NATURE AND THE NATURE RESEARCH JOURNALS PRESS RELEASE
For papers that will be published online on 06 September 2009.
This press release is copyrighted to the Nature journals mentioned below.
This press release contains:
· Summaries of newsworthy papers:
Genetics: Three new targets in Alzheimer’s disease
Neuroscience: Channels for stroke treatment
Chemical Biology: Holding off HIV
Geoscience: Driving down ozone
Methods: Ten thousand embryos - and counting
Geoscience: Black burial
And finally... Genetics: Susceptibility to ALS
· 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 http://press.nature.com. Press contacts for the Nature journals are listed at the end of this release.
PICTURES: To obtain artwork from any of the journals, you must first obtain permission from the copyright holder (if named) or author of the research paper in question (if not).
NOTE: Once a paper is published, the digital object identifier (DOI) number can be used to retrieve the abstract and full text from the journal web site (abstracts are available to everyone, full text is available only to subscribers). To do this, add the DOI to the following URL: http://dx.doi.org/ (For example, http://dx.doi.org/10.1038/ng730). For more information about DOIs and Advance Online Publication, see http://www.nature.com/ng/aop/.
HYPE: We take great care not to hype the papers mentioned on our press releases, but are sometimes accused of doing so. If you ever consider that a story has been hyped, please do not hesitate to contact us at [email protected], citing the specific example.
PLEASE CITE THE SPECIFIC NATURE JOURNAL AND WEBSITE AS THE SOURCE OF THE FOLLOWING ITEMS. IF PUBLISHING ONLINE, PLEASE CARRY A HYPERLINK TO THE APPROPRIATE JOURNAL’S WEBSITE.
[1] & [2] Genetics: Three new targets in Alzheimer’s disease
DOI: 10.1038/ng.439
DOI: 10.1038/ng.440
Three new genetic associations to late onset Alzheimer’s disease are reported in two papers online this week in Nature Genetics. These are among the first robustly replicated genetic associations to the disease since the now well established association to APOE. Alzheimer’s disease (AD) is the most common form of dementia worldwide.
Philippe Amouyel, Julie Williams and their respective colleagues report two independent genome-wide association studies to late onset AD. In addition to replicating the well established genetic association to APOE, they report three new genetic loci associated with progression of the disease. Two of the newly associated genes - CLU (Clusterin) and CR1 - have been shown to play a role in clearance of the amyloid beta peptide, a major component of the plaques that form in the brain of patients with AD. Clusterin, a major brain apolipoprotein, has been shown to interact with amyloid beta proteins, and is found in amyloid plaques.
The genetic risk for AD has been estimated to account for as much as 80% of the overall risk of progression to AD. While the genetic association to APOE has been robustly established through numerous studies over the past decade, the current studies are amongst the first well powered genetic association studies that are able to identify and replicate additional common genetic variants associated with late onset AD.
Author contacts:
Philippe Amouyel (Institut Pasteur de Lille, France) Author paper [1]
Tel: +33 3 20 87 77 10; E-mail: [email protected]
Julie Williams (Cardiff University, UK) Author paper [2]
Tel: +44 29 20687067; E-mail: [email protected]
[3] Neuroscience: Channels for stroke treatment
DOI: 10.1038/nn.2395
Nerve cell death and memory deficits in a rat model of stroke can be prevented by the suppression of a certain ion channel, reports a study published online this week in Nature Neuroscience. This research has potential implications for treatment of stroke in humans.
About 17 million people die of stroke every year and it is a leading cause of disability. Brain ischemia, or lack of blood flow, in stroke leads to a host of devastating consequences, including neuronal death and loss of brain function, which ultimately lead to deficits in motor skills, speech, and memory.
Michael Tymianski and colleagues have devised a treatment to ameliorate these consequences in rats that underwent stroke-like brain ischemia. The researchers suppressed a specific type of channel, TRPM7, in the brains of rats, specifically in hippocampal neurons which are known to be crucial for memory. This suppression prevented the death of the brain cells and preserved their shape and function. Furthermore, in memory tests, these rats performed as well as non-ischemic rats. Rats that underwent the stroke-like brain ischemia, but did not have TRPM7 suppressed showed expected nerve cell death and deficits in memory.
