NATURE RESEARCH JOURNALS PRESS RELEASE
For papers that will be published online on 08 April 2007
This press release is copyrighted to the Nature journals mentioned below.
This press release contains:
· Summaries of newsworthy papers:
- Chemical control of neural stem cells – Nature Chemical Biology
- Amplification of oestrogen receptor gene in breast cancer – Nature Genetics
- Natural genetic variant influencing rice grain weight – Nature Genetics
- Stabilization contra retardation – Nature Neuroscience
- How one’s own DNA can cause autoimmunity – Nature Immunology
- Enrichment of metabolites with chemical probes – 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.
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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 CHEMICAL BIOLOGY ****************************
(http://www.nature.com/nchembio)
[1] Chemical control of neural stem cells
DOI: 10.1038/nchembio873
Chemicals that regulate neurotransmitter signalling in neurons can also prevent neural stem cell proliferation, according to a paper in the May issue of Nature Chemical Biology. Neural stem cells are a potentially important therapeutic target for neurological diseases and brain tumours. However, very little is known about the potential for using small molecules to regulate neural stem cell differentiation and proliferation.
Using cultures of neural precursor cells, Peter B. Dirks and colleagues screened a chemical library for inhibitors of neural precursor cell proliferation. Within the ‘hits’ were a number of small molecules that are known to influence neurotransmitter signalling in neurons. These unexpected results indicate that neurotransmitter signalling pathways may also function in neural stem cells and raises the possibility of using existing drugs that regulate neurotransmitter signalling in the treatment of brain tumours.
Author contact:
Peter B. Dirks (The Hospital for Sick Children and University of Toronto, Canada)
Tel: +1 416 813 6426; E-mail: [email protected]
Additional contact for comment on paper:
Mike Tyers, (Mount Sinai Hospital, Toronto, Canada)
Tel: +1 416 586 8371; E-mail: [email protected]
*****************************NATURE GENETICS **************************************
(http://www.nature.com/naturegenetics)
[2] Amplification of oestrogen receptor gene in breast cancer
DOI: 10.1038/ng2006
A fifth of breast tumours have extra copies of the gene encoding one form of the oestrogens receptor ESR1, suggests a study published online this week in Nature Genetics. A small-scale initial study shows that women treated with tamoxifen, which blocks the activity of the oestrogens receptor, survive longer if their tumour has this gene amplification.
Oestrogens receptor expression is one of the most important known factors in the development of breast cancer, and assessing its status is important for determining the use of anti-oestrogens receptor therapies like tamoxifen. Ronald Simon and colleagues examined more than 2,000 breast cancer samples for evidence of amplification of ESR1, and detected it in 20.6 % of the tumours. In a small follow-up study of 175 women with breast cancer who were being treated with tamoxifen, they found that women with the amplification survived longer than those who did not, even though the tumours in both groups of women expressed ESR1. The authors suggest that ESR1 amplification may identify a subgroup of breast cancers that would be particularly likely to respond to anti-oestrogens therapy.
Author contact:
Ronald Simon (University Medical Center Hamburg Eppendorf, Germany)
Tel: +49 42803 7214; E-mail: [email protected]
[3] Natural genetic variant influencing rice grain weight
DOI: 10.1038/ng2014
A study published in Nature Genetics this week identifies a gene that influences rice grain weight and yield. This is only the second such gene that has been found and functionally characterized, and is a step toward understanding and improving grain yield in crops.
Rice is a staple food, and the world’s most important cereal crop. Hong-Xuan Lin and colleagues examined two varieties of rice that exhibit significant differences in grain size, and mapped the gene responsible for this variation in size – GW2. The version of GW2 found in the large-grain variety of rice increased the width and weight of rice grains and increases grain yield per plant by nearly 20%, although the authors caution that its effect on grain yield needs to be further assessed in randomized blocks of plants in paddies.
