NATURE AND THE NATURE RESEARCH JOURNALS PRESS RELEASE
For papers that will be published online on 29 April 2007
This press release is copyrighted to the Nature journals mentioned below.
This press release contains:
• Summaries of newsworthy papers:
Mice and easy memory recovery – Nature
Life without Dad – Nature
New hypothesis for amyloid disease – Nature
Chromatin link to mental retardation? – Nature
Plastic power – Nature Materials
A gel to absorb solvent spills – Nature Materials
Recovering from amblyopia – Nature Neuroscience
The wisdom of youth – Nature Neuroscience
New player in inflammatory ‘shut down’ – Nature Immunology
Ancient diversity – Nature Immunology
Standards for the analysis of metagenomes – Nature Methods
• 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/.
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.
*****************************NATURE******************************
(http://www.nature.com/nature)
[1] Neuroscience: Mice and easy memory recovery
DOI: 10.1038/nature05772
Long-term memories lost after brain damage can be restored in mice, according to a paper published online this week in Nature. Li-Huei Tsai and colleagues report that environmental enrichment reinstated learning and long-term memories, as did compounds known as histone deacetylase (HDAC) inhibitors, which might represent a potential therapeutic approach to treating dementia.
It has previously been shown that environmental enrichment and HDAC inhibitors improve learning of new memories in mice. In the present study, the authors tested transgenic mice in which they were able to turn ‘on’ and ‘off’ a protein that induces neuronal damage, giving them control over when the mice were able to form memories relative to the time of neuronal damage. They report that environmental enrichment and HDAC inhibitors allowed the recovery of previously learned long-term memories, despite the severe brain damage suffered by the mice.
These findings support the notion that ‘memory loss’ in this context is more likely a reflection of inaccessible memories, and that, in mice, HDAC inhibitors allow access to these memories to be regained. Future work will aim to determine whether a similar approach is successful in human patients.
Author contact:
Li-Huei Tsai (MIT Brain and Cognitive Sciences, Cambridge, MA, USA)
Tel: +1 617 324 1660; E-mail: [email protected]
[2] Genetics: Life without Dad
DOI: 10.1038/nature05770
Genomic imprinting is not always essential for seed development, a study published online this week in Nature suggests. The finding may have implications for stem cell research.
Genomic imprinting is a form of gene regulation that starts early in life. It causes certain genes to be expressed from just the maternally inherited DNA, whilst others are expressed only from the paternal DNA. The phenomenon is well known in mammals, but it also occurs in flowering plants.
In a fertilized seed the endosperm provides nutrients to the developing embryo. Arp Schnittger and colleagues created a mutant plant in which the endosperm is derived solely from maternal DNA. They find that, in a certain mutant background that affects chromatin remodelling, the endosperm can develop normally without a paternal contribution, suggesting that genomic imprinting per se is not essential for seed development. Mammalian embryos lacking appropriate imprints die, but the uniparental endosperm seedlings in this study are viable albeit smaller than normal.
Imprinting is a hot topic in stem cell research, because researchers are trying to clone viable, healthy embryos from cells lacking imprints. So the study contributes useful information to this field and also says something about the evolution of endosperm.
Author contact:
Arp Schnittger (University of Cologne, Germany)
Tel: +49 221 506 2627; E-mail: [email protected]
[3] Neuroscience: New hypothesis for amyloid disease
DOI: 10.1038/nature05695
Degenerative diseases such as Alzheimer’s, Parkinson’s and type 2 diabetes may share common structural features at the molecular level, reports a paper published online by Nature. The findings suggest an atomic-level hypothesis for these conditions and may aid the design of future therapies.
It’s already known that amyloid diseases share certain similarities — in each disease a different protein folds abnormally, yielding clumps known as amyloid fibrils. But the fibril aggregates are always remarkably similar.
David Eisenberg and colleagues have now identified 30 short fibril-forming peptides taken from a large range of amyloid diseases and solved the atomic structure of 13 of them. They reveal one common feature: the ‘steric zipper’ that ‘glues’ together pairs of interwoven amino acids called beta-sheets.
The new finding may help to explain why amyloid fibrils from different diseases are so strong, despite the fact that they are formed from different proteins. It may also throw up new possible drug targets for these devastating illnesses.
