NATURE RESEARCH JOURNALS PRESS RELEASE
For papers that will be published online on 15 April 2007
This press release is copyrighted to the Nature journals mentioned below.
This press release contains:
· Summaries of newsworthy papers:
The smallest pipette – Nature Materials
Genetic susceptibility to Crohn disease – Nature Genetics
Mutation leads to male infertility – Nature Genetics
Astrocytes kill neurons in ALS – Nature Neuroscience
Increasing bad cholesterol levels – Nature Structural & Molecular Biology
· 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 MATERIALS ****************************** (http://www.nature.com/naturematerials)
[1] The smallest pipette
DOI: 10.1038/nmat1894
A pipette that dispenses zeptolitre droplets — a million-trillionth of a litre and containing between 10,000 and a million atoms — is described online this week in Nature Materials.
Eli and Peter Sutter made their pipettes from germanium nanowires with a reservoir of germanium–gold alloy at one end. Next they covered both the nanowire and reservoir in a few thin layers of carbon. The pipette was then heated and a hole punctured in the reservoir end of the carbon shell, through which the alloy escapes to form a droplet. The dispensed droplets are ideal for studying crystallization in this size regime, which is too large for easy computer simulation, but small enough to show different behaviour from the bulk alloy.
Author contact:
Eli Sutter (Brookhaven National Laboratory, Upton, NY, USA)
Tel: +1 631 344 7179 ; E-mail: [email protected]
Other papers from Nature Materials to be published online at the same time and with the same embargo:
[2] Multifunctional chondroitin sulphate for cartilage tissue–biomaterial integration
DOI: 10.1038/nmat1890
****************************NATURE GENETICS **************************************
(http://www.nature.com/naturegenetics)
[3] Genetic susceptibility to Crohn disease
DOI: 10.1038/ng2032
A genome-wide assessment of genetic variation in individuals with Crohn disease has identified seven genes or regions that are associated with elevated risk of the disease, according to a study to be published online this week in Nature Genetics. Three of the genes were previously known, but four are newly associated with the disease.
Crohn disease is one of the most common forms of inflammatory bowel disease, affecting 100–150 per 100,000 individuals of European ancestry. John Rioux and colleagues assessed more than 300,000 genetic variants in individuals with Crohn disease, as well as controls, and identified three previously reported risk factors (CARD15, IL23R, and ATG16L1), and four new ones (PHOX2B, NCF4, FAM92B, and a region on chromosome 10).
In combination with other studies, these ‘genome-wide association studies’ promise to flesh out the entire catalogue of genetic variants that predispose to Crohn disease, as well as provide new insight into the causes of the disease. In this case, the authors show that ATG16L1 might have a role in the degradation and processing of bacteria by the body’s inflammatory response—a process known as autophagy. This is consistent with other evidence that an inappropriate response to bacteria in the gut is important in the initiation of Crohn disease.
Author contact:
John Rioux (University of Montreal, Québec, Canada)
Tel: +1 514 376 3330; E-mail: [email protected]
[4] Mutation leads to male infertility
DOI: 10.1038/ng2027
A mutation in a gene called AURKC (Aurora Kinase C) has been identified in 14 infertile men of North African descent, reports a paper online this week in Nature Genetics. While deletions of some portion of the Y chromosome have been found in infertile men, this is a rare example in which a mutation in a single gene causes male infertility.
Estimates suggest that at least 80 million individuals worldwide are infertile. Pierre Ray and colleagues studied 14 men whose infertility seemed to have a similar origin. Their sperm were characterized by large heads, increased DNA content, and a variable number of flagella—the whip-like tails that propel the sperm. A genome-wide scan identified a mutation in AURKC that severely truncates the protein. AURKC encodes an enzyme that phosphorylates other proteins, and the authors show that the mutation abolishes this activity. An analysis of the genomic region around AURKC shows that these individuals have other markers in common, suggesting that this mutation appeared in a North African common ancestor approximately 1,500 years ago. The authors note that a larger study of the prevalence of this mutation in North Africans is now warranted.
