NATURE AND THE NATURE RESEARCH JOURNALS PRESS RELEASE
For papers that will be published online on 08 November 2009
This press release is copyrighted to the Nature journals mentioned below.
This press release contains:
· Summaries of newsworthy papers:
Nature: Speeding up ‘ethical stem-cell’ production
Genetics: Variants associated with hearing loss in children receiving chemotherapy medication
Neuroscience: The long shadows of adversity
Geoscience: Low-level seismicity in Southern California
Genetics: Smoking and autoimmunity affect rheumatoid arthritis susceptibility
Medicine: Arthritis is spreading
Genetics: A deletion is associated with neurodevelopmental problems
Immunology: Disrupting lasting memory
Chemical Biology: When chemicals attack
· 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.
[1] Nature: Speeding up ‘ethical stem-cell’ production
DOI: 10.1038/nature08592
The process of reprogramming mature cells into a stem-cell-like state can be accelerated, a Nature paper reveals. The results shed light on the processes underlying the production of induced pluripotent stem (iPS) cells — the ethical ‘embryo-free’ alternative to stem cells touted to hold great promise for regenerative medicine.
Rudolf Jaenisch and colleagues studied the ability of mature immune cells to generate iPS cells upon continued exposure to four previously defined reprogramming factors. Nearly all of the donor cells were able to form iPS cells, although they took different lengths of time to do so. The results indicate that reprogramming is not the sole preserve of an elite subset of cells, but a continuous, essentially random process that almost any cell can undergo given the right conditions.
Critically, the process can be accelerated, and the team identify two methods that do just that. One method depends on the rate at which the donor cells divide; the other method does not. So the results also establish a new model in which cell division number, rather than the absolute time of reprogramming factor expression, drives the kinetics of iPS cell production.
Author contact:
Rudolf Jaenisch (Whitehead Institute for Biomedical Research, Massachusetts Institute of Technology, Cambridge, MA, USA)
Tel: +1 617 258 5186; E-mail: [email protected]
[2] Genetics: Variants associated with hearing loss in children receiving chemotherapy medication
DOI: 10.1038/ng.478
An association between a chemotherapy-induced hearing loss and specific genetic variants has been identified, according to a new study published online in this week’s Nature Genetics. The study suggests that these genetic variants may be useful to identify individuals with increased risk of chemotherapy-induced hearing loss, which could help to manage treatment.
Cisplatin is a commonly used chemotherapy drug, although its side-effects include serious hearing loss in 10-25% of adults and 41-61% of children. In order to identify genetic variants that may be associated with increased risk of cisplatin-induced hearing loss, Colin Ross and colleagues analyzed 220 drug-metabolism genes from over 150 children receiving cisplatin chemotherapy. The scientists found that in these children, variants in the genes TPMT and COMT are significantly associated with cisplatin-induced hearing loss.
Further research is needed to determine whether these findings will be useful in guiding treatment options in a clinical setting.
Author contact:
Colin Ross (University of British Columbia, Vancouver, Canada)
Tel: +1 604 875 2000, x5238; E-mail: [email protected]
[3] Neuroscience: The long shadows of adversity
DOI: 10.1038/nn.2436
Severe stress suffered at an early age can cause long-lasting changes to gene expression patterns in the mouse brain, reports a study published online in this week’s Nature Neuroscience.
Previous studies have shown that children growing up under stressful or traumatic circumstances carry an elevated risk of developing depression later in life. To elucidate the underlying neurobiological causes, Dietmar Spengler and colleagues studied mouse pups that were repeatedly separated from their mothers during the first ten days of life. This stressful separation caused a specific loss of suppression mechanisms at the gene encoding the stress-related hormone AVP, which in turn led to elevated levels of this hormone.
One year after the stressful phase in the pups’ lives, Spengler and colleagues still found the aberrant gene modification, AVP elevation, and ensuing physiological over-reaction towards other stressful situations. The researchers conclude that the long-lasting behavioral, and sometimes psychiatric, consequences of early-life stress may be due in part to persistent changes of gene regulation in the brain.