Author contact:
Michael Tymianski (Toronto Western Hospital Research Institute, Toronto, Canada)
Tel: +1 416 603 5899; E-mail: [email protected]
[4] Chemical Biology: Holding off HIV
DOI: 10.1038/nchembio.207
Scientists have discovered a new strategy to inhibit HIV entry into host cells, as published online this week in Nature Chemical Biology.
HIV normally enters cells when gp120, a protein on the surface of HIV, binds to receptors on the host cell. In this process, gp120 first binds to one receptor - CD4 - which causes the structure of the protein to change so that it can bind to a second receptor, such as CCR5 or heparan sulfate.
Hugues Lortat-Jacob and colleagues have now made a molecule that contains a sequence of amino acids to mimic CD4 and a sequence of carbohydrates to mimic heparan sulfate to bind to both sites on gp120. This new strategy results in very effective inhibition of HIV infection in cellular assays, and so may have implications for further antiviral efforts.
Author contact:
Hugues Lortat-Jacob (CNRS, Grenoble, France)
Tel: +33 438 784 485; E-mail: [email protected]
[5] Geoscience: Driving down ozone
DOI: 10.1038/ngeo604
Twenty-first-century climate change will alter atmospheric circulation, increasing the flux of ozone from the upper to the lower atmosphere, and changing the amount of ultraviolet radiation reaching the Earth’s surface, according to a study published online in Nature Geoscience.
Michaela Hegglin and Theodore Shepherd used a computer model to examine the impact of climate change on circulation patterns of ozone in the upper atmosphere. They show that climate change will increase the transport of ozone from the upper to the lower atmosphere, and shift the distribution of ozone in the upper atmosphere. The latter change will result in a 20% increase in the amount of ultraviolet radiation reaching the southern high latitudes during spring and summer, and a 9% decrease in ultraviolet radiation reaching the northern high latitudes, by 2095.
In an accompanying News & Views, David Stevenson writes "climate change could have significant consequences for the distribution of ozone and Earth’s UV budget".
Author contacts:
Michaela Hegglin (University of Toronto, Canada)
Tel: +1 416 978 2661; E-mail: [email protected]
Theodore Shepherd (University of Toronto, Canada)
Tel: +1 416 978 2931; E-mail: [email protected]
David Stevenson (University of Edinburgh, UK) News & Views author
Tel: +44 131 650 6750; E-mail: [email protected]
[6] Methods: Ten thousand embryos - and counting
DOI 10.1038/nmeth.1370
A technique to collect large numbers of worm embryos, all precisely the same age, is reported online this week in Nature Methods. It will allow for detailed studies of early events during embryogenesis.
The worm Caenorhabditis elegans is a popular animal model for biologists, and many genes essential for the early events in embryo development have been identified. Yet, to date, it has not been possible to collect large numbers of embryos at the same developmental stage, a prerequisite to studying gene expression and protein interactions on a genome-wide scale. The current method of choice is collecting the embryos by hand, which is time consuming and does not yield adequate sample size for large-scale studies.
Nikolaus Rajewsky and colleagues improve the process using fluorescence-activated cell sorting (FACS). They create embryos that express a stage-specific protein fused to a fluorescent marker; when the embryo reaches the particular stage, it fluoresces. This is an ideal way to rapidly collect tens of thousands of embryos at the same stage.
Making use of this technique, the scientists carried out high-throughput sequencing to profile small RNA populations in embryos, and gained insight into how gene expression changes during the first cell cycles in a worm embryo.
Author contact:
Nikolaus Rajewsky (Max Delbruck Center for Molecular Medicine, Berlin, Germany)
Tel: +49 94 06 29 99; E-mail [email protected]
[7] Geoscience: Black burial
DOI: 10.1038/ngeo617
Charcoal in boreal forest soils in Scandinavia is easier to break down than previously thought, according to a study published online this week in Nature Geoscience. Forest fires convert a fraction of the burning vegetation into charred residues, which have been considered difficult to break down, and therefore a potential long-term carbon sink.
Mikael Ohlson and colleagues sampled hundreds of boreal forest soils in Norway and Sweden, and found that the charcoal content varies considerably between samples. Radiocarbon dating revealed that the charcoal has a median age of 652 years, which is younger than they expected, given that forest fires have been occurring in the region for the past 10,000 years.