Author contact:
David Eisenberg (University of California, Los Angeles, CA, USA)
Tel: +1 310 825 3754; E-mail: [email protected]
[4] Molecular biology: Chromatin link to mental retardation?
DOI: 10.1038/nature05823
A protein previously implicated in mental retardation has now been shown to influence gene expression by modifying histones. The finding, appearing in a paper published online by Nature, may shed light on a molecular mechanism behind neurological disorders.
Histones are the major proteins that package DNA into chromatin to form chromosomes. Enzymes can add or remove modifications such as methyl groups to these histones and in turn influence DNA-based events such as gene transcription. Yujiang Shi and colleagues have shown that a protein called SMCX (or JARID1C) acts as a demethylating enzyme. The molecule removes tri-methyl groups from histone H3 at lysine residue 4 and can repress transcription of certain neuronal genes.
The gene encoding SMCX is frequently mutated in X-linked mental retardation, in which defects in genes on the X chromosome are inherited. Mutations in SMCX might contribute to disease by impairing regulation of neuronal genes.
Author contact:
Yujiang Shi (Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA)
Tel: +1 617 525 8097; E-mail: [email protected]
Other papers from Nature to be published online at the same time and with the same embargo:
[5] Control of alternative RNA splicing and gene expression by eukaryotic riboswitches
DOI: 10.1038/nature05769
********************** NATURE MATERIALS ************************
(http://www.nature.com/naturematerials)
[6] Plastic power
DOI: 10.1038/nmat1903
A flexible plastic sheet that can wirelessly transmit power to electronic devices is described online this week in Nature Materials.
The increasing use of electronic devices, gadgets and sensors in our daily lives places a demand on flexible and convenient power-transmission systems. The wireless transmission system presented by Takao Someya and colleagues is made using printing techniques that are already in use for the large-scale manufacture of organic electronic circuits, and therefore can cover entire floors, walls or desks. The power-transmission sheets use small position-sensing coils that are able to detect similar coils attached to the targeted electronic device. Once a target device is brought near to the transmission sheet, the sheet senses the receiver coils and tiny switches activate the nearest sender coil to transmit a wireless power signal.
The overall efficiency of the transmission is an impressive 81%, and a transfer of up to 40 Watts was achieved. This efficiency as well as the cheap manufacturing process suggest the future common use of such sheets to power electronic devices in everyday environments.
Author contact:
Takao Someya (University of Tokyo, Japan)
Tel: +81 3 5841 6820; E-mail: [email protected]
[7] A gel to absorb solvent spills
DOI: 10.1038/nmat1904
A gel that swells up to 500 times its size in a range of solvents is reported by Kazuki Sada and colleagues online in Nature Materials this week. The gels should prove useful for absorbing industrial spills.
Polyelectrolyte gels are already known as super-absorbent polymers. Their ability to swell and absorb several hundred times their dry weight of water or other polar solvents means that they find many uses such as in nappies and for absorbing water spills. Until now, however, such gels haven’t been effective at absorbing less-polar organic solvents — such as dichloromethane and tetrahydrofuran, which are widely used in industry — because they collapse rather than swell. Sada and colleagues have simply added bulky side-groups that are more attractive to less-polar solvents onto the polyelectrolyte molecules. This enables the gels to swell rather than collapse.
Author contact:
Kazuki Sada (Kyushu University, Fukuoka, Japan)
Tel: +81 92 802 2821; E-mail: [email protected]
Other papers from Nature Materials to be published online at the same time and with the same embargo:
[8] Spin-torque oscillator using a perpendicular polarizer and a planar free layer
DOI:10.1038/nmat1905
***********************NATURE NEUROSCIENCE ********************
(http://www.nature.com/natureneuroscience)
[9] Recovering from amblyopia
DOI: 10.1038/nn1899
Environmental enrichment in adulthood promotes recovery from amblyopia, according to a study in the June issue of Nature Neuroscience. These results suggest that the loss of visual acuity caused by abnormal visual experience early in life may be treatable in adults.