Author contact:
Dietmar Spengler (Max Planck Institute of Psychiatry, Munich, Germany)
Tel: +49 89 30622 559 or +49 89 30622 221; E-mail: [email protected]
[4] Geoscience: Low-level seismicity in Southern California
DOI: 10.1038/ngeo684
The San Jacinto fault in Southern California is the site of frequent moderate earthquakes because it can adjust to applied stresses slowly and continuously at relatively shallow depths, suggests a paper published online this week in Nature Geoscience. This behaviour is in contrast to the nearby, and more quiescent, Southern San Andreas fault, in which the two sides of the fault stick together to a greater depth, and thus accumulates strain over longer periods.
Shimon Wdowinski compared seismic activity in the San Jacinto and Southern San Andreas fault systems. He found that only the top 10 km of crust at the San Jacinto fault accumulates strain, whereas the section deeper down in the crust adjusts through frequent small earthquakes and through continuous creep. Because of the limited amount of strain accumulation, the San Jacinto fault is unlikely to produce large earthquakes, instead experiencing frequent small or moderate events. In contrast, the neighbouring Southern San Andreas fault system accumulates strain throughout the entire 17 km of brittle crust, and releases its strain in larger seismic events.
Author contact:
Shimon Wdowinski (University of Miami, FL, USA)
Tel: +1 305 421 4730; E-mail: [email protected]
[5] & [6] Genetics: Smoking and autoimmunity affect rheumatoid arthritis susceptibility
DOI: 10.1038/ng.480
DOI: 10.1038/ng.479
New insights into the genetic basis of rheumatoid arthritis are reported in two papers published online this week in Nature Genetics.
Rheumatoid arthritis (RA) is an acquired, chronic autoimmune disease, characterized by inflammation of the lining of multiple joints. RA is the most common inflammatory form of arthritis and is influenced by both genetic and environmental factors.
Karin Lundberg and colleagues explore the susceptibility to RA and the interaction of established genetic, environmental and autoimmune factors. These factors include several previously studied genes, environmental factors such as smoking, and a particular immune system antibody. The scientists find that the interaction between the different factors depends on a specific protein, which may mediate the autoimmune response underlying this gene-environment interaction.
In a second paper, Soumya Raychaudhuri and colleagues report three genetic variants found to be associated with RA. They began with a unique approach of analyzing genome-wide association study datasets, using a computational method called GRAIL that predicts functional relationships between genes, and then replicated their findings in an independent set of nearly 8000 RA cases.
Author contacts:
Karin Lundberg (Imperial College, London, UK) Author paper [5]
Tel: +44 208 383 4768; E-mail: [email protected]
Soumya Raychaudhuri (Brigham and Women’s Hospital, Boston, MA, USA and Broad Institute, Cambridge, MA, USA) Author paper [6]
Tel: +1 617 324 4948; E-mail: [email protected]
[7] Medicine: Arthritis is spreading
DOI: 10.1038/nm.2050
A mechanism that accounts for the spreading of arthritis between joints is presented in a study published online in this week’s Nature Medicine.
Rheumatoid arthritis starts in a few joints but subsequently spreads to affect most joints, though the pathways that account for this progression were previously unknown. Elena Neumann and her colleagues tested whether synovial fibroblasts – cells present in the fluid that bathes the joints and also implicated in cartilage destruction in arthritis patients – could spread the disease.
Using mice, the scientists implanted healthy human cartilage plus synovial fibroblasts from arthritis patients into one side of their bodies, and healthy cartilage without the fibroblasts into the opposite side. Synovial fibroblasts actively moved from one side to the other via blood vessels, leading to marked cartilage destruction.
Author contact:
Elena Neumann (Justus-Liebig-University Giessen, Bad Nauheim, Germany)
Tel: +49 6032 996 2801; E-mail: [email protected]
[8] Genetics: A deletion is associated with neurodevelopmental problems
DOI: 10.1038/ng.481
A small deletion at a specific region on chromosome 15 is associated with a range of neurodevelopmental problems, including developmental delays and seizures, according to a new study published online in this week’s Nature Genetics.
