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This press release is copyright Nature.
VOL.471 NO.7339 DATED 24 MARCH 2011
This press release contains:
· Summaries of newsworthy papers:
Developmental biology: ‘Test-tube’ sperm
Genomics: Multiple myeloma genome sequenced
Cancer: Getting under the skin of melanoma
Outlook: Pioneer of chemoprevention champions new research effort
Cancer: Improving targeted treatment of lung cancer
Comment: Journey to the mantle of the Earth
Geoscience: San Andreas fault has a soft streak
Evolutionary biology: Questioning eusocial arguments
Chemistry: Catching some Z olefins
Neuroscience: Serotonergic sexual discrimination
Quantum physics: A new resource for precision measurement
And finally… The smell of pain
· Mention of papers to be published at the same time with the same embargo
· Geographical listing of authors
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[1] Developmental biology: ‘Test-tube’ sperm (pp 504-507; N&V)
Scientists have successfully cultured mouse testes cells and induced them to produce sperm. The findings, published in this week’s Nature, might have clinical applications in the field of male infertility.
Sperm production (spermatogenesis) is a long and complex process that has been difficult to reproduce in mammals. Takehiko Ogawa and colleagues have created an organ culture system that can support complete spermatogenesis in spermatogonia of mice outside the testes. The resulting sperm and spermatids produced healthy and fertile mice. Moreover, the testes tissue was still viable after being frozen for months.
CONTACT
Takehiko Ogawa (Yokohama City University, Japan)
Tel: +81 45 787 2679; E-mail: ogawa(at)med.yokohama-cu.ac.jp
Shahin Rafii (Weill Medical College, New York, NY, USA) N&V author
Tel: +1 212 746 2070; E-mail: srafii(at)med.cornell.edu
[2] Genomics: Multiple myeloma genome sequenced (pp 467-472)
An analysis of several multiple myeloma genomes is published in this week’s Nature. The study reveals a variety of mutated genes that are involved in the disease and identifies mechanisms that could be the target of therapeutic strategies.
The pathogenesis of multiple myeloma — an aggressive and incurable malignancy — is poorly understood. Recent examples of individual cancer genomes have shown that sequencing of whole genomes can reliably identify acquired somatic mutations. Todd Golub and colleagues sequenced 38 tumour genomes and compared them with normal DNA sequences. They found that mutations in genes involved in protein translation, histone methylation and blood coagulation are associated with multiple myeloma pathogenesis. Moreover, as mutations of a kinase called BRAF were observed, BRAF inhibition might be worth evaluating in multiple myeloma clinical trials.
CONTACT
Todd Golub (Broad Institute of Harvard and MIT, Cambridge, MA, USA)
Tel: +1 617 252 1927; E-mail: golub(at)broad.harvard.edu
[3] & [4] Cancer: Getting under the skin of melanoma (pp 513-522)
Molecules that speed and slow the growth of melanoma are described in two Nature papers published this week. The research helps unravel the mechanisms that underlie this skin cancer, and may aid therapeutic development.
The studies, both led by Leonard Zon, use a zebrafish model of melanoma. One demonstrates how the histone-methylating enzyme SETDB1 cooperates with a common melanoma mutation to accelerate melanoma development. The other indicates that neural crest progenitor cells that fail to differentiate properly may somehow fuel the cancer; treatment with leflunomide, an inhibitor of neural crest stem cells, slows melanoma growth in tissue culture and mouse models.
Leflunomide is an FDA-approved drug for the treatment of rheumatoid arthritis, and this second study suggests that it may be a useful anti-cancer drug, which might work best in combination with another type of drug called a BRAF inhibitor.
CONTACT
Leonard Zon (Children's Hospital Boston, MA, USA)
Tel: +1 617 919 2069; E-mail: zon(at)enders.tch.harvard.edu
Outlook: Pioneer of chemoprevention champions new research effort (pp S2-S3)
Cancer chemoprevention should be of higher priority within the research and clinical community, says Michael Sporn in a Perspective piece in this week’s Nature Outlook: Cancer prevention. Sporn — who is acknowledged as the father of chemoprevention — calls on pharmaceutical firms, regulatory agencies, governments and academic researchers to reassess their attitudes and practices to help develop chemopreventive drugs through clinical testing into clinical practice.