Initial experiments also show that rice with the high-yield variant of GW2 has no reduction in cooking or eating quality, suggesting that it will be useful for high-yield crop breeding. GW2 encodes a protein that belongs to a family of enzymes that target other proteins for degradation, and the authors speculate that it could affect grain size by regulating the cell division cycle.
Author contact:
Hong-Xuan Lin (Shanghai Institute for Biological Sciences, China)
Tel: +86 21 5492 4129; E-mail: [email protected]
Other papers from Nature Genetics to be published online at the same time and with the same embargo:
[4] Comprehensive analysis of the gene encoding filaggrin uncovers prevalent and rare mutations in ichthyosis vulgaris and atopic eczema
DOI: 10.1038/ng2020
[5] Genetic reconstruction of a functional transcriptional regulatory network
DOI: 10.1038/ng2012
****************************NATURE NEUROSCIENCE ***********************************
(http://www.nature.com/natureneuroscience)
[6] Stabilization contra retardation
DOI: 10.1038/nn1893
A paper published online in Nature Neuroscience this week explores the mechanisms underlying fragile X syndrome – the most common inherited form of mental retardation. This disorder is caused by loss of a protein, dubbed FMRP, which interacts with messenger RNAs. (mRNAs are the templates that a cell ‘reads’ to correctly build specific proteins.) The details of how FMRP affects mRNAs and protein synthesis, and how subtle misregulation in absence of FMRP causes mental retardation, are still unclear.
Claudia Bagni and Kirsten S. Dickson and colleagues now report that FMRP stabilizes the mRNA that encodes the protein PSD-95. PSD-95 is crucial for the structure and function of neural synapses. In the brains of mice lacking FMRP, the authors found that the PSD-95 mRNA was rapidly degraded. The level of PSD-95 protein was reduced especially in the hippocampus, a structure crucial for learning, memory and certain kinds of reasoning.
This work suggests an important role for mRNA stabilization in the circuit wiring and communication of nerve cell networks. Though it is unlikely that all fragile X mental retardation symptoms can be explained by instability of PSD-95 mRNA, it may well represent an important part of the disease mechanism.
Author contacts:
Claudia Bagni (Universita di Roma, Italy)
Tel: +39 06 501 703 213; E-mail: [email protected]
Kirsten S. Dickson (University of Edinburgh, UK)
E-mail: [email protected]
Other papers from Nature Neuroscience to be published online at the same time and with the same embargo:
[7] Olfactory processing and behavior downstream from highly selective receptor neurons
DOI: 10.1038/nn1881
[8] Choice of cranial window type for in vivo imaging affects dendritic spine turnover in the cortex
DOI: 10.1038/nn1883
[9] CLOCK and NPAS2 have overlapping roles in the suprachiasmatic nuclei circadian clock
DOI: 10.1038/nn1884
************************NATURE IMMUNOLOGY ************************************
(http://www.nature.com/natureimmunology)
[10] How one’s own DNA can cause autoimmunity
DOI: 10.1038/ni1457
A study in the May issue of Nature Immunology may shed light on the cause of immune activation associated with systemic lupus erythematosus (SLE) – the second most common autoimmune disease in humans.
Found more often in women than in men, SLE is associated with the abnormal production of antibodies that ‘attack’ normal molecules in the body, including a person’s own DNA. As a result, debilitating inflammation, including skin rashes, hypertension, arthritis, and kidney and nervous system problems, ensues. Anthony Coyle and colleagues studied a protein called HMGB1 that normally binds to DNA in the cell nucleus. HMGB1 is also found in blood plasma, where it can bind to DNA released from dying cells. In many SLE patients, such DNA is also often the target of ‘abnormal’ lupus antibodies. As a result, antibody–HMGB1–DNA protein complexes form. The new study by Coyle and colleagues finds that antibody–HMGB1–DNA complexes in blood plasma from SLE patients can stimulate immune cells to produce potent inflammatory proteins associated with autoimmunity.
