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Article Released Sun-15th-November-2009 18:56 GMT
Contact: Ruth Institution: Nature Publishing Group
 Elevating arsenic

Summaries of newsworthy papers: Medicine: Location, location, location, Understanding schizophrenia, Costing the Earth, Nitrogen fix for early Earth, Common genetic risk variants for Parkinson’s disease, Inducible microRNA sponges for intact organisms and Ouch, that hurts!


For papers that will be published online on 15 November 2009

This press release is copyrighted to the Nature journals mentioned below.

This press release contains:

· Summaries of newsworthy papers:

Medicine: Location, location, location

Geoscience: Elevating arsenic

Neuroscience: Understanding schizophrenia

Nature: Opinion: Costing the Earth

Geoscience: Nitrogen fix for early Earth

Genetics: Common genetic risk variants for Parkinson’s disease

Methods: Inducible microRNA sponges for intact organisms

And finally…Nature: Ouch, that hurts!

· Mention of papers to be published at the same time with the same embargo

· Geographical listing of authors

PDFs of all the papers mentioned on this release can be found in the relevant journal’s section of Press contacts for the Nature journals are listed at the end of this release.

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[1] Medicine: Location, location, location
DOI: 10.1038/nm.2056

A drug that inhibits excitatory activity in the brain can either improve or worsen the progression of Huntington’s disease (HD) depending on where on neurons its targets are located. The finding, published online this week in Nature Medicine, may offer a new therapeutic approach towards Huntington’s disease.

HD is a condition characterized by neuronal death in the brain region termed striatum – which plays an important role in planning and executing movement. The disease is caused by mutations in the gene encoding the protein huntingtin, and results in the formation of huntingtin aggregates in the affected neurons; these aggregates may have a protective role early in the disease.

Stuart Lipton and his colleagues looked at the link between HD, the excessive excitatory brain activity observed, and the huntingtin aggregate formation. Using mice that express mutant forms of huntingtin, the team tested the effect on neurons of different doses of the drug memantine on neurons. This drug inhibits the NMDA receptors in the brain, which are a key subtype of the main excitatory receptors in the brain.

They found that a low dose of memantine blocked NMDA receptors found outside of the synapse and therefore reduced the severity of HD in the mice – such as neuronal death and behavioral deficits. By contrast, the scientists found, that a high dose of memantine that blocked NMDA receptors found on both the synapse and outside of the synapse decreased the number of huntingtin clumps and in fact worsened the disease.

Lipton and colleagues also established that the location of NMDA receptors on the neuron determines whether their activation will lead to aggregate formation and neuronal survival or to aggregate dissolution and neuronal death. Importantly, memantine is already used in the clinic to treat patients with Alzheimer’s disease, therefore tinkering with its dose to only target NMDA receptors in certain cellular locations may help with Huntington’s treatment.

Author contact:
Stuart Lipton (Burnham Institute for Medical Research, La Jolla, CA, USA)
Tel: +1 858 713 6261; E-mail:

[2] Geoscience: Elevating arsenic
DOI: 10.1038/ngeo685

Human-made ponds drive the arsenic contamination of groundwater in Bangladesh, according to a study published online this week in Nature Geoscience.

It is known that organic carbon triggers arsenic release from sediments into groundwater, but the source of this carbon has remained uncertain. Charles Harvey and colleagues modelled groundwater flow in a typical agricultural area in Bangladesh and found that human-made ponds are a key source of organic carbon. The scientists report that groundwater pumping for agriculture carries organic carbon underground, where it can trigger arsenic release.

To prevent this, they suggest that the development of artificial ponds above the wells that supply drinking water should be avoided.

Author contact:
Charles Harvey (Massachusetts Institute of Technology, Cambridge, MA, USA)
Tel: +1 617 258 0392; E-mail:

[3] Neuroscience: Understanding schizophrenia
DOI: 10.1038/nn.2447

Dysfunction of neurotransmitter signalling can cause pathological behaviour similar to that seen in schizophrenia, according to a paper published online in the journal Nature Neuroscience. This finding may prove important for developing future therapeutic targets for disorders associated with psychosis.