Cancer does not arise overnight. Breast cancer, for example, doesn’t begin when a lump is first felt. In some cases, it can take up to twenty years after a malignant mutation for a tumour to grow to be detectable, giving ample opportunity to block the development of invasive and metastatic disease. The author contends that we need to drop the “bizarre misperception that people are ‘healthy’ until they have actual symptoms of invasive cancer”. In truth, Sporn says, they are at risk for many years beforehand and medical intervention should be considered. Changing this mindset will take education alongside a coordinated scientific endeavour.
Preventing cancer makes common sense, but it has been subordinate to finding cures, he argues. By emulating the spirit of cooperative research that led to past triumphs over childhood leukaemia and Hodgkin’s disease, it will be possible to design better drugs and drug-combinations to combat the earliest signs of cancer — stopping this deadly disease before it even starts.
CONTACT
Michael Sporn (Dartmouth Medical School, Hanover, NH, USA)
Please note this author is travelling from 21-28 March.
Tel: +1 603 650 6557; E-mail: Michael.B.Sporn(at)Dartmouth.edu
[5] Cancer: Improving targeted treatment of lung cancer (pp 523-526)
A potential strategy for improving patient-specific treatment of lung cancer is reported in Nature this week.
Targeted therapies that specifically inhibit mutated EGFR in lung cancer have varying outcomes, and some tumours even develop resistance. Charles Sawyers and colleagues identified factors that modify the response to EGFR inhibition; they may provide companion drug targets to enhance the response to EGFR inhibitors.
Inhibition of FAS and NF-kappa B signalling enhances the response to treatment with EGFR inhibitors. Sawyers’ team noted that, in lung cancer patients treated with EGFR inhibitors, expression of the NF-kappa B inhibitor I-kappa B is associated with a better response and longer survival. These findings suggest that combining NF-kappa B pathway and EGFR inhibitors may prove clinically useful.
CONTACT
Charles Sawyers (Memorial Sloan-Kettering Cancer Center, New York, NY, USA)
Tel: +1 646 888 2138; E-mail: sawyersc(at)mskcc.org
Comment: Journey to the mantle of the Earth (pp 437-439)
This spring, researchers will mark the 50-year anniversary of an ambitious project by taking another step towards the same dream. They aim to drill through Earth’s crust under the ocean floor and down into the mantle and, for the first time ever, pull up a sample. In a Comment in Nature this week, the two co-chief scientists of that upcoming mission — Damon Teagle and Benoît Ildefonse — say that drilling into Earth’s mantle is now possible, and should hopefully begin within a decade.
The mantle makes up the bulk of our planet, stretching from the bottom of the crust — at 30–60 kilometres under the continents but just 6 kilometres under the oceans — down to the core 2,890 kilometres below. Retrieving a sample direct from the mantle would provide scientists with “a treasure trove comparable to the Apollo lunar rocks”, they write, and it would provide insight into the origins and evolution of our planet. But this goal has proven as difficult as going to the Moon: so far no one has drilled deeper than about 2 kilometres into the crust — a third of the way through.
The idea to drill into the mantle was born at a drinking club of notable earth scientists in 1957. ‘Project Mohole’ sailed in 1961. It took the first scientific core from the sea floor, and developed techniques for ocean drilling that are still used by the oil industry today. But it failed at its mission. Over the next few years, scientists will practise their deep drilling and assess three Pacific Ocean sites, looking for the best place to reawaken this dream.
CONTACT
Damon Teagle (University of Southampton, UK)
Tel: +44 23 8059 2723 E-mail: Damon.Teagle(at)soton.ac.uk
Benoît Ildefonse (CNRS, Université Montpellier 2, France)
E-mail: benoit.ildefonse(at)um2.fr
[6] Geoscience: San Andreas fault has a soft streak (AOP)
DOI: 10.1038/nature09927
***This paper will be published electronically on Nature's website on 23 March at 1800 London time / 1400 US Eastern Time as part of our AOP (ahead of print) programme. Although we have included it on this release to avoid multiple mailings it will not appear in print on 24 March, but at a later date. ***
Measurements taken from the San Andreas Fault Observatory at Depth (SAFOD) reveal the abundance of a weak clay mineral in a creeping zone of this fault. These measurements, which are published in Nature this week, provide strong evidence that the weakness in this portion of the fault is caused by the presence of weak minerals rather than by high fluid pressure or other proposed mechanisms.