Despite the relatively rapid turnover time, the researchers estimate that, if these results are applicable to other soils, the charcoal sink in boreal forest soils amounts to 1 peta gram of carbon, which is equivalent to 1% of the plant carbon stock in boreal forests.
Author contact:
Mikael Ohlson (Norwegian University of Life Sciences, Aas, Norway)
Tel: + 47 6496 5000; Email: [email protected]
[8] Genetics: Susceptibility to ALS
DOI: 10.1038/ng.442
Two new genetic associations to amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease, are reported in a study published online this week in Nature Genetics. The identified associations may suggest pathways involved in the characteristic neural degeneration.
ALS is a progressive neurodegenerative disorder characterized by loss of motor neurons in the spinal cord, brainstem and motor cortex of the brain, which leads to atrophy of the muscles and eventually paralysis.
Leonard van den Berg and colleagues report a large scale genome-wide association study to sporadic ALS, the most common form of the disease. In addition to replicating some of the previous genetic associations to this disorder, they identify two genetic regions newly associated with ALS. One of the candidate genes is UNC13A, encoding a presynaptic protein that is found within central and neuromuscular synapses. This protein regulates the release of neurotransmitters, which suggests a mechanism for its involvement in the characteristic motor neuron degeneration associated with the disease’s progression. The second genetic association occurs at a region previously implicated in individuals with a familial form of ALS and a specific type of dementia.
Author contact:
Leonard van den Berg (University Medical Center Utrecht, The Netherlands)
Tel: +31 88 7557978; E-mail: [email protected]
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Items from other Nature journals to be published online at the same time and with the same embargo:
Nature (http://www.nature.com/nature)
[9] Active turnover modulates mature microRNA activity in Caenorhabditis elegans
DOI: 10.1038/nature08349
[10] Bursts of retrotransposition reproduced in Arabidopsis
DOI: 10.1038/nature08351
[11] Selective epigenetic control of retrotransposition in Arabidopsis
DOI: 10.1038/nature08328
NATURE CELL BIOLOGY (http://www.nature.com/naturecellbiology)
[12] Oxidant-induced apoptosis is mediated by oxidation of the actin-regulatory protein cofilin
DOI: 10.1038/ncb1968
[13] NEK11 regulates CDC25A degradation and the IR-induced G2/M checkpoint
DOI: 10.1038/ncb1969
[14] Brassinosteroid signal transduction from cell-surface receptor kinases to nuclear transcription factors
DOI: 10.1038/ncb1970
[15] Ageing-related chromatin defects through loss of the NURD complex
DOI: 10.1038/ncb1971
NATURE CHEMICAL BIOLOGY (http://www.nature.com/nchembio)
[16] Genetic mapping of targets mediating differential chemical phenotypes in Plasmodium falciparum
DOI: 10.1038/nchembio.215
[17] Augmented photoswitching modulates immune signaling
DOI: 10.1038/nchembio.214
NATURE GENETICS (http://www.nature.com/naturegenetics)
[18] A multistage genome-wide association study detects a new risk locus near IRS1 for type 2 diabetes, insulin resistance and hyperinsulinemia
DOI: 10.1038/ng.443
NATURE IMMUNOLOGY (http://www.nature.com/natureimmunology)
[19] Peli1 facilitates TRIF-dependent Toll-like receptor signaling and proinflammatory cytokine production