Author contact:
Pierre Ray (University Hospital of Grenoble, France)
Tel: +33 476 76 55 73; E-mail: [email protected]
Other papers from Nature Genetics to be published online at the same time and with the same embargo:
[5] Duplication of the MYB oncogene in T cell acute lymphoblastic leukemia
DOI: 10.1038/ng2025
[6] Direct quantitative trait locus mapping of mammalian metabolic phenotypes in diabetic and normoglycemic rat models
DOI: 10.1038/ng2026
****************************NATURE NEUROSCIENCE ***********************************
(http://www.nature.com/natureneuroscience)
[7] & [8] Astrocytes kill neurons in ALS
DOI: 10.1038/nn1876
DOI: 10.1038/nn1885
Astrocytes carrying a mutated version of a protein that causes amyotrophic lateral sclerosis (ALS, also known as Lou Gehrig’s disease) are responsible for the death of motor neurons, report two papers in the May issue of Nature Neuroscience. These findings suggest that stem cell therapy focused on replacing damaged neurons may not be feasible in ALS, because diseased astrocytes would be expected to damage the replacement neurons.
Mutations in the gene for superoxide dismutase (SOD1) cause some cases of ALS, in which progressive degeneration of motor neurons leads to paralysis and eventually death. In both studies, the authors expressed this mutant protein in single cell types in culture. Motor neurons degenerated and died when cocultured with astrocytes expressing mutant SOD1, while mutant SOD1 in neurons, fibroblasts or microglia did not cause neuronal death.
Przedborski and colleagues additionally report that the astrocytes expressing mutant SOD1 killed only the neurons that degenerate in ALS, not other types of neurons, and that this was due to a soluble toxic factor released by the astrocytes. If this toxic factor can be identified in future studies, this finding may offer novel strategies for therapy.
Author contacts:
Serge Przedborski (Columbia University, New York, NY, USA) Paper [7]
Tel: +1 212 305 1540; E-mail: [email protected]
Kevin Eggan (Harvard University, Cambridge, MA, USA) Paper [8]
Tel: +1 617 496 5611; E-mail: [email protected]
Additional contact for comment on papers:
Jean-Pierre Julien (Laval University, Québec, Canada)
Tel: +1 418 654 2296; E-mail: [email protected]
Other papers from Nature Neuroscience to be published online at the same time and with the same embargo:
[9] Double dissociation between long-term depression and dendritic spine morphology in cerebellar Purkinje cells
DOI: 10.1038/nn1889
[10] Channelrhodopsin-2–assisted circuit mapping of long-range callosal projections
DOI: 10.1038/nn1891
**********************NATURE STRUCTURAL AND MOLECULAR BIOLOGY************************
(http://www.nature.com/natstructmolbiol)
[11] Increasing bad cholesterol levels
DOI: 10.1038/nsmb1235
A study in the May issue of Nature Structural & Molecular Biology suggests how the gene PCSK9 maintains cholesterol balance in the body.
Low-density lipoproteins (LDLs, also known as ‘bad cholesterol’) are removed from the bloodstream by binding to LDL receptors (LDLRs) present on the surface of cells. After binding, cells internalize both the receptor and cholesterol, the cholesterol is processed by the cell and LDLR is recycled back to the surface, where it can bind new cholesterol molecules. The amount of surface LDLR is decreased by the PCSK9 protein, resulting in high blood cholesterol, but how PCSK9 does this was not known.
Xiayang Qiu and colleagues have now found that PCSK9 binds very tightly to LDLR. This tight binding may lower LDLR levels on the cell surface by sequestering LDLRs inside cells, preventing their recycling back to the cell surface. A mutation in PCSK9 associated with high cholesterol shows even tighter binding to LDLR, supporting this model. These findings should improve our understanding of cholesterol regulation, and may help in the development of drugs to treat cardiovascular disease.