Kazu Nakazawa and colleagues created a line of mice that lacked a particular functional receptor for the neurotransmitter glutamate in the inhibitory neurons located in brain regions responsible for cognitive function, emotion and memory. These mice developed various psychotic symptoms including changes in spatial working memory and increased anxiety. However, when the authors engineered the mice so that the receptor dysfunction would not occur until after adolescence, the mice showed no psychosis-like symptoms, suggesting that dysfunction of glutamate signalling specifically during development was responsible for the irregular behaviour.

Although there is thought to be a genetic contribution to schizophrenia, this disorder has not been linked to specific mutations in glutamate receptorsThis mouse model aims to specifically test the 'glutamate' hypothesis in schizophrenia, which is based on evidence that various drugs of abuse that affect glutamate signalling also induce a variety of symptoms which are typically seen in schizophrenia, including social withdrawal and psychosis.

Regardless of whether these specific changes in glutamate transmission are found in human patients, this mouse model can be used to understand the changes that lead to psychotic behaviour.

Author contact:
Kazu Nakazawa (National Institute of Mental Health, Bethesda, MD, USA)
Tel: +1 301 451 3499; E-mail:

Nature: Opinion: Costing the Earth

The value of biodiversity must be accounted for, says Pavan Sukhdev, in a Nature Opinion article published online this week. Some estimate that half of the species alive today will be extinct by 2100, and poor people will be hardest hit by such losses, because their livelihoods often depend on nature’s ‘public goods’. Sukhdev argues that it is time for governments to invest to secure the flows of these commodities.

To stop people and business taking natural systems and processes for granted, governments must “encourage the participation of stakeholders as responsible stewards rather than short-term optimizers … by reforming the way property and access rights are assigned, and through better targeting of taxes and subsidies,” Sukhdev writes. The author is study leader of The Economics of Ecosystems and Biodiversity (TEEB) study which releases its TEEB for Policy Makers report (one of a series of TEEB reports being released over the next 12 months) on 13 November. “Good ideas for change are close at hand. We just have to lean forwards and pick them up” he concludes

Author contact:
Pavan Sukhdev (The Economics of Ecosystems and Biodiversity (TEEB) project, Bonn, Germany)
Please contact this author via the Communications office:
Georgina Langdale
Tel: +49 1707 617 138 E-mail:

[4] Geoscience: Nitrogen fix for early Earth
DOI: 10.1038/ngeo692

Higher levels of atmospheric nitrogen — almost double today’s levels — were the key to warming the early Earth, suggests a paper published online this week in Nature Geoscience. The paper could help shed light on why the Earth was not covered in glaciers 2.5 billion years ago even though the Sun was much weaker than it is today, a problem known as the “faint young Sun paradox.”

Colin Goldblatt, Tim Lenton, and colleagues used numerical modelling to show that, although atmospheric nitrogen itself is not a greenhouse gas, higher levels of atmospheric nitrogen gas would increase the potency of greenhouse gases such as carbon dioxide in the early atmosphere. A doubling of present-day atmospheric nitrogen levels would lead to a warming of 4.4 ºC.

The authors suggest that the excess nitrogen has since been removed from the atmosphere by biological activity and chemical reactions in the deep ocean, and that it is now stored in the Earth’s crust and mantle.

Author contact:
Colin Goldblatt (NASA Ames Research Center, Moffett Field, CA, USA)
Tel: +1 650 604 5514; Mobile: +1 650 814 4559; E-mail:

Tim Lenton (University of East Anglia, Norfolk, UK)
Tel: +44 1603 591414; E-mail:

[5] & [6] Genetics: Common genetic risk variants for Parkinson’s disease
DOI: 10.1038/ng.485
DOI: 10.1038/ng.487

Two independent studies report that common variants at five genes are risk factors for sporadic Parkinson’s disease. These studies, published online this week in Nature Genetics, are the largest genome-wide association studies to date for Parkinson’s disease and add to our understanding of the common genetic variants that increase risk of Parkinson’s in the general population.

