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This press release is copyright Nature.
VOL.461 NO.7261 DATED 10 SEPTEMBER 2009
This press release contains:
· Summaries of newsworthy papers:
Cancer: A prostate stem cell linked to cancer
Geology: An ocean of magma
Prions: Symptomless deer produce infectious faeces
Geochemistry: The rise of oxygen
Opinion: Data sharing
Developmental biology: Source-sink mechanism aids embryonic patterning
Materials science: Ultrathin catalysts made to order
And finally… Save our spuds!
· Mention of papers to be published at the same time with the same embargo
· Geographical listing of authors
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[1] Cancer: A prostate stem cell linked to cancer (AOP)
DOI: 10.1038/nature08361
***This paper will be published electronically on Nature's website on 09 September at 1800 London time / 1300 US Eastern time (which is also when the embargo lifts) 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 10 September, but at a later date.***
Prostate cancer could be caused by the aberrant activity of a newly identified stem cell type, a mouse study in this week’s Nature paper suggests. The finding has implications for therapeutic design.
The rare cells, identified by Michael Shen and colleagues, are found among the epithelial cells that line the inner cavity of the prostate gland. They can form copies of themselves, and also generate different, more mature cell types — the hallmarks of a true stem cell. Critically, the team show that when a particular tumour suppressor gene is deleted in the cells, they give rise to prostate cancer in mice.
Stem cells have been suggested to underlie other forms of cancer, for example some leukaemias. The find suggests that these putative prostate stem cells can, under certain circumstances, cause prostate cancer.
CONTACT
Michael Shen (Columbia University Medical Center, New York, NY, USA)
Tel: +1 212 851 4723; E-mail: [email protected]
[2] Geology: An ocean of magma (pp 236-240)
Geochemical evidence published in Nature this week refines our understanding of the ocean of molten rock that once covered the surface of the Moon. Scientists have mapped the lunar highland crust at key locations to better constrain the composition of this ‘magma ocean’. The data will be important for understanding the dynamics of the magma ocean and the subsequent evolution of the Moon.
Most scientists believe the Moon was formed as a result of a giant impact on the proto-Earth — with the ejected material eventually accumulating into a separate planetary body. Owing to the huge amount of energy released, much of the Moon’s surface is thought to have initially been completely molten. The lunar highland crust then solidified after crystallization and flotation of the mineral plagioclase, but the exact mechanism by which such a crust formed remains unclear.
Makiko Ohtake and colleagues use reflectance spectroscopy data from the SELENE spacecraft to produce the first clear and high-resolution picture of the Moon’s crustal composition. They find that the widely distributed highland rocks have compositions of nearly 100% plagioclase — higher than previous estimates. The data should provide a valuable constraint on future models of lunar magma ocean evolution.
CONTACT
Makiko Ohtake (Japan Aerospace Exploration Agency, Kanagawa, Japan)
Tel: +81 42 759 8188; Email: [email protected]
[3] Prions: Symptomless deer produce infectious faeces (AOP)
DOI: 10.1038/nature08289
***This paper will be published electronically on Nature's website on 09 September at 1800 London time / 1300 US Eastern time (which is also when the embargo lifts) 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 10 September, but at a later date.***
Deer infected with chronic wasting disease excrete infectious prions long before they develop any symptoms of the prion disease, a Nature study reveals. The findings support the idea that the fatal neurodegenerative disease may spread when infectious faeces enter the food chain of the animals, and helps explain the horizontal spread of the disease between deer.
Stanley Prusiner and colleagues injected irradiated deer faeces into mouse brains, and found that samples collected from infected deer 7–11 months before they became ill could still cause disease in mice. It is already known that infected, symptomatic deer excrete infectious prions in their faeces, but this study shows that the faeces of infected, asymptomatic deer are contagious too. The same may be true for sheep with the prion disease scrapie, the authors suggest.
CONTACT
Stanley Prusiner (University of California, San Francisco, San Francisco, California, USA)
Tel: +1 415 476 4482; Email: [email protected]
[4] Geochemistry: The rise of oxygen (pp 250-253; N&V)
Scientists have developed a geochemical tracer system capable of unravelling small-scale fluctuations in the Earth’s ancient climate. The system, using chromium isotopes to track the rise of oxygen, will help researchers to build a better picture of how, when and why life evolved on our planet.
The rise of atmospheric oxygen, referred to as the ‘Great Oxidation Event’, plays a central role in the emergence and evolution of life, but the precise details of when and how this evolution occurred are still uncertain.
In Nature this week, Robert Frei and colleagues track the presence of chromium isotopes in banded iron formations — thick deposits with high concentrations of iron oxides, presumed to have formed in anoxic Precambrian oceans. Chromium is highly sensitive to changes in oxygen levels, so the team was able to reveal a more detailed picture of the oxygenation history of the Earth’s atmosphere–hydrosphere system.