David Lockner and colleagues discuss measurements of fault core materials from a drill hole (2.7 kilometres deep) located near the southern end of the creeping zone in the San Andreas fault, northwest of Parkfield, California. They report that the fault is profoundly weak at this location and depth, owing to the presence of a magnesium-rich clay mineral called saponite ― one of the weakest phyllosilicates known.
The saponites in this actively creeping shear zone in the San Andreas fault have a low frictional strength and are sandwiched by stronger crusts. This characteristic indicates that the mineral make-up alone is sufficient to explain fault strength, the researchers suggest.
CONTACT
David Lockner (US Geological Survey, Menlo Park, CA, USA)
Tel: +1 415 329 4826; E-mail: dlockner(at)usgs.gov
Evolutionary biology: Questioning eusocial arguments (pp E1-E10)
The field of evolutionary biology has been up in arms since the publication in Nature last August of a paper claiming that natural selection alone can be used to explain the evolution of eusocial behaviour without the need for kin selection theory. This week, five Brief Communications Arising (BCA) articles question that argument and the original authors respond.
Eusocial behaviour involves the forming of hierarchies where some individuals in a species do not reproduce, but assist in raising the offspring of others. The field has long believed that kin selection, an elegant extension of natural selection that takes into account relatedness, can explain this behaviour. Last year, Martin Nowak and colleagues put forward a mathematical analysis that suggested natural selection was all that was needed and kin selection is not necessary. Kin selection, formalised as inclusive fitness, only applies in limited cases, and where it is found, their calculations suggest natural selection is a more useful explanation.
A group of 137 researchers in the field outline three areas that they take issue with: firstly they feel the distinction between kin selection and standard natural selection is incorrect, secondly they disagree with the original authors’ ‘stringent assumptions’ about kin selection, and finally they wholeheartedly dispute the main claim that kin selection does not provide any additional biological insight.
Jacobus Boomsma and colleagues believe that the original paper overlooked the observation that eusociality has only arisen where relatedness is as high between siblings as it is between parents and offspring. Joan Strassmann et al. argue that inclusive fitness has been very useful for understanding the evolution of eusociality; Régis Ferrière and Richard Michod assert that the only paradigm is natural selection driven by interactions, and Edward Allen Herre and William Wcislo also defend kin selection and challenge the Nature paper.
The original authors respond, concluding that ‘we have shown that we cannot rely on inclusive fitness theory to describe how interactions among related individuals affect evolution.’ They still believe the theory is neither useful nor necessary to explain the evolution of eusociality and urge the field of social evolution to move beyond the limitations it imposes.
CONTACT
Stuart West (University of Oxford, UK) Author BCA
E-mail: stuart.west(at)ox.ac.uk
Jacobus Boomsma (University of Copenhagen, Denmark) Author BCA
Tel: +45 35 32 13 40; E-mail: JJBoomsma(at)bio.ku.dk
Joan Strassmann (Rice University, Houston, TX, USA) Author BCA
Tel: +1 832 978 5961; E-mail: [email protected]
Régis Ferrière (CNRS, Ecole Normale Supérieure, Paris, France) Author BCA
Tel: +33 144 322 340; E-mail: Regis.ferriere(at)ens.fr
Edward Allen Herre (Smithsonian Tropical Research Institute, Balboa, Panama) Author BCA
Tel: +507 212 8000; E-mail: herrea(at)si.edu
Martin Nowak (Harvard University, Cambridge, MA, USA) Author of original paper and of BCA
Tel: +1 617 496 4737; E-mail: martin_nowak(at)harvard.edu
[7] Chemistry: Catching some Z olefins (pp 461-466; N&V)
A new chemical method for synthesizing a specific class of carbon-carbon double bonds is reported in this week's issue of Nature. The authors demonstrate that a molybdenum-containing catalyst is able to generate the higher-energy isomer of an alkene from two simpler compounds.