DOI: 10.1038/ni.1777
[20] Ras orchestrates exit from the cell cycle and light-chain recombination during early B cell development
DOI: 10.1038/ni.1785
[21] Thymic self-reactivity selects natural interleukin 17-producing T cells that can regulate peripheral inflammation
DOI: 10.1038/ni.1783
NATURE MATERIALS (http://www.nature.com/naturematerials)
[22] One-dimensional imidazole aggregate in aluminium porous coordination polymers with high proton conductivity
DOI: 10.1038/nmat2526
[23] Nanoscale manipulation of the properties of solids at high pressure with relativistic heavy ions
DOI: 10.1038/nmat2528
[24] Spotted vesicles, striped micelles and Janus assemblies induced by ligand binding
DOI: 10.1038/nmat2512
[25] Self-assembly and transformation of hybrid nano-objects and nanostructures under equilibrium and non-equilibrium conditions
DOI: 10.1038/nmat2496
Nature MEDICINE (http://www.nature.com/naturemedicine)
[26] Integrin avb3-c-Src oncogenic unit promotes anchorage-independence and tumor progression
DOI: 10.1038/nm.2009
[27] Inhibition of calpain increases LIS1 and partially rescues in vivo phenotypes in a mouse model of lissencephaly
DOI: 10.1038/nm.2023
NATURE NANOTECHNOLOGY (http://www.nature.com/nnano)
[28] All-electric quantum point contact spin-polarizer
DOI: 10.1038/nnano.2009.240
[29] Thermochemical nanopatterning of organic semiconductors
DOI: 10.1038/nnano.2009.254
[30] Selective and sensitive detection of metal ions by plasmonic resonance energy transfer-based nanospectroscopy
DOI: 10.1038/nnano.2009.258
Nature NEUROSCIENCE (http://www.nature.com/natureneuroscience)
[31] Epac2 induces synapse remodeling and depression and its disease-associated forms alter spines
DOI: 10.1038/nn.2386
[32] The timing of external input controls the sign of plasticity at local synapses
DOI: 10.1038/nn.2388
[33] Approach sensitivity in the retina processed by a multifunctional neural circuit
DOI: 10.1038/nn.2389
[34] EFHC1 interacts with microtubules to regulate cell division and cortical development
DOI: 10.1038/nn.2390
[35] Neuron-glia communication via EphA4/ephrin-A3 modulates LTP through glial glutamate transport
DOI: 10.1038/nn.2394
[36] Hippocampal development and neural stem cell maintenance require Sox2-dependent regulation of Shh
DOI: 10.1038/nn.2397
Nature PHYSICS (http://www.nature.com/naturephysics)
[37] Arrested Kondo effect and hidden order in URu2Si2
DOI: 10.1038/nphys1392
[38] Assessment of carrier-multiplication efficiency in bulk PbSe and PbS
DOI: 10.1038/nphys1393
[39] Antiferromagnetic criticality at a heavy-fermion quantum phase transition
DOI: 10.1038/nphys1374
Nature STRUCTURAL & MOLECULAR BIOLOGY (http://www.nature.com/natstructmolbiol)
[40] Single-molecule imaging of DNA curtains reveals intrinsic energy landscapes for nucleosome deposition
DOI: 10.1038/nsmb.1655
[41] The histone variant macroH2A is an epigenetic regulator of key development genes
DOI: 10.1038/nsmb.1665
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GEOGRAPHICAL LISTING OF AUTHORS
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.
AUSTRALIA
Queensland: 1
BELGIUM
Antwerp: 1, 2
Leuven: 8
Liege: 32
BRAZIL
Porto Alegre: 12
CANADA:
Halifax: 32
London: 3
Montreal: 18
Toronto: 3, 5, 18
CHINA
Hebei: 14
DENMARK
Aarhus: 18
Copenhagen: 7, 13, 18, 41
Gentofte: 18
Glostrup: 18
FINLAND
Helsinki: 18
Kuopio: 1
Oulu: 18
FRANCE
Aubiere: 9, 10, 11
Bordeaux: 1
Corbeil-Essonnes: 18
Dijon: 1