Alessandro Sale and colleagues deprived rats of visual input in one eye during development, a manipulation known to cause permanent changes in visual acuity (amblyopia). Later, during adulthood, animals were deprived of input to the other eye, and placed in an enriched environment, which led to increased exploratory behaviour and sensory-motor stimulation. After two to three weeks in the new environment, the animals fully recovered from amblyopia, despite being well beyond the traditional critical period for neural plasticity.
Physiological recordings suggested that the change in environmental conditions re-activated neural plasticity that had ended before adulthood. Pharmacological experiments indicated that the crucial factor in increasing this plasticity was a decrease in inhibition within the visual cortex. These findings raise the possibility that environmental enrichment may have therapeutic potential to promote recovery of normal visual functions in adults with amblyopia caused by childhood conditions such as strabismus – in which the eyes do not align properly with each other.
Author contact:
Alessandro Sale (Scuola Normale Superiore, Pisa, Italy)
Tel: +39 050 315 3205; E-mail: [email protected]
[10] The wisdom of youth
DOI: 10.1038/nn1894
Older adults have an asymmetric neural response to monetary gains and losses, finds a new study in the June issue of Nature Neuroscience. Compared to a younger group, older adults have a lower response to losses but not gains.
Gregory Larkin and colleagues compared adults aged 19-27 years with another group who were over 65 years old. While being scanned by functional magnetic resonance imaging (fMRI), both groups completed a task in which they had to respond to a cue either to get a monetary reward or to avoid a loss. On each trial, both groups also rated their positive or negative arousal at the prospect of the potential gain or loss.
The authors found that while both the young and older adults had similar positive arousal at the prospect of an impending gain, the older group had less negative arousal to anticipated losses. The neural response mirrored this behaviour – activity in a part of brain called the striatum was similarly changed by the amount of gain in both the young and old adults, but only the young adults showed a change in activity paralleling the amount of anticipated loss. Previous work has identified the striatum in reward processing, and this study shows that the functioning of this area depends on age as well. These findings suggest that older and younger adults could weigh gains and losses differently when making decisions.
Author contact:
Gregory Larkin (Stanford University, CA, USA)
Tel: +1 650 799 5715; E-mail: [email protected]
Other papers from Nature Neuroscience to be published online at the same time and with the same embargo:
[11] Contribution of olfactory neural stem cells to tissue maintenance and regeneration
DOI: 10.1038/nn1882
[12] Differential neural coding of acoustic flutter within primate auditory cortex
DOI: 10.1038/nn1888
[13] Rapid learning in cortical coding of visual scenes
DOI: 10.1038/nn1895
[14] Cortical spreading depression causes and coincides with tissue hypoxia
DOI: 10.1038/nn1902
************************NATURE IMMUNOLOGY ******************
(http://www.nature.com/natureimmunology)
[15] New player in inflammatory ‘shutdown’
DOI: 10.1038/ni1464
Scientists show that a protein within immune cells stands poised to dampen inflammation, according to an article published this week online in Nature Immunology.
Inflammatory proteins are produced by immune cells following microbial infection. After clearance of the invading pathogen the inflammatory response must be switched off to avoid excessive damage to host tissues.
Tsuneyaso Kaisho and colleagues now demonstrate that a protein called PDLIM2 continuously targets the p65 subunit of the proinflammatory transcription factor NF-kappaB for destruction. PDLIM2 marks p65 for degradation and routes p65 into cellular compartments containing demolition machinery.
Consequently, mice lacking PDLIM2 suffer from lethal uncontrolled inflammation. These findings pinpoint another potential target for therapeutic efforts to suppress excessive inflammatory responses.
Author contact:
Tsuneyasho Kaisho (RIKEN Research Center for Allergy and Immunology, Kanagawa, Japan)
Tel: +81 45 503 7065; E-mail: [email protected]
[16] Ancient diversity
DOI: 10.1038/ni1463
An ancient enzyme drives diversification of immune receptors in lampreys, and resembles an enzyme with a similar function in mammals, according to a report published online this week in Nature Immunology.
Zeev Pancer and colleagues used computational analyses – ‘genomic mining’ – to look for molecular signatures in the lamprey genome. Clues to how lampreys diversify their antigen receptors, allowing them to combat any array of potential microbial threats, came from their identification of hundreds of short gene segments that encode bits of the antigen receptors. The authors also discovered evidence that these pieces can combine in almost an infinite array, thereby explaining how a diverse repertoire of receptors can be made.
