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This press release is copyright Nature. VOL.448 NO.7149 DATED 05 July 2007
This press release contains:
· Summaries of newsworthy papers:
Planetary Science: Cassini snaps sponge-like moon
Genetics: Variation associated with childhood asthma
Oncology: New cancer mutation found
Neurodegeneration: Newly discovered protein may help treat Parkinson’s?
And finally… Look-alikes can be good for your health
· Mention of papers to be published at the same time with the same embargo
· Geographical listing of authors
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[1] & [2] Planetary Science: Cassini snaps sponge-like moon (pp 50-53; pp 54-56)
High-resolution images of Hyperion reveal that Saturn’s eighth-largest and irregularly shaped satellite has an unusual sponge-like appearance at scales of a few kilometres.
The satellite is peppered with relatively well-preserved craters, each around two to ten kilometres in size, report Peter C. Thomas and colleagues in this week’s Nature. But their distribution is unusual, and Hyperion is highly porous. This high porosity may enhance crater preservation, they say.
The surface is quite reflective, but the bottoms of the craters are much darker, report Dale P. Cruikshank and colleagues in a second paper that also analyses images of Hyperion snapped by Cassini. The dark material from the crater bottoms seems to be similar to stuff on two of Saturn’s other moons: the dark side of Iapetus and the surface of Phoebe.
CONTACT
Peter C. Thomas (Cornell University, Ithaca, NY, USA) Author paper [1]
Tel: +1 607 255 5908 or 3507; E-mail: [email protected]
Dale P. Cruikshank (NASA Ames Research Center, Moffett Field, CA, USA) Author paper [2]
Please contact the author through:
Ruth Malaire (Media Contact, NASA Ames Research Center, Moffett Field, CA, USA)
Tel: +1 650 604 4709 or 9000; E-mail: [email protected]
[3] Genetics: Variation associated with childhood asthma (AOP)
DOI: 10.1038/nature06014
***This paper will be published electronically on Nature's website on 04 July 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 05 July, but at a later date.***
Variations in expression of a gene called ORMDL3 are associated with the development of childhood asthma, according to a report published online this week in Nature. The study suggests that this gene should be examined further in patient groups.
Asthma is caused by a combination of poorly understood genetic and environmental factors. William Cookson and colleagues here set out to find genes contributing to childhood onset asthma, using a genome-wide association scan to investigate the effects of single nucleotide polymorphisms (SNPs). They compared DNA from thousands of patient cases and controls, and report that multiple markers at the chromosome 17q21 locus are strongly and reproducibly associated with childhood asthma. Moreover, they show that the SNPs linked with childhood asthma are associated with expression levels of the gene ORMDL3.
ORMDL3 is the third member of a novel class of genes whose precise function is unknown — it is believed to encode a transmembrane protein that is anchored within an intracellular structure known as the endoplasmic reticulum. The authors propose that ORMDL3 should be explored in greater detail in large-scale, multicentre studies.
CONTACT
William Cookson (National Heart and Lung Institute, Imperial College London, UK)
Tel: +44 20 7351 8144; E-mail: [email protected]
[4] Oncology: New cancer mutation found (AOP)
DOI: 10.1038/nature05933
***This paper will be published electronically on Nature's website on 04 July 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 05 July, but at a later date.***
A newly identified genetic mutation found in several types of cancer makes cultured cells cancerous and induces leukaemia in mice. The find, reported in this week's Nature, aids our basic understanding of cancer biology and may influence drug design and prescription.
AKT proteins have been implicated in many cellular processes including metabolism, programmed cell death and proliferation. But while AKT signalling has been implicated in cancer, activating point mutations have so far not been reported in human tumours. Studies by Kerry L. Blanchard and colleagues suggest a direct role of AKT1 mutations in human cancer.
The team identified a recurrent mutation in the AKT1 gene in biopsy samples from breast, colorectal and ovarian cancer. They then analysed the structure of the mutant protein, and found that it tends to be located near the cell’s plasma membrane, where active AKT proteins are known to function. Critically, the mutation appears to activate the AKT protein, stimulating a cascade of downstream signals and making cultured cells cancerous. This mutant form of AKT1 also induced leukaemia in a mouse model.
CONTACT
Kerry L. Blanchard (Eli Lilly & Company, Indianapolis, IN, USA)
Tel: +1 317 276 5111; E-mail: [email protected]
[5] Neurodegeneration: Newly discovered protein may help treat Parkinson’s? (pp 73-77)
A new neuron-nourishing protein that may prove useful for treating Parkinson’s disease is revealed in this week’s Nature.