Fontenay aux Roses: 4
Grenoble: 4
Lille: 1, 18, 38
Montpellier: 1
Orsay: 4, 18
Paris: 1, 4, 8, 18, 32
Poitiers: 18
Rouen: 1
Villejuif: 18
GERMANY
Berlin: 2, 6, 15
Bonn: 2, 8
Breisgau: 36
Darmstadt: 23
Duisburg: 2
Erlangen: 2
Essen: 2
Freiburg: 2
Halle: 17
Hamburg: 2, 35
Heidelberg: 15
Kiel: 8
Martinsried: 35
Munich: 2, 8, 35
Neuherberg: 2, 8
Tuebingen: 11, 32
Ulm: 8
GREECE
Thessaloniki: 2
IRELAND
Dublin: 2, 8
ISRAEL
Beer-Sheva: 38
Jerusalem: 8
ITALY
Bari: 1
Bologna: 1
Florence: 1
Milan: 1, 13
Milano: 36
Monza: 1
Pisa: 1, 29
Rome: 1, 6
Troina: 1
Verona: 8
JAPAN
Aichi: 27
Fukui: 27
Kanazawa: 22
Kyoto: 3, 22, 27
Osaka: 27
Saitama: 27
Shizuoka: 9
Tokyo: 27
KOREA
Seoul: 30
NETHERLANDS
Amsterdam: 8, 38
Maastricht: 15
Nijmegen: 8
Rotterdam: 8
Utrecht: 8
NORWAY
Aas: 7
Oslo: 7
POLAND
Krakow: 8
SPAIN
Barcelona: 41
Madrid: 1
Oviedo: 1
Santander: 1
Terrassa: 41
Victoria-Gasteiz: 1
SWEDEN
Malmo: 18
Umea: 8
Uppsala: 35
SWITZERLAND
Basel: 9, 32
Geneva: 9, 10, 11
UNITED KINGDOM
Bristol: 2, 25
Cadiff: 2
Cambridge: 2, 18
Grenoble: 39
Hinxton: 18
Lancaster: 29
London: 2, 8, 18, 29, 35
Nottingham: 2
Oxford: 2, 32
Salford: 2
Southampton: 2
Toulouse: 39
UNITED STATES OF AMERICA
Arkansas
Jefferson: 12
California
Berkeley: 30
La Jolla: 26, 35
Los Angeles: 8, 32
San Francisco: 14, 27
Stanford: 14
Connecticut
New Haven: 21
Storrs: 32
District of Columbia
Washington: 28
Florida
Jacksonville: 2, 3
Georgia
Atlanta: 8
Illinois
Chicago: 20, 31
Indiana
Indianapolis: 31
Maryland
Bethesda: 12, 15, 16
Frederick: 12
Massachusetts
Boston: 8
Charlestown: 8, 20
Worcester: 8
Michigan
Ann Arbor: 23
Minnesota
Rochester: 2
Missouri
St Louis: 2
New Jersey
Piscataway: 37
New York
New York: 6, 16, 40
Ohio
Athens: 28
Cincinnati: 28
Cleveland: 18
Pennsylvania
Philadelphia: 24
Texas
Houston: 19
PRESS CONTACTS
For media inquiries relating to embargo policy for all the Nature Research Journals:
Rachel Twinn (Nature London)
Tel: +44 20 7843 4658; E-mail: [email protected]
Neda Afsarmanesh (Nature New York)
Tel: +1 212 726 9231; E-mail: [email protected]
Ruth Francis (Head of Press, Nature, London)
Tel: +44 20 7843 4562; E-mail: [email protected]
For media inquiries relating to editorial content/policy for the Nature Research Journals, please contact the journals individually:
Nature Cell Biology (London)
Bernd Pulverer
Tel: +44 20 7843 4892; E-mail: [email protected]
Nature Chemical Biology (Boston)
Andrea Garvey
Tel: +1 617 475 9241, E-mail: [email protected]
Nature Genetics (New York)
Myles Axton
Tel: +1 212 726 9324; E-mail: [email protected]
Nature Geoscience (London)
Heike Langenberg
Tel: +44 20 7843 4042; E-mail: [email protected]
Nature Immunology (New York)
Laurie Dempsey
Tel: +1 212 726 9372; E-mail: [email protected]
Nature Materials (London)
Vincent Dusastre
Tel: +44 20 7843 4531; E-mail: [email protected]
Nature Medicine (New York)
Juan Carlos Lopez
Tel: +1 212 726 9325; E-mail: [email protected]
Nature Methods (New York)
Hugh Ash
Tel: +1 212 726 9627; E-mail: [email protected]
Nature Nanotechnology (London)
Peter Rodgers
Tel: +44 20 7014 4019; Email: [email protected]
Nature Neuroscience (New York)
Kalyani Narasimhan
Tel: +1 212 726 9319; E-mail: [email protected]
Nature Physics (London)
Alison Wright
Tel: +44 20 7843 4555; E-mail: [email protected]
Nature Structural & Molecular Biology (New York)
Michelle Montoya
Tel: +1 212 726 9326; E-mail: [email protected]
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