Previously, larger deletions that remove 1.5 million base pairs on chromosome 15 were reported in individuals with mental retardation, seizures and schizophrenia. Now, Arthur Beaudet and colleagues report that smaller deletions of about 680,000 base pairs at this region of chromosome 15 were found in ten individuals from four unrelated families that presented with similar neurodevelopmental problems. These smaller deletions remove the entire CHRNA7 gene and part of the OTUD7A gene.
Both OTUD7A and CHRNA7 are genes that are expressed in the brain. CHRNA7 encodes a protein that regulates the flow of ions in neurons; defects in this class of protein have frequently been associated with epilepsy.
Author contact:
Arthur Beaudet (Baylor College of Medicine, Houston, TX, USA)
Tel: +1 713 798 4795; E-mail: [email protected]
[9] Immunology: Disrupting lasting memory
DOI: 10.1038/ni.1820
A new protein holds the key to making long-lasting antibody responses in the body, according to a report published online this week in Nature Immunology.
The immune system utilizes different types of immune cells – such as T cells and B cells – to ward off attacks from foreign agents. B cells make antibodies against microbes; after an infection, B cells remember or gain long-lasting 'memory' against future attacks by that particular microbe so the body can rapidly respond and clear infection.
Chris Goodnow, Richard Cornall, and their colleagues generated a battery of mutant mice, and then screened the mice for various aberrant immune responses. Two independent types of mutant mouse groups were found that could make early antibody responses towards microbes but failed to generate longer lasting and more specialized antibody responses. The scientists were able to identify a single gene that is responsible for this immune defect seen in both strains of mice.
The gene, Dock8, encodes a protein that helps the antibody-producing B cells form stable complexes with other immune cells. These immune complexes allow information to pass between the interacting cells and provide instructions to the B cells on how to generate more effective antibodies and become memory cells.
These results are corroborated by recent findings that DOCK8 mutations also occur in humans and are associated with immunodeficiency disease.
Author contacts:
Chris Goodnow (The Australian National University, Canberra, Australia)
Tel: +61 2 6125 3621; E-mail: [email protected]
Richard Cornall (Oxford University, UK)
Tel: +44 186 528 7790; E-mail: [email protected]
[10] Chemical Biology: When chemicals attack
DOI: 10.1038/nchembio.252
A new way to watch chemical warfare between bacteria is presented in a study published online this week in Nature Chemical Biology. These findings have implications in microbial ecology and antibacterial drug development.
Many currently used antibiotics were originally identified as natural products made by bacteria, such as penicillin. In their natural environment, bacteria also use these compounds as antibiotics against other types of bacteria that are competing for resources.
Now Pieter Dorrestein and colleagues have created a method to directly monitor the production and release of these compounds using imaging mass spectrometry – a technique that yields a quantitative picture of which and how many chemicals are made to fight off a bacterial competitor. The method should significantly simplify the ability to study bacterial interactions and may provide new pathways to identify and develop antibacterial compounds.
Author contacts:
Pieter Dorrestein (University of California, San Diego, CA, USA)
Tel: +1 858 534 6607; E-mail: [email protected]
Paul Straight (Texas A&M University, College Station, TX, USA)
