samples that Schweitzer isolated from the T. rex fossil were buried deep within the fossil's large, dense bones, which probably provided a protective casing for the protein.



    No one thought protein from a 68-million-year-old bone could be preserved.

    Science
    Horner is optimistic that similarly well-preserved fossils and their resident proteins can be isolated if palaeontologists are willing to dig through enough rock to find them. "If we spend a lot of time getting as deep into the sediment as we can in places where there has been very little air or water contamination, I think we're going to find that many specimens are like this," he says.

    But others question whether there will be enough such finds to be useful. "I think you're not going to be able to get this kind of material from the vast majority of fossils," says Norell. "Most of the stuff we work on has been heated to hundreds and hundreds of degrees and smashed by geological pressure."

    "If we can only get rare sequence data it will remain just a curiosity," says Derek Briggs, a curator at Yale University's Peabody Museum of Natural History in New Haven, Connecticut.

    Close to a chicken

    So far, seven fragments of protein sequence have been gleaned from the T. rex fossil. Trawling through the limited amount of data available on collagen sequences, the authors determined that these are closest to the collagen of chickens.

    This is in keeping with the dominant view that birds and dinosaurs are closely related. But the researchers hasten to point out that this does not mean that T. rex's closest modern relative is the chicken - just that the chicken is the closest relative for which collagen sequence is available in public databases. Crocodile and alligator collagen sequences, for example, were not available for comparison.

    Schweitzer hopes the results will also encourage palaeontologists to open their collections to molecular investigation - even though that will mean dissolving the samples to get at any proteins inside. "Most curators of dinosaur palaeontology don't like me," says Schweitzer. "They like to keep their bones intact."

    References
    1. Schweitzer M. H., et al. Science, 316 . 277 - 280 (2007).
    2. Asara J. M., et al. Science, 316 . 280 - 285 (2007).




































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  • http://www.nature.com/news/2007/070409/full/070409-9.html / Published online: 12 April 2007; | doi:10.1038/news070409-9

    US Senate passes stem-cell bill - again

    Bush promises to veto attempt to expand federal funding.

    Meredith Wadman



    For the second time in nine months, the US Senate has voted to lift restrictions on federal funding for human embryonic stem-cell research. But once again, the measure is expected to be vetoed by President Bush.

    "This bill crosses a moral line that I and many others find troubling. If it advances all the way through Congress to my desk, I will veto it," the president said in a statement issued shortly after the Senate vote.

    Senator Tom Harkin (Democrat, Iowa), the bill's leading proponent, urged the president to reconsider. "Tonight I am appealing to President Bush to re-examine the substance of this bill, and to reconsider his threat to veto it."



     


    Le président américain George W. Bush a annoncé mercredi qu'il opposerait son veto à un projet de loi adopté en soirée par le Sénat visant à favoriser la recherche sur les cellules souches embryonnaires

     

    http://www.la-croix.com/article/index.jsp?docId=2300105&rubId=5547  

     


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  • Published online: 11 April 2007; | doi:10.1038/news070409-6 / http://www.nature.com/news/2007/070409/full/070409-6.html

    How to stop cancer from spreading

    Breast cancer kept from the lungs of mice with simple drug cocktail.

    Helen Pearson



    Targetting four genes with drugs can stop at least one type of breast cancer from spreading in mice.

    Getty
    Breast cancer has been prevented from spreading in mice with a simple cocktail of drugs, some of which are already approved for human use.

    The spread, or metastasis, of cancer is the most dreaded aspect of the disease: tumours formed this way are responsible for 90% of cancer deaths. But the process has been difficult to fathom - two tumours may by all appearances be identical, yet one will spread and one will not. And a tumour may shed hundreds or thousands of cells into the bloodstream every day, of which only a tiny fraction will successfully lodge in a new site and start to proliferate into a new cancer.

    In 2005, Joan Massagué at the Memorial Sloan-Kettering Cancer Center in New York identified a roster of genes that seem to help breast cancer cells to metastasize to the lung. Now Massagué's team has shown how four of these genes specifically work in concert to fuel metastasis. Addressing these four genes with drugs, they show in mice, has a dramatic effect.