Parkinson’s disease (PD) is a neurodegenerative disease that affects 1-2% of people above the age of 65 and is characterized by tremors, sluggish movement, muscle stiffness, and difficulty with balance. Although there are medical treatments available that may improve symptoms, there are no treatments that can slow down or halt the progression of PD.

Tatsushi Toda and colleagues analyzed 2000 Japanese patients and found strong associations with risk of PD to the genes PARK16, BST1, SNCA and LRRK2. In the second study, Andrew Singleton and colleagues analyzed the genomes of about 5000 patients of European ancestry and detected strong associations of PD risk to variants within the genes SNCA and MAPT. Both teams compared their data with each other and suggested that variants at PARK16, SNCA and LRRK2 confer a risk of PD in both the Japanese and European populations, while risk variants at BST1 and MAPT are population-specific.

Mutations in SNCA, LRRK2 and MAPT have previously been linked to rare, dominant forms of parkinsonism or dementia with parkinsonian features, indicating that the same genes involved in rare forms of parkinsonism also contribute to the complex genetic basis of typical PD.

Author contacts:
Tatsushi Toda (Kobe University, Japan) Author paper [5]
Tel: +81 78 382 6286; E-mail:

Andrew Singleton (National Institutes of Health, Bethesda, MD, USA) Author paper [6]
Tel: +1 301 451 6079; E-mail:

[7] Methods: Inducible microRNA sponges for intact organisms
DOI 10.1038/nmeth.1402

A method for the tissue-specific inhibition of microRNAs – which play a key role in regulating gene expression – is published online this week in Nature Methods. This method was used to investigate the formation of neuromuscular junctions in the fruit fly and could also be used to study microRNA function in other tissues.

MicroRNAs bind to a partially complementary target sequence of an RNA transcript and thereby either destine the RNA for degradation or prevent its translation into protein. The most effective way to study the role of microRNAs is to eliminate the gene that encodes them, but this is a time- and labor-intensive process.

A quicker alternative is to over-express their short target sequences, termed microRNA sponges, which will soak up the microRNA and move it away from its natural target. David Van Vactor and colleagues designed microRNA sponges in the fruit fly that are expressed at a precise time and in particular tissues of choice during a fly’s development to adulthood. The scientists show that their sponges copy the effect of removing the microRNA gene, and they demonstrate that a particular microRNA affects the formation of the neuromuscular junction through its activity in the muscle and not the neurons.

This precise dissection of microRNA-driven gene regulation should also shed light on microRNA function in organisms beyond the fly.

Author contact:
David Van Vactor (Harvard Medical School, Boston, MA, USA)
Tel: +1 617 432 2195; E-mail:

[8] And finally…Nature: Ouch, that hurts!
DOI: 10.1038/nature08505

Even the lightest touch to a recently broken limb can be intensely painful, and researchers have now identified a new class of nerve cells that may be responsible. The data, presented in this week’s Nature, suggest new approaches for pain management.

The sensory nerve cells relay information from the site of injury to the spinal cord, but researchers have now looked at a poorly understood subset that expresses a particular version of a protein required for the release of the chemical messenger glutamate. Robert Edwards and colleagues demonstrate that mice lacking the protein VGLUT3 are much less sensitive to intense mechanical pain and are no longer hypersensitive to light touch after injury.

Author contact:
Robert Edwards (University of California at San Francisco, CA, USA)
Tel: +1 415 502 5687; E-mail:

Items from other Nature journals to be published online at the same time and with the same embargo:

Nature (

[9] Controlling photonic structures using optical forces
DOI: 10.1038/nature08584


[10] Direct photosynthetic recycling of carbon dioxide to isobutyraldehyde
DOI: 10.1038/nbt.1586

[11] A recombinant polypeptide extends the in vivo half-life of peptides and proteins in a tunable manner
DOI: 10.1038/nbt.1588

[12] High-resolution analysis of DNA regulatory elements by synthetic saturation mutagenesis
DOI: 10.1038/nbt.1589


[13] AMPH-1/Amphiphysin/Bin1 functions with RME-1/Ehd1 in endocytic recycling
DOI: 10.1038/ncb1998