Parkinson’s disease destroys nerve cells that produce the neurotransmitter dopamine, leading to movement and balance problems. The new molecule, dubbed conserved dopamine neurotrophic factor (CDNF), can prevent the degeneration of dopamine-producing neurons in a rat model of Parkinson’s disease. But Mart Saarma and colleagues go one step further, showing that CDNF actually stops ongoing cell death and can help damaged dopaminergic neurons to recover, easing symptoms in their animal model.
Current anti-Parkinsonian drugs do not prevent neuronal degeneration and death, and their effects can be patchy and short-lived. The results suggest that CDNF has great potential as a therapeutic protein for Parkinson’s disease.
CONTACT
Mart Saarma (University of Helsinki, Finland)
Tel: +358 9 191 59359 or +358 50 500 2726; E-mail: [email protected]
[6] And finally… Look-alikes can be good for your health (pp 64-68; N&V)
Mimicry in the animal kingdom can benefit both the model and the wannabe, a Nature paper suggests. The finding, from a laboratory-based predator–prey set-up, helps to resolve conflicting theories about the nature of mimicry.
There are many examples of species that have evolved to resemble others to evade predators or dupe prey. Some, like the various species of yellow-and-black-striped bees and wasps, not only look alike, but also share the defence that wards off predators, such as being able to sting. Others like the sting-less ash borer moth (Podosesia syringae), which mimics the common wasp (Vespula vulgaris), go on looks alone.
Hannah M. Rowland and colleagues now show that both types of mimicry can be beneficial for both parties. Unequally defended mimics — including those that are edible — gain survival benefits from their association with one another. This goes against the school of thought that says that a moderately defended species might dilute the protection of a better defended one.
CONTACT
Hannah M. Rowland (The University of Liverpool, UK)
Tel: +44 151 795 4355; E-mail: [email protected]
Thomas N. Sherratt (Carleton University, Ottawa, Canada) N&V author
Tel: +1 613 520 2600 x1748; E-mail: [email protected]
ALSO IN THIS ISSUE…
[7] Low-energy acoustic plasmons at metal surfaces (pp 57-59)
[8] Early geochemical environment of Mars as determined from thermodynamics of phyllosilicates (pp 60-63; N&V)
[9] TRIC channels are essential for Ca21 handling in intracellular stores (pp 78-82)
[10] Structural snapshots along the reaction pathway of ferredoxin–thioredoxin reductase (pp 92-96)
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.
AUSTRIA
Feldkirch: 3
Vienna: 3
DENMARK
Aarhus: 7
ESTONIA
Tallinn: 5
FINLAND
Helsinki: 5
Jyvaskyla: 6
FRANCE
Evry: 3
Meudon: 2
Nantes: 2
Orsay: 2, 8
GERMANY
Berlin: 1, 2
Bochum: 3
Cologne: 3
Dresden: 3
Freiburg: 3
Munich: 3
Neuherberg: 3
Ulm: 3
Wesel: 3
ITALY
Forli: 1
Genova: 7
Naples: 2
Rome: 1, 2
JAPAN
Ibaraki: 9
Kyoto: 9
Miyagi: 9
Saitama: 9
NETHERLANDS
Maastricht: 8
NORWAY
Oslo: 10
SINGAPORE
Singapore: 4
SPAIN
Basque Country: 7
Madrid: 7
San Sebastian: 7
SWEDEN
Uppsala: 10
SWITZERLAND
Geneva: 10
Neuchatel: 10
Zurich: 10
UNITED KINGDOM
Liverpool: 6
London: 3
Oxford: 3
UNITED STATES OF AMERICA
Arizona
Phoenix: 4
Scottsdale: 4
Tuscon: 1, 2
Arkansas
Fayetteville: 8
California
Los Angeles: 1
Moffett Field: 2
Mountain View: 2
Pasadena: 1, 2
Colorado
Boulder: 1
Denver: 2, 10
Connecticut
New Haven: 5
Indiana
Indianapolis: 4
Maryland
Laurel: 1
Michigan
Ann Arbor: 3
New Hampshire
Durham: 7
New Jersey
Piscataway: 9
New York
Ithaca: 1, 2
Ohio
Cincinnati: 10
Washington
Winthrop: 2
PRESS CONTACTS…
For North America and Canada
Katie McGoldrick, Nature Washington
Tel: +1 202 737 2355; E-mail: [email protected]
For Japan, Korea, China, Singapore and Taiwan
Mika Nakano, Nature Tokyo
Tel: +81 3 3267 8751; E-mail: [email protected]
For the UK/Europe/other countries not listed above
Helen Jamison, Nature London
Tel: +44 20 7843 4658; E-mail [email protected]
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