Author contact:
Xiayang Qiu (Pfizer, Groton, CT, USA)
Tel: +1 860 715 6718; E-mail: [email protected]
Other papers from Nature Structural and Molecular Biology to be published online at the same time and with the same embargo:
[12] Structure-based design of a pathway-specific nuclear import inhibitor
DOI: 10.1038/nsmb1229
[13] The uncoupled chloride conductance of a bacterial glutamate transporter homolog
DOI: 10.1038/nsmb1230
[14] H-NS cooperative binding to high-affinity sites in a regulatory element results in transcriptional silencing
DOI: 10.1038/nsmb1233
***************************************************************************************************************
Items from other Nature journals to be published online at the same time and with the same embargo:
NATURE CHEMICAL BIOLOGY (http://www.nature.com/nchembio)
[15] Zinc pyrithione-mediated activation of voltage-gated KCNQ potassium channels rescues epileptogenic mutants
DOI: 10.1038/nchembio874
[16] Engineering Escherichia coli for production of functionalized terpenoids using plant P450s
DOI: 10.1038/nchembio875
Nature PHYSICS (http://www.nature.com/naturephysics)
[17] Plasma mirrors for ultrahigh-intensity optics
DOI: 10.1038/nphys595
[18] Spin-valley phase diagram of the two-dimensional metal–insulator transition
DOI: 10.1038/nphys596
[19] Microscopic manifestation of the spin phase transition at filling factor 2/3
DOI: 10.1038/nphys588
Nature MEDICINE (http://www.nature.com/naturemedicine)
[20] MIF is a noncognate ligand of CXC chemokine receptors in inflammatory and atherogenic cell recruitment
DOI: 10.1038/nm1567
[21] Rhesus monkey TRIM5alpha restricts HIV-1 production through rapid degradation of viral Gag polyproteins
DOI: 10.1038/nm1562
[22] Osteopontin has a crucial role in allergic airway disease through regulation of dendritic cell subsets
DOI: 10.1038/nm1580
Nature BIOTECHNOLOGY (http://www.nature.com/naturebiotechnology)
[23] Isolation of engineered, full-length antibodies from libraries expressed in Escherichia coli
DOI: 10.1038/nbt1296
[24] Chloroplastic photorespiratory bypass increases photosynthesis and biomass production in Arabidopsis thaliana
DOI: 10.1038/nbt1299
Nature IMMUNOLOGY (http://www.nature.com/natureimmunology)
[25] A crucial function of SGT1 and HSP90 in inflammasome activity links mammalian and plant innate immune responses
DOI: 10.1038/ni1459
NATURE CELL BIOLOGY (http://www.nature.com/naturecellbiology)
[26] N-terminal alpha-methylation of RCC1 is necessary for stable chromatin association and normal mitosis
DOI: 10.1038/ncb1572
[27] DEAD-box RNA helicase subunits of the Drosha complex are required for processing of rRNA and a subset of microRNAs
DOI: 10.1038/ncb1577
[28] The neural progenitor-specifying activity of FoxG1 is antagonistically regulated by CKI and FGF
DOI: 10.1038/ncb1573
[29] The outer plate in vertebrate kinetochores is a flexible network with multiple microtubule interactions
DOI: 10.1038/ncb1576
NATURE METHODS (http://www.nature.com/nmeth)
[30] Multiplexed single-molecule assay for weak enzymatic activity on flow-stretched DNA
DOI: 10.1038/nmeth1037
[31] A model system for analyzing somatic mutations in Drosophila melanogaster
DOI: 10.1038/nmeth1027
***************************************************************************************************************
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
Adelaide: 20
Victoria: 20
BELGIUM
Ghent: 5
Leuven: 5
Liege: 5
Yvoir: 5
CANADA:
Montreal: 3
Toronto: 3, 17
FRANCE
Cachan: 14
Gif-sur-Yvette: 17
Grenoble: 4
Lyon: 4
La Tronche: 4
Palaiseau: 17
Paris: 14
GERMANY
Aachen: 20, 24
Cologne: 20
Garching: 19
Munich: 20
Stuttgart: 19
GREECE
Athens: 22
ISRAEL
Rehovot: 19
ITALY
Milan: 20
JAPAN
Ibaraki: 27
Saitama: 27
Tokyo: 27
MOROCCO
Rabat: 4
NETHERLANDS
Bilthoven: 31
Leiden: 20
Rotterdam: 5, 22
SINGAPORE
Singapore: 2
SOUTH AFRICA
Rondebosch: 28
SPAIN
Pamplona: 5
SWITZERLAND
Epalinges: 25
Lausanne: 25
UNITED KINGDOM
Cambridge: 28
Edinburgh: 28
Leicester: 28
London: 6, 22
Manchester: 28
Oxford: 6
UNITED STATES OF AMERICA
California
Berkeley: 16
Foster City: 2
Los Angeles: 3
Novato: 31
Connecticut
New Haven: 3, 20
Illinois
Chicago: 3
Maryland
Baltimore: 2, 3, 9, 15
Bethesda: 13
Massachusetts
Boston: 3, 25
Cambridge: 3, 7, 30
Michigan
Ann Arbor: 11
Minnesota
Rochester: 21
New Jersey
Princeton: 18
New York
Albany: 29
Cold Spring Harbor: 10
New York: 7
Upton: 1
Pennsylvania
Pittsburgh: 3
Texas
Austin: 23
Dallas: 12
Houston: 27
San Antonio: 31
Virginia
Ashburn: 10
Charlottesville: 26
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 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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