Tel: +1 979 845 4231; E-mail: [email protected]
************************************************************************************
Items from other Nature journals to be published online at the same time and with the same embargo:
Nature (http://www.nature.com/nature)
[11] CD81 T lymphocyte mobilization to virus-infected tissue requires CD41 T-cell help
DOI: 10.1038/nature08511
[12] The abscisic acid receptor PYR1 in complex with abscisic acid
DOI: 10.1038/nature08591
NATURE CELL BIOLOGY (http://www.nature.com/naturecellbiology)
[13] The let‑7 target gene mouse Lin‑41 is a stem cell specific E3 ubiquitin ligase for the miRNA pathway protein Ago2
DOI: 10.1038/ncb1987
[14] TAp63 induces senescence and suppresses tumorigenesis in vivo
DOI: 10.1038/ncb1988
[15] Regulation of a Golgi flippase by phosphoinositides and an ArfGEF
DOI: 10.1038/ncb1989
[16] A subdomain of the endoplasmic reticulum forms a cradle for autophagosome formation
DOI: 10.1038/ncb1991
NATURE CHEMICAL BIOLOGY (http://www.nature.com/nchembio)
[17] An artificial di-iron oxo-protein with phenol oxidase activity
DOI: 10.1038/nchembio.257
NATURE CHEMISTRY (http://www.nature.com/nchem)
[18] Identification of active Zr–WOx clusters on a ZrO2 support for solid acid catalysts
DOI: 10.1038/nchem.433
NATURE GENETICS (http://www.nature.com/naturegenetics)
[19] Etv4 and Etv5 are required downstream of GDNF and Ret for kidney branching morphogenesis
DOI: 10.1038/ng.476
NATURE GEOSCIENCE (http://www.nature.com/ngeo)
[20] Permanent storage of carbon dioxide in geological reservoirs by mineral carbonation
DOI: 10.1038/ngeo683
NATURE IMMUNOLOGY (http://www.nature.com/natureimmunology)
[21] Different modes of ubiquitination of the adaptor TRAF3 selectively activate the expression of type I interferons and proinflammatory cytokines
DOI: 10.1038/ni.1819
[22] Nod1 and Nod2 direct autophagy by recruiting ATG16L1 to the plasma membrane at the site of bacterial entry
DOI: 10.1038/ni.1823
NATURE MATERIALS (http://www.nature.com/naturematerials)
[23] Quasi-ballistic thermal transport from nanoscale interfaces observed using ultrafast coherent soft X-ray beams
DOI: 10.1038/nmat2568
[24] Self-assembling chimeric polypeptide–doxorubicin conjugate nanoparticles that abolish tumours after a single injection
DOI: 10.1038/nmat2569
[25] Large modulation of carrier transport by grain-boundary molecular packing and microstructure in organic thin films
DOI: 10.1038/nmat2570
[26] Metastable and unstable cellular solidification of colloidal suspensions
DOI: 10.1038/nmat2571
Nature MEDICINE (http://www.nature.com/naturemedicine)
[27] Identification of miR-145 and miR-146a as mediators of the 5q–syndrome phenotype
DOI: 10.1038/nm.2054
NATURE METHODS (http://www.nature.com/nmeth)
[28] Automated high throughput mapping of promoter-enhancer interactions in zebrafish embryos
DOI: 10.1038/nmeth.1396
[29] Optical interrogation of neural circuits in Caenorhabditis elegans
DOI: 10.1038/nmeth.1397
[30] Imaging neural activity in worms, flies and mice with improved GCaMP calcium indicators
DOI: 10.1038/nmeth.1398
[31] A genetically-encoded reporter of synaptic activity in vivo
DOI: 10.1038/nmeth.1399
NATURE NANOTECHNOLOGY (http://www.nature.com/nnano)
[32] Effective repair of traumatically injured spinal cord by nanoscale block copolymer micelles
DOI: 10.1038/nnano.2009.303
[33] Self-assembly of carbon nanotubes into two-dimensional geometries using DNA origami templates
DOI: 10.1038/nnano.2009.311
[34] Self-organized photosynthetic nanoparticle for cell-free hydrogen production
DOI: 10.1038/nnano.2009.315
[35] Principles and applications of nanofluidic transport
DOI: 10.1038/nnano.2009.332
Nature NEUROSCIENCE (http://www.nature.com/natureneuroscience)