    Massagué hopes that this approach will work better than existing treatments, because it is targeted against genes now proven to fuel tumour growth and metastasis. And, he notes, two of the drugs are already in clinical use, which should speed clinical trials. "You couldn't have it better," he says. Other researchers say they would like to see data from human patients before getting too excited.

    Four together

    The researchers proved the action of the four genes by silencing them in a line of human breast cancer cells, before injecting them into mice. The gene silencing halted the growth of breast tumours in the mice, and almost completely blocked the formation of lung metastases, they report in Nature. Silencing only one of the genes at a time, by contrast, had far less effect.

    The team propose that the four genes (called EREG, MMP1, MMP2 and COX2) are vital both for aggressive growth of the primary tumour and for metastasis : they help to hijack a network of blood vessels to nourish the tumour's own growth, help tumour cells escape into these same blood vessels to reach the lung, and help them to weasel their way through the capillary wall, set up shop and grow.

    The researchers showed that a combination of existing drugs known to inhibit the genes' action - two approved drugs called cetuximab and celecoxib, plus an experimental one called GM6001 - had a similar effect to silencing the genes. The two approved drugs on their own also served to stop the cancer spread.

    Massagué says the next step is to find women whose breast tumours are relying on these four genes, and to test whether this combination of drugs would help to protect them from lung cancer. He is now working with doctors to initiate clinical trials.

    Born to kill

    The study challenges a long-standing idea that the tendency to metastasize is picked up late in a tumour's life. Massagué's results support an alternative hypothesis, that certain tumour cells possess the ability to metastasize from the outset - and in this case, the same genes that drive the growth of the primary tumour are the ones that drive the cells to metastasize.

    Researchers don't yet know whether these four genes are also involved in the metastasis of other cancer types. There are now thought to be hundreds of different cancer types and it is conceivable that each uses slightly different ploys for growing and spreading. That would make it much harder to treat. "I hope there are rules," says Christoph Klein, who studies metastasis at the University of Regensburg, Germany.

    There are many other aspects of metastasis that remain mysterious. Some patients turn up at the doctor with metastases even though, mysteriously, their primary tumour is never found. And little is known about why particular cancers show a proclivity for spreading to particular tissues, such as breast cancer's particular preference to target bone and lung.

    References
    1. Minn A. J., et al. Nature, 436 . 518 - 524 (2005). 
    2. Gupta G. P., et al. Nature, 446 . 765 - 770 (2007).


























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  • Published online: 11 April 2007; Updated online: 12 April 2007 | doi:10.1038/news070409-7 / http://www.nature.com/news/2007/070409/full/070409-7.html

    Alien plants may come in all colours but blue

    Model shows the rainbow of plant life possible in the Universe.

    Heidi Ledford



    The local sunlight and atmosphere helps determine what colours a plant will absorb.

    A picnic on a far-flung planet orbiting a red dwarf might involve spreading your blanket on black grass and munching on purple veggies, according to a new model.

    Given that we have yet to find bacteria, let alone little green men or purple palms, on any other planet, it might seem slightly ridiculous to spend time working out what colour plants elsewhere in the Universe must be. But scientists say that the thought experiment could be useful in helping us to look for lush landscapes in other solar systems.

    Nancy Kiang, a biometeorologist at the NASA Goddard Institute for Space Studies in New York, modelled the solar and atmospheric conditions of other planets to see which ones might be suitable for photosynthetic life, and what those photosynthesizers might look like.

    Red dwarfs, for example, emit only a fraction of the visible light produced by our own Sun, meaning that plants on planets around these stars will probably hoard all the visible light they can absorb, rather than reflecting back any particular wavelength, Kiang hypothesizes. That means they would probably look black.

    Is there a colour that a plant couldn't be? Kiang thinks that it's unlikely that plants will be blue, no matter what planetary environs are out there.










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