The data suggest a brief elevation in atmospheric and surface ocean oxygenation before the first great rise of oxygen 2.45–2.2 billion years ago (the Great Oxidation Event) and a decline is recorded in younger deposits. This suggests that the Great Oxidation Event did not lead to a persistent stepwise increase in atmospheric oxygen.
CONTACT
Robert Frei (University of Copenhagen, Denmark)
Tel: +45 35 32 24 50; Email: [email protected]
Timothy Lyons (University of California, Riverside, CA, USA) N&V author
Tel: +1 951 827 3106; E-mail: [email protected]
Opinion: Data sharing (pp 160-163; 168-173)
Sharing knowledge is essential for the progress of science, but researchers do not always release data and research materials, even after publication of work. Earlier this year, two research communities held meetings with a broad range of stakeholders to discuss this issue, and they report their proposals to promote data sharing in biology in two Opinion articles in this week’s Nature.
Data producers and users met at a workshop in Toronto in May to discuss the benefits and best practices of rapid data release prior to publication. Ewan Birney, Tom Hudson and colleagues report the main conclusions of these discussions in a community statement, free to access online. They propose that the principles for early release of genomics data should be extended to other large data sets in biology and medicine. A grace period should be allowed, if requested, to enable data producers to analyse and publish their data set, but this should be limited to one year. The authors suggest a set of best practices for funding agencies, scientists and journal editors.
Mouse researchers, along with funding agencies and publishers, also met in May in Rome to address the barriers preventing more effective sharing of data and biomaterials — particularly mouse strains and embryonic stem cells. Their agenda, also free to access online, outlines guidelines to enable sharing of materials under the least restrictive terms, avoiding material transfer agreements where possible. Paul Schofield and the other participants argue that funding organization, journals and researchers need to work together to encourage better use of public repositories.
The recommendations are intended to spark community discussion on this subject. Ewan Birney, Tom Hudson and Paul Schofield will respond to reader comments in two online forums on Nature Network which will go live after the embargo has lifted:
http://network.nature.com/groups/naturenewsandopinion/forum/topics/5433 http://network.nature.com/groups/naturenewsandopinion/forum/topics/5434
Also in this issue, a News Feature examines the technical and cultural hurdles that can keep scientists from sharing data. Exploring issues from antiquated technology to a lack of trust in other scientists, the article highlights a range of potential solutions.
CONTACT
Ewan Birney (The European Bioinformatics Institute, Hinxton, UK)
Tel: +44 1223 494 420; E-mail: [email protected]
Tom Hudson (Ontario Institute for Cancer Research, Toronto, Canada)
This author is best contacted through:
Rhea Cohen (Media relations, Ontario Institute for Cancer Research, Toronto, Canada)
Tel: +1 416 673 6642; Mobile: +1 416 671 2846; E-mail: [email protected]
Paul Schofield (University of Cambridge, UK)
Tel: +44 1223 333 878; E-mail: [email protected]
Tania Bubela (University of Alberta, Edmonton, Canada)
E-mail: [email protected]
[5] Developmental biology: Source-sink mechanism aids embryonic patterning (AOP)
DOI: 10.1038/nature08931
***This paper will be published electronically on Nature's website on 09 September at 1800 London time / 1300 US Eastern time (which is also when the embargo lifts) 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 10 September, but at a later date.***
A technique that enables researchers to track the movement and concentration of single protein molecules has shed light on a fundamental mechanism underlying embryonic development. The discovery is revealed in this week’s Nature.
It is well known that the patterning and fate of cells in developing embryos is influenced by concentration gradients of diffusible proteins called morphogens. But how these gradients form has been the subject of debate. Michael Brand and colleagues use fluorescence correlation spectroscopy to show that gradients of the morphogen Fgf8 in living zebrafish embryos are formed by a simple source-sink mechanism — cells release the protein, which then diffuses away though the extracellular space into a ‘sink’ in the target tissue.
CONTACT
Michael Brand (University of Technology, Dresden, Germany)
Tel: +49 351 4634 0345; Email: [email protected]
[6] Materials science: Ultrathin catalysts made to order (pp 246-249; N&V)
Some clever chemistry has been used to improve the properties of a type of catalyst widely used in the chemical and petrochemical industries. The new synthesis strategy creates crystalline sheets of zeolite only two nanometres thick, which have higher catalytic activity and better resistance to poisoning by reaction products than their conventional counterparts.
Zeolites — microporous crystals of aluminosilicate — owe their powerful catalytic activity to their plentiful and uniform micropores, which selectively accelerate desirable chemical reactions by restricting the size and shape of molecules that can enter and leave the pores. But these tiny pores also hinder the diffusion of reactants and products, thereby limiting catalytic activity. This problem can be addressed by reducing the thickness of the zeolite crystals, but until now no direct synthesis method has produced crystals thinner than five nanometres.