By demonstrating a role for HMGB1 in SLE inflammation, Coyle and colleagues provide unique insight into the pathogenesis associated with increasingly prevalent autoimmune diseases such as SLE. However, whether blocking the inflammatory function of HMGB1 will help SLE patients remains a question for future investigation.
Author contact:
Anthony Coyle (MedImmune Inc, Gaithersberg, MD, USA)
Tel: +1 301 398 4520; E-mail: [email protected]
Other papers from Nature Immunology to be published online at the same time and with the same embargo:
[11] Production of Ins(1,3,4,5)P4 mediated by the kinase Itpkb inhibits store-operated calcium channels and regulates B cell selection and activation
DOI: 10.1038/ni1458
*********************NATURE METHODS******************************************
(http://www.nature.com/nmeth)
[12] Enrichment of metabolites with chemical probes
DOI: 10.1038/nmeth1038
A general strategy for enriching various classes of metabolites directly from biological samples is described online in Nature Methods this week. The method allows researchers to profile small molecule metabolites that are difficult to detect with more conventional discovery-based methods.
The proteomics community has greatly benefited from chemical enrichment methods allowing the targeted isolation of proteins with similar functional or structural properties. The ‘metabolome,’ or entire spectrum of small molecules found in an organism, is even greater than the proteome in terms of numbers and chemical complexity. Benjamin Cravatt and colleagues reasoned that metabolomics researchers would therefore also benefit from targeted chemical enrichment strategies.
The authors synthesized chemical probes to target specific functional groups on small molecules. The probes were attached to a solid bead for easy isolation of the captured small molecules. The captured metabolites were then released from the probe and analyzed by liquid chromatography-mass spectrometry. They demonstrated that the method was able to isolate and profile low mass and polar small molecules, which are usually missed with conventional analysis without enrichment.
Author contact:
Benjamin Cravatt (The Scripps Research Institute, La Jolla, CA, USA)
Tel: +1 858 784 8633; E-mail: [email protected]
Other papers from Nature Methods to be published online at the same time and with the same embargo:
[13] Multiplexed analysis of glycan variation on native proteins captured by antibody microarrays
DOI: 10.1038/nmeth1035
[14] A genomic integration method to visualize localization of endogenous mRNAs in living yeast
DOI: 10.1038/nmeth1040
**************************************************************************
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)
[15] Efficient unidirectional nanoslit couplers for surface plasmons
DOI: 10.1038/nphys584
[16] Gigahertz quantized charge pumping
DOI: 10.1038/nphys582
[17] Spin–lattice instability to a fractional magnetization state in the spinel HgCr2O4
DOI: 10.1038/nphys586
NATURE MATERIALS (http://www.nature.com/naturematerials)
[18] Extrafluorescent electroluminescence in organic light-emitting devices
DOI: 10.1038/nmat1885
[19] Solution-phase deposition and nanopatterning of GeSbSe phase-change materials
DOI: 10.1038/nmat1887
[20] Giant sharp and persistent converse magnetoelectric effects in multiferroic epitaxial heterostructures
DOI: 10.1038/nmat1886
Nature MEDICINE (http://www.nature.com/naturemedicine)
[21] Cyclic AMP–regulated exocytosis of Escherichia coli from infected bladder epithelial cells
DOI: 10.1038/nm1572
[22] Sema3a establishes arrhythmia-free hearts via sympathetic innervation patterning