The surprise the authors found in the lamprey genomic sequence was that these fish encode two enzymes similar to an enzyme called AID, which is essential for the production of different types of antibodies in mammals. In fact, further experiments performed in test tubes showed the lamprey enzymes can mutate target genes much like the mammalian AID enzyme. The new work suggests the ability to diversify antigen receptors occurred much earlier in evolution then previously thought and hence is an ‘ancient adaptation’.
Author contact:
Zeev Pancer (University of Maryland Biotechnology Institute, Baltimore, MD, USA)
Tel: +1 410 234 8834; E-mail: [email protected]
Additional contact for comment on paper:
David Schatz (Yale University School of Medicine, New Haven, CT, USA)
Tel: +1 203 737 4403; E-mail: [email protected]
Other papers from Nature Immunology to be published online at the same time and with the same embargo:
[17] The NEMO adaptor bridges the nuclear factor-kappa B and interferon regulatory factor signaling pathways
DOI:10.1038/ni1465
*************************NATURE METHODS*******************
(http://www.nature.com/nmeth)
[18] Standards for the analysis of metagenomes
DOI: 10.1038/nmeth1043
Simulated datasets for the evaluation of metagenomic analysis programs are presented online in Nature Methods this week.
Metagenomics is the study of microbial organisms in a common habitat with genomic techniques such as sequencing. Rather than isolating and cultivating individual strains, scientists work with material obtained from the natural environment representing a complex mix of different microbes. To assemble the data and identify individual species and their genes, researchers use programs developed for the analysis of individual genomes. The main problem with this approach is that the error rate cannot be determined, since the correct answer to which and how many microbes exist in a given sample is not known. Therefore it is currently not possible to compare the efficiency of different programs.
To address this problem, Konstantinos Mavromatis and colleagues created three complex datasets. They ran them on three commonly used programs and discuss the strength and limitations of each. These datasets are publicly available so that the scientific community can use them as standards to test and improve metagenomic analysis programs.
Author contact:
Konstantinos Mavromatis (Joint Genome Institute Genome Biology, Walnut Creek, CA, USA)
Tel: +1 925 296 5815; E-mail: [email protected]
Other papers from Nature Methods to be published online at the same time and with the same embargo:
[19] Quantifying force-dependent and zero-force DNA intercalation by single-molecule stretching
DOI: 10.1038/nmeth1044
*******************************************************************
Items from other Nature journals to be published online at the same time and with the same embargo:
Nature PHYSICS (http://www.nature.com/naturephysics)
[20] Achievement of robust high-efficiency 1MW oscillation in the hard-self-excitation region by a 170GHz continuous-wave gyrotron
DOI: 10.1038/nphys599
NATURE NANOTECHNOLOGY (http://www.nature.com/nnano)
[21] In situ nucleation of carbon nanotubes by the injection of carbon atoms into metal particles
DOI: 10.1038/nnano.2007.107
[22] Mesoporous silica nanoparticles deliver DNA and chemicals into plants
DOI: 10.1038/nnano.2007.108
[23] Creation of multiple nanodots by single ions
DOI: 10.1038/nnano.2007.109
Nature MEDICINE (http://www.nature.com/naturemedicine)
[24] MicroRNA-133 controls cardiac hypertrophy
DOI: 10.1038/nm1582
[25] SIK1 is a class II HDAC kinase that promotes survival of skeletal myocytes
DOI: 10.1038/nm1573
Nature BIOTECHNOLOGY (http://www.nature.com/naturebiotechnology)
[26] Genome sequence of the animal pathogen Dichelobacter nodosus