In this week’s Nature, Minkee Choi and colleagues report their use of specially designed organic template molecules to direct the growth of the thinnest possible zeolite nanosheets: only one unit cell thick. The large surface area gives high catalytic activity, and undesirable by-products easily diffuse out of the thin sheets. This synthesis strategy should work for a variety of zeolite structures, with appropriate organic molecules designed for each one.
CONTACT
Minkee Choi (Korea Advanced Institute of Science and Technology, Daejeon, Korea)
Email: [email protected]
Avelino Corma (Polytechnic University of Valencia, Spain) N&V author
Tel: +34 96 387 78 00; Email: [email protected]
[7] And finally… Save our spuds! (AOP)
DOI: 10.1038/nature08358
***This paper will be published electronically on Nature's website on 09 September at 1800 London time / 1300 US Eastern time (which is also when the embargo lifts) 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 10 September, but at a later date.***
The genome of the water mould responsible for the Irish potato famine is reported online this week in Nature. Phytophthora infestans remains a critical threat to global food security, and it’s hoped that the information will help researchers to devise ways of combating this devastating plant disease.
Phytophthora is a group of plant-maiming organisms that are responsible for destroying billions of dollars of crops each year. Chad Nusbaum and colleagues sequenced P. infestans, a fungus-like water mould that causes potato blight and by far the most destructive member of the family.
They identify several genes that are induced during infection that could help P. Infestans to cause disease, by meddling with normal metabolic processes inside the host plant. Many of these genes are seen in families that are expanded specifically in this organism. These fast-evolving effector genes are localized to highly dynamic and expanded regions of the genome. Strikingly abundant ‘transposons’ — dynamic regions of DNA that can jump around to different positions in the genome — might help P. Infestans to evolve quickly to environmental pressures. This, say the researchers, could account for the success of the organism and its remarkable ability to adapt to control strategies aimed at limiting its spread.
CONTACT
Chad Nusbaum (Broad institute Genome Sequencing and Analysis, Cambridge, USA)
Tel: +1 617 714 7880 Email: [email protected]
Sophien Kamoun (The Sainsbury Laboratory, Norwich, UK) Co-author paper [7]
Tel: +44 1603 450 410; E-mail: [email protected]
Paul Birch (Scottish Crop Research Institute, University of Dundee, UK) Co-author paper [7]
Tel: +44 1382 562 731 ext 2520; E-mail: [email protected]
ALSO IN THIS ISSUE…
[8] Quantum Optical Pulse Sequencer (pp 241-245)
[9] Nucleotides released by apoptotic cells act as a “find-me” signal to promote phagocytic clearance (pp 282-286)
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.
AUSTRALIA
Canberra: 8
COLOMBIA
Bogota: 7
DENMARK
Copenhagen: 4
Odense: 4
GERMANY
Dresden: 5
Karlsruhe: 5
Stuttgart: 7
ISRAEL
Tel Aviv: 7
JAPAN
Chiba: 2
Fukushima: 2
Ibaraki: 2
Iwate: 2
Kanagawa: 2
Kyoto: 2
Nagoya: 2
Osaka: 2, 6
Tokyo: 2
Wakayama: 2
KOREA
Daejeon: 6
NETHERLANDS
Wageningen: 7
NEW ZEALAND
Dunedin: 8
SWEDEN
Stockholm: 6, 7
Uppsala: 7
SWITZERLAND
Neuchatel: 2
UNITED KINGDOM
Aberdeen: 7
Dundee: 7
Edinburgh: 7
Glasgow: 7
Newcastle: 4
Norwich: 7
Warwick: 7
UNITED STATES OF AMERICA
Arizona
Stuttgart: 7
California
Riverside: 7
San Francisco: 3
Colorado
Fort Collins: 3
Delaware
Newark: 7
Maryland
Baltimore: 7
Beltsville: 7
Rockville: 7
Massachusetts
Boston: 7
Cambridge: 7
New Jersey
Bridewater: 1
New Brunswick: 1
Piscataway: 1
Princeton: 1
Rahway: 1
Skillman: 1
New York
Ithaca: 7
New York: 1
North Carolina
Chapel Hill: 9
Raleigh: 7
Ohio
Bowling green: 7
Wooster: 7
Oregon
Corvallis: 7
Pennsylvania
Easton: 7
Rhode Island
Providence: 2
Tennessee
Knoxville: 7
Nashville: 7
Virginia
Charlottesville: 9
Washington
Madison: 7
Wisconsin
Madison: 7
URUGUAY
Montevideo: 4
PRESS CONTACTS…
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For Japan, Korea, China, Singapore and Taiwan
Mika Nakano, Nature Tokyo
Tel: +82 3 3267 8752; E-mail: [email protected]
For the UK/Europe/other countries not listed above
Ruth Francis, Nature London
Tel: +44 20 7843 4562; E-mail [email protected]
Jen Middleton, Nature London
Tel: +44 20 7843 4502; E-mail: [email protected]
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