Alkenes, or olefins, are found in a large number of pharmaceuticals and natural products, and the 2005 Nobel Prize in Chemistry was awarded to three chemists, including one of the authors of this paper, for the development of catalytic reactions that can be used to synthesize carbon-carbon double bonds via 'olefin metathesis.' Currently available olefin metathesis catalysts can be used to produce E olefins, but Z olefins are higher-energy compounds and are consequently harder to synthesize. Amir Hoveyda and colleagues show that their molybdenum-containing catalyst is able to facilitate a Z-selective 'cross-metathesis' reaction — an olefin metathesis reaction in which two different alkene-containing molecules are fused into a single molecule.
The authors show that this method can be used to synthesize the antioxidant C18 (plasm)-16:0 (PC), found in electrically active tissue, and the potent immunostimulant KRN7000.
CONTACT
Amir Hoveyda (Boston College, Chestnut Hill, MA, USA)
Tel: +1 617 552 3618; E-mail: amir.hoveyda(at)bc.edu
Daesung Lee (University of Illinois, Chicago, IL, USA) N&V author
Tel: +1 312 996 5189; E-mail: dsunglee(at)uic.edu
[8] Neuroscience: Serotonergic sexual discrimination (AOP)
DOI: 10.1038/nature09822
***This paper will be published electronically on Nature's website on 23 March at 1800 London time / 1400 US Eastern Time as part of our AOP (ahead of print) programme. Although we have included it on this release to avoid multiple mailings it will not appear in print on 24 March, but at a later date. ***
Neuron signalling triggered by serotonin seems to influence the sexual discrimination behaviour of mice, according to research in Nature this week. The work could stimulate further studies into the role of neurotransmitters in mammalian social relationships.
Scientists have known for some time that rodent mating depends on many social and chemical cues, but very little is known about the molecular and cellular mechanisms underlying this behaviour. Yi Rao and colleagues engineered male mice to lack the neurotransmitter 5-hydroxytryptamine (5-HT) and the result was loss of discrimination between male and female sexual partners. This demonstration of a role for serotonergic signalling in mouse sexual preference should stimulate further studies into the part that 5-HT plays in sexual interactions in particular and the roles of neurotransmitters in mammalian social relationships in general.
CONTACT
Yi Rao (Peking University, Beijing, China)
Tel: +86 135 0115 3876; E-mail: yrao(at)pku.edu.cn
[9] Quantum physics: A new resource for precision measurement (pp 486-489)
The quest for ever-more precise measurements takes a new turn in this week’s Nature, with the demonstration of a way to surpass a fundamental limit on the sensitivity of a quantum measurement. Using interacting photons to probe an atomic ensemble, Mario Napolitano and colleagues achieve sensitivity beyond the so-called Heisenberg limit — showing that interparticle interactions could be a useful resource for quantum metrology.
The laws of quantum physics place certain restrictions on the act of measurement, limiting the sensitivity that can be attained. In a measurement involving quantum interference among N probe particles, the sensitivity improves as N increases, scaling as 1/N1/2 if the particles are independent, and as 1/N (the Heisenberg limit) if they are quantum-mechanically ‘entangled’. Recent theoretical work has suggested that the sensitivity can be improved still further if the particles interact with one another, so that the behaviour of any one particle depends on the presence of others.
Napolitano and colleagues designed an experimental system to achieve this ‘super-Heisenberg’ scaling, using nonlinear optical effects in an ensemble of cold atoms to generate interactions among photons used to probe the ensemble’s magnetization. The authors succeed in observing super-Heisenberg scaling (proportional to 1/N3/2), but note that translating this into improved absolute sensitivity will depend in detail on experimental conditions.
CONTACT
Mario Napolitano (Institute of Photonic Sciences, Castelldefels, Spain)
Tel: +34 935 534 019 or tel: +34 935 534 013; E-mail: mario.napolitano(at)icfo.es
[10] And finally… The smell of pain (AOP)
DOI: 10.1038/nature09975
***This paper will be published electronically on Nature's website on 23 March at 1800 London time / 1400 US Eastern Time as part of our AOP (ahead of print) programme. Although we have included it on this release to avoid multiple mailings it will not appear in print on 24 March, but at a later date. ***
A genetic link between the loss of two major senses — smell and pain — is identified in a paper in this week's Nature. The study may help to improve our understanding of the genetic factors involved in smell perception and associated deficits.