DOI: 10.1038/nm1570
[23] Reverse signaling through GITR ligand enables dexamethasone to activate IDO in allergy
DOI: 10.1038/nm1563
[24] Derivation of engraftable skeletal myoblasts from human embryonic stem cells
DOI: 10.1038/nm1533
[25] Noninvasive detection of macrophages using a nanoparticulate contrast agent for computed tomography
DOI: 10.1038/nm1571
NATURE CELL BIOLOGY (http://www.nature.com/naturecellbiology)
[26] p53 gain-of-function cancer mutants induce genetic instability by inactivating ATM
DOI: 10.1038/ncb1571
[27] A functional genomic screen identifies a role for TAO1 kinase in spindle-checkpoint signalling
DOI: 10.1038/ncb1569
[28] Priming, initiation and synchronization of the segmentation clock by deltaD and deltaC
DOI: 10.1038/ncb1578
[29] Flies without a spindle checkpoint
DOI: 10.1038/ncb1570
[30] Voltage-dependent anion channels are dispensable for mitochondrial-dependent cell death
DOI: 10.1038/ncb1575
[31] Cdk1 coordinates cell-surface growth with the cell cycle
DOI: 10.1038/ncb1568
Nature STRUCTURAL & MOLECULAR BIOLOGY (http://www.nature.com/natstructmolbiol)
[32] Iron-regulatory proteins limit hypoxia-inducible factor-2alpha expression in iron deficiency
DOI: 10.1038/nsmb1222
[33] Homology-driven chromatin remodeling by human RAD54
DOI: 10.1038/nsmb1223
[34] Bluetongue virus VP4 is an RNA-capping assembly line
DOI: 10.1038/nsmb1225
[35] Structure of the human GINS complex and its assembly and functional interface in replication initiation
DOI: 10.1038/nsmb1231
**************************************************************************
FOR IMMEDIATE RELEASE***
The following paper was published on Nature Neuroscience’s website on Thursday 29 March, so is not under embargo. It is included here to avoid multiple mailings.
[36] Conditional gene targeting reveals key roles for Raf kinase signaling in neuron differentiation and axon growth
DOI:10.1038/nn1898
The rest of this press release is under embargo as normal, until Sunday 08 April, 1800 London time (BST) / 1300 US Eastern time.
****************************************************************************
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.
AUSTRIA
Graz: 15
Vienna: 4, 36
CANADA:
Hamilton: 13
Toronto: 1
CHINA
Chengdu: 16
Shanghai: 3
DENMARK
Aalborg: 15
FRANCE
Dijon: 15
Gif-sur-Yvette: 29
Paris: 25
Strasbourg: 15
GERMANY
Braunschweig: 16
Hamburg: 2
Heidelberg: 10, 26, 32
Ulm: 20
IRELAND
Dublin: 4
ISRAEL
Rehovot: 14
ITALY
Perugia: 23
Rome: 6
JAPAN
Chiba: 17
Hyogo: 17
Ibaraki: 17
Osaka: 35
Nagoya: 22
Saitama: 35
Sapporo: 22
Tokyo: 22
NETHERLANDS
Maastricht: 4
Utrecht: 23
SAUDI ARABIA
Riyadh: 2
SPAIN
Barcelona: 15
Madrid: 15, 20
Zaragoza: 15
SWITZERLAND
Basel: 2
UNITED KINGDOM
Cambridge: 16, 20
Dundee: 4
Glasgow: 4
Hinxton: 6
Leeds: 26
London: 34
Oxford: 34
Teddington: 16
UNITED STATES OF AMERICA
California
Duarte: 24
La Jolla: 12, 26, 31
Los Angeles: 5, 36
San Diego: 11
San Francisco: 4
San Jose: 19
Santa Cruz: 31
Connecticut
New Haven: 28
Illinois
Glenview: 13
Maryland
Gaithersburg: 10
Massachusetts
Boston: 7, 10, 27, 31, 33
Cambridge: 18, 27
Lexington: 10
Worcester: 9, 10
Michigan
Ann Arbor: 13
Grand Rapids: 13
New York
Cold Spring Harbor: 27
New York: 8, 10, 24, 25
Yorktown Heights: 19
North Carolina
Chapel Hill: 36
Durham: 21
Ohio
Cincinnati: 30
Pennsylvania
Philadelphia: 33
Texas
Austin: 5
Houston: 30
Virginia
Charlottesville: 17
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 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)
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 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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