DOI: 10.1038/nbt1302
NATURE GENETICS (http://www.nature.com/naturegenetics)
[27] p38alpha suppresses normal and cancer cell proliferation by antagonizing the JNK–c-Jun pathway
DOI: 10.1038/ng2033
[28] p38alpha MAP kinase is essential in lung stem and progenitor cell proliferation and differentiation
DOI: 10.1038/ng2037
[29] MMTV insertional mutagenesis identifies genes, gene families and pathways involved in mammary cancer
DOI: 10.1038/ng2034
[30] IFT80, which encodes a conserved intraflagellar transport protein, is mutated in Jeune asphyxiating thoracic dystrophy
DOI: 10.1038/ng2038
Nature STRUCTURAL & MOLECULAR BIOLOGY (http://www.nature.com/natstructmolbiol)
[31] Essential function of the built-in lid in the allosteric regulation of eukaryotic and archaeal chaperonins
DOI: 10.1038/nsmb1236
[32] Structural basis of Na+/K+-ATPase adaptation to marine environments
DOI: 10.1038/nsmb1237
*****************************************************************
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
Melbourne: 26
Sydney: 26
AUSTRIA
Vienna: 27
CANADA:
Montreal: 17
DENMARK
Copenhagen: 3
Maaloev: 14
FRANCE
Caen: 23
Grenoble: 3, 8
Toulouse: 8
GERMANY
Bonn: 2
Cologne: 2, 28
Duisburg: 23
Goettingen: 1
Mainz: 21
Marburg: 31
ITALY
Milan: 24
Monterotondo: 28
Pisa: 9
Rome: 24
JAPAN
Fukuoka: 7
Ibaraki: 20
Kanagawa: 15
Osaka: 25
Tokyo: 6
MEXICO
San Luis Potosi: 21
NETHERLANDS
Amsterdam: 29
NORWAY
Oslo: 2
Tronndheim: 24
PUERTO RICO
San Juan: 32
ROMANIA
Brasov: 8
RUSSIA
Novosibirsk: 16
SPAIN
Barcelona: 28
Madrid: 28
TURKEY
Istanbul: 30
UNITED KINGDOM
Birmingham: 30
Leeds: 30
London: 30
UNITED STATES OF AMERICA
Arizona
Tucson: 26
California
Berkeley: 10, 13
La Jolla: 24, 25
Los Angeles: 3
Palo Alto: 25
Pleasanton: 31
Stanford: 10, 31
Walnut Creek: 18
Colorado
Boulder: 30
Connecticut
New Haven: 5
Florida
Gainesville: 4
Tallahassee: 21
Iowa
Ames: 22
Maryland
Baltimore: 11, 12, 16
Bethesda: 10, 16, 32
Rockville: 26
Massachusetts
Boston: 4, 15, 19
Cambridge: 1
South Hadley: 19
Minnesota
Minneapolis: 19
Nebraska
Omaha: 16
New York
Rochester: 14, 16
Yorktown Heights: 18
Ohio
Cincinnati: 24
Columbus: 24
Tennessee
Nashville:17
Texas
Houston: 31
PRESS CONTACTS…
For media inquiries relating to embargo policy for all the Nature Research Journals:
Katherine Anderson (Nature London)
Tel: +44 20 7843 4502; E-mail: [email protected]
Ruth Francis (Senior Press Officer, 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 Biotechnology (New York)
Peter Hare
Tel: +1 212 726 9284; E-mail: [email protected]
Nature Genetics (New York)
Orli Bahcall
Tel: +1 212 726 9311; E-mail: [email protected]
Nature Immunology (New York)
Laurie Dempsey
Tel: +1 212 726 9372; E-mail: [email protected]
Nature Materials (London)
Maria Bellantone
Tel: +44 20 7843 4556; E-mail: [email protected]
Nature Medicine (New York)
Juan Carlos Lopez
Tel: +1 212 726 9325; E-mail: [email protected]
Nature Methods (New York)
Allison Doerr
Tel: +1 212 726 9393; E-mail: [email protected]
Nature Nanotechnology (London)
Peter Rodgers
Tel: +44 20 7014 4019; Email: [email protected]
Nature Neuroscience (New York)
Sandra Aamodt (based in California)
Tel: +1 530 795 3256; 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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Nature Publishing Group (NPG) is a division of Macmillan Publishers Ltd, dedicated to serving the academic, professional scientific and medical communities. NPG's flagship title, Nature, was first published in 1869. Other publications include Nature research journals, Nature Reviews, Nature Clinical Practice and a range of prestigious academic journals including society-owned publications. NPG also provides news content through [email protected] and scientific career information through Naturejobs.
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