Individuals with congenital general anosmia have a total inability to sense odours. The causative genes for this class of disorders have not been identified. Frank Zufall and colleagues find that both humans and mice with mutations in the gene coding for the voltage-gated sodium ion channel Nav1.7, previously shown to cause insensitivity to pain, are also unable to perceive odours.
Absence of Nav1.7, caused by loss-of-function mutations in the gene SCN9A, does not affect action potentials in olfactory sensory neurons (which are involved in smell detection). However, they prevent the transmission of information from neural synapses to downstream neural circuits, Zufall’s team report.
CONTACT
Frank Zufall (Saarland University, Homburg, Germany)
Tel: +49 6841 1626 450; E-mail: frank.zufall(at)uks.eu
ALSO IN THIS ISSUE…
[11] Fault lubrication during earthquakes (pp 494-498)
[12] A cis-regulatory map of the Drosophila genome (pp 527-531; N&V)
ADVANCE ONLINE PUBLICATION
***These papers will be published electronically on Nature's website on 23 March at 1800 London time / 1400 US Eastern Time as part of our AOP (ahead of print) programme. Although we have included them on this release to avoid multiple mailings it will not appear in print on 24 March, but at a later date. ***
[13] Redox freezing and melting in the Earth’s deep mantle resulting from carbon–iron redox coupling
DOI: 10.1038/nature09899
[14] Mapping and analysis of chromatin state dynamics in nine human cell types
DOI: 10.1038/nature09906
GEOGRAPHICAL LISTING OF AUTHORS…
The following list of places refers to the whereabouts of authors on the papers numbered in this release. For example, London: 4 - this means that on paper number four, there will be at least one author affiliated to an institute or company in London. The listing may be for an author's main affiliation, or for a place where they are working temporarily. Please see the PDF of the paper for full details.
CANADA
Toronto: 2
CHINA
Beijing: 8, 11
Shanghai: 8
FRANCE
Paris: 3, 9, 10
GERMANY
Homburg: 10
ISRAEL
Rehovot: 2
ITALY
Padua: 11
Rome: 3, 11
JAPAN
Chiba: 11
Ibaraki: 1
Kochi: 11
Yokohama: 1
SOUTH KOREA
Daejon: 11
Seoul: 10
SPAIN
Barcelona: 5
Castelldefels: 9
SWEDEN
Stockholm: 12
SWITZERLAND
Zurich: 13
UNITED KINGDOM
Cambridge: 2, 10, 12
Durham: 11
London: 10
Norwich: 4
UNITED STATES OF AMERICA
Arizona
Phoenix: 2
Scottsdale: 2
California
Duarte: 2
La Jolla: 12
Menlo Park: 6
Connecticut
New Haven: 10, 12
Norwalk: 2
Georgia
Atlanta: 2
Illinois
Chicago: 2, 12
Maryland
Chevy Chase: 2
Massachusetts
Boston: 2, 3, 4, 12, 14
Cambridge: 2, 3, 4, 7, 12, 14
Chestnut Hill: 7
Worcester: 3
Michigan
Ann Arbor: 2, 4
Minnesota
Rochester: 2
Missouri
St Louis: 2, 8
New Jersey
Hackensack: 2
New York
Cold Spring Harbor: 5
New York: 2, 3, 5
North Carolina
Durham: 5, 12
Ohio
Columbus: 2
Texas
Houston: 12
PRESS CONTACTS…
From North America and Canada
Neda Afsarmanesh, Nature New York
Tel: +1 212 726 9231; E-mail: n.afsarmanesh(at)us.nature.com
From Japan, Korea, China, Singapore and Taiwan
Mika Nakano, Nature Tokyo
Tel: +81 3 3267 8751; E-mail: m.nakano(at)natureasia.com
From the UK
Rebecca Walton, Nature, London
Tel: +44 20 7843 4502; E-mail: r.walton(at)nature.com
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