[14] Adaptive force transmission in amoeboid cell migration
DOI: 10.1038/ncb1992

[15] A ubiquitin-selective AAA-ATPase mediates transcriptional switching by remodelling a repressor–promoter DNA complex
DOI: 10.1038/ncb1997


[16] Dynamic hook-and-eye nanoparticle sponges
DOI: 10.1038/nchem.432

[17] Cooperative molecular dynamics in surface reactions
DOI: 10.1038/nchem.440


[18] Genome-wide association study of ulcerative colitis identifies three new susceptibility loci, including the HNF4A region
DOI: 10.1038/ng.483

[19] A genome-wide association study identifies three new susceptible loci for ulcerative colitis in the Japanese population
DOI: 10.1038/ng.482

[20] Common variants at five new loci associated with early-onset inflammatory bowel disease
DOI: 10.1038/ng.489


[21] Stronger winds over a large lake in response to weakening air-to-lake temperature gradient
DOI: 10.1038/ngeo693

[22] A seafloor microbial biome hosted within incipient ferromanganese crusts
DOI: 10.1038/ngeo696


[23] Recognition of RNA virus by RIG-I results in activation of CARD9 and inflammasome signaling for interleukin 1beta production
DOI: 10.1038/ni.1824


[24] Gel-expanded to gel-condensed transition in neurofilament networks revealed by direct force measurements
DOI: 10.1038/nmat2566

[25] Giant Zeeman splitting in nucleation-controlled doped CdSe:Mn2+ quantum nanoribbons
DOI: 10.1038/nmat2572

[26] Size and shape effects on the order–disorder phase transition in CoPt nanoparticles
DOI: 10.1038/nmat2574


[27] Modulating hedgehog signaling can attenuate the severity of osteoarthritis
DOI: 10.1038/nm.2055


[28] Cell stimulation with optically manipulated microsources
DOI: 10.1038/ nmeth.1400

[29] An auxin-based degron system for the rapid depletion of proteins in non-plant cells
DOI: 10.1038/ nmeth.1401


[30] Efficient narrow-band light emission from a single carbon nanotube p–n diode
DOI: 10.1038/nnano.2009.319

[31] In vivo magnetic enrichment and multiplex photoacoustic detection of circulating tumour cells
DOI: 10.1038/nnano.2009.333

[32] A tunable phonon–exciton Fano system in bilayer graphene
DOI: 10.1038/nnano.2009.334


[33] Glial precursors clear sensory neuron corpses during development via Jedi-1, an engulfment receptor
DOI: 10.1038/nn.2446

[34] Leucine-rich repeat transmembrane proteins instruct discrete dendrite targeting in an olfactory map
DOI: 10.1038/nn.2442

[35] Attention improves performance primarily by reducing interneuronal correlations
DOI: 10.1038/nn.2439

[36] Self-modulation of neocortical pyramidal neurons by endocannabinoids
DOI: 10.1038/nn.2430

[37] Thrombospondin 1 accelerates synaptogenesis in hippocampal neurons through neuroligin 1
DOI: 10.1038/nn.2459

Nature PHYSICS (

[38] Realization of a programmable two-qubit quantum processor
DOI: 10.1038/nphys1453

[39] Experimental probing of the interplay between ferromagnetism and localization in (Ga, Mn)As
DOI: 10.1038/nphys1455


[40] Physical determinants of strong voltage sensitivity of K+ channel block
DOI: 10.1038/nsmb.1717

[41] A stepwise 2′-hydroxyl activation mechanism for the bacterial transcription termination factor Rho helicase
DOI: 10.1038/nsmb.1711

[42] The chromosomal association of condensin II is regulated by a noncatalytic function of PP2A
DOI: 10.1038/nsmb.1708

[43] The chaperonin TRiC blocks a huntingtin sequence element that promotes the conformational switch to aggregation
DOI: 10.1038/nsmb.1700

[44] IDN1 and IDN2 are required for de novo DNA methylation in Arabidopsis thaliana
DOI: 10.1038/nsmb.1690

[45] An acetylated form of histone H2A.Z regulates chromosome architecture in Schizosaccharomyces pombe
DOI: 10.1038/nsmb.1688


***The following paper will be published electronically on Nature Neuroscience’s website on 10 November at 2000 London time / 1500 US Eastern time. The paper is under embargo until this time, though the rest of the above articles on this release remain under embargo until 15 November at 1800 London time / 1300 US Eastern time ***

[46] Dissociable cost and benefit encoding of future rewards by mesolimbic dopamine


The following list of places refers to the whereabouts of authors on the papers numbered in this release. 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.

Buenos Aires: 3

Brisbane: 18

Dhaka: 2

Toronto: 17, 20, 27, 45
Vancouver: 1

Hong Kong: 37
Lanzhou: 32
Shanghai: 32

Bordeaux: 36
Chatillon: 26
Marseille: 26
Montpellier: 41
Orleans: 41
Paris: 14, 26

Bonn: 6, 23
Kiel: 6
Lubeck: 6
Martinsried: 14
Munich: 23
Neuherberg: 6, 23
Stuttgart: 14
Tubingen: 6

Dublin: 18

Tel Aviv: 20

Rome: 20, 36
San Giovanni Rotondo: 20

Fukuoka: 19
Hiroshima: 5
Ibaraki: 42
Kobe: 5
Kodaira: 5
Mishima: 34
Okinawa: 42
Osaka: 23, 29
Sagamihara: 5
Saitama: 5, 23, 42
Sapporo: 19
Sendai: 5, 19, 39
Shizuoka: 29, 42
Suita: 5
Takamatsu: 5
Tokyo: 5, 19, 23, 26, 39, 42
Tsukuba: 5
Yokohama: 5, 19, 42
Yonago: 5

Amsterdam: 6

Warsaw: 39

Coimbra: 6

Moscow: 31
Saratov: 31

Daegu: 25
Pohang: 25
Seoul: 25

Burjassot: 33

Epalinges: 23

Bristol: 18
Cambridge: 18, 45
Cardiff: 18
Dundee: 18
Edinburgh: 18, 20, 45
Exeter: 18
Glasgow: 20
Leicester: 18
Liverpool: 17
London: 6, 18
Manchester: 18
Middleborough: 18
Newcastle: 18
Norwich: 4
Oxford: 18, 45
Sheffield: 18
Torbay: 18


Birmingham: 3, 20

Fayetteville: 31
Little Rock: 31

Berkeley: 26, 32
Davis: 10
La Jolla: 1, 22, 44
Los Angeles: 10, 20, 33, 44
Menlo Park: 22
Moffett Field: 4
Mountain View: 11
Parlier: 28
Pasadena: 34
San Francisco: 8, 20, 28, 33, 34, 43, 45
Santa Barbara: 24
Stanford: 34, 43

Boulder: 22, 38

New Haven: 28

District of Columbia
Washington: 6

Gainesville: 6
Jupiter: 6

Atlanta: 20, 31

Chicago: 20
Evanston: 16

Notre Dame: 25

Baltimore: 8, 43
Bethesda: 3
College Park: 3

Boston: 7, 20, 35
Cambridge: 2

Detroit: 3

Duluth: 21

St Louis: 6

Omaha: 13

New Jersey
Princeton: 13

New York
Ithaca: 9
Lake Placid: 45
New York: 12, 45
Stony Brook: 30
Yorktown Heights: 30

Cincinnati: 20

Beaverton: 22
Corvallis: 44

Hershey: 6
Philadelphia: 20, 40

Rhode Island
Providence: 15

Nashville: 33

Austin: 25
Houston: 20, 33

Salt Lake City: 20

Richland: 22
Seattle: 4, 12, 46

Madison: 21
Milwaukee: 20

Laramie: 8


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Tel: +44 20 7843 4658; E-mail:

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Nature Chemical Biology (Boston)
Andrea Garvey
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Nature Chemistry (London)
Stuart Cantrill
Tel: +44 20 7014 4018; E-mail:

Nature Genetics (New York)
Myles Axton
Tel: +1 212 726 9324; E-mail:

Nature Geoscience (London)
Heike Langenberg
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Nature Immunology (New York)
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Nature Materials (London)
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Nature Medicine (New York)
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Nature Methods (New York)
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