[36] Vascular niche factor PEDF modulates Notch-dependent stemness in the adult subependymal zone
DOI: 10.1038/nn.2437
[37] Experience-dependent compartmentalized dendritic plasticity in rat hippocampal CA1 pyramidal neurons
DOI: 10.1038/nn.2428
[38] Microcircuitry coordination of cortical motor information in self-initiation of voluntary movements
DOI: 10.1038/nn.2431
Nature PHYSICS (http://www.nature.com/naturephysics)
[39] Non-adiabatic spin-torques in narrow magnetic domain walls
DOI: 10.1038/nphys1436
[40] Nernst effect and dimensionality in the quantum limit
DOI: 10.1038/nphys1437
[41] Melting temperature of diamond at ultrahigh pressure
DOI: 10.1038/nphys1438
Nature STRUCTURAL & MOLECULAR BIOLOGY (http://www.nature.com/natstructmolbiol)
[42] Basis of substrate binding and conservation of selectivity in the CLC family of channels and transporters
DOI: 10.1038/nsmb.1704
[43] Non-specifically bound proteins spin while diffusing along DNA
DOI: 10.1038/nsmb.1716
[44] Solution structure and functional analysis of the influenza B proton channel
DOI: 10.1038/nsmb.1707
[45] Recognition of the bacterial second messenger cyclic diguanylate by its cognate riboswitch
DOI: 10.1038/nsmb.1701
[46] Structural basis of ligand binding by a c-di-GMP riboswitch
DOI: 10.1038/nsmb.1702
************************************************************************************
***The following paper will be published electronically on Nature Structural & Molecular Biology’s website on 5 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 08 November at 1800 London time / 1300 US Eastern time ***
[47] Structural insights into the mechanism of abscisic acid signaling by PYL
DOI: 10.1038/nsmb.1730
************************************************************************************
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
Garran: 9
Melbourne: 9
New South Wales: 9
BELGIUM
Brussels: 22
BRAZIL
Sao Paula: 40
CANADA:
Hamilton: 19
Montreal: 2
Toronto: 6, 22, 27
Vancouver: 2, 27
CHINA
Beijing: 47
Hangzhou: 40
Jiangsu: 28
FRANCE
Cavaillon: 26
Gif-sur-Yvette: 15
Grenoble: 12, 39
Orsay: 39
Paris: 22, 40
Villeurbanne: 26
GERMANY
Bad Nauheim: 7
Berlin: 13, 19
Eggenstein: 28
Giessen: 7
Mainz: 13
Meldorf: 8
Munich: 3, 8
Munster: 7
Neuherberg: 13
Regensburg: 7
INDIA
Bangalore: 43
ITALY
Napoli: 17
JAPAN
Chiba: 38
Nagoya: 19
Osaka: 16
Saitama: 38
Shiga: 16
Tokyo: 21, 38
NETHERLANDS
Amsterdam: 6
Enschede: 35
Leiden: 6
POLAND
Warsaw: 8
PUERTO RICO
San Juan: 30
SINGAPORE
Singapore: 6
SPAIN
Barcelona: 14
Burjassot: 36
Valencia: 12
SWEDEN
Stockholm: 5, 6
Uppsala: 5
SWITZERLAND
Basel: 19
Zurich: 7
TAIWAN
Taipei: 21
UNITED KINGDOM
Aberdeen: 6
Birmingham: 28
Cambridge: 31
Leeds: 6
London: 2, 5, 6, 9, 17
Manchester: 5, 6
Oxford: 6, 9
Sheffield: 6
UNITED STATES OF AMERICA
California
Alameda: 6
Berkeley: 15, 23, 41
Carlsbad: 43
Davis: 6
La Jolla: 21, 39
Livermore: 41
Los Angeles: 24
Menlo Park: 25
Palo Alto: 25
Pasadena: 33
Pleasanton: 6
Riverside: 12
San Diego: 10
San Francisco: 6, 9
Stanford: 14, 25, 43
Colorado
Boulder: 23
Connecticut
New Haven: 11, 46
Florida
Miami: 4
Illinois
Evanston: 25
Skokie: 25
Indiana
West Lafayette: 32
Iowa
Iowa City: 42
Maryland
Bethesda: 6, 9, 19
Massachusetts
Boston: 6, 7, 11, 44
Cambridge: 1, 6, 23, 29, 37, 43
Charlestown: 29
Worcester: 19
Michigan
Ann Arbor: 22
Missouri
Kansas City: 30
St Louis: 19
Montana
Kansas City:
New York
Cold Spring Harbor: 14
IManhasset: 6
Melville: 14
New York: 19, 20, 30, 36, 37
Rochester: 41
Upton: 43
North Carolina
Durham: 24
Pennsylvania
Bethlehem: 18
Philadelphia: 17
Pittsburgh: 7, 19
Tennessee
Memphis: 21
Nashville: 8, 15
Oak Ridge: 34
Texas
Austin: 8
College Station: 10
Houston: 6, 8, 18
Knoxville: 34
Virginia
Ashburn: 30, 37
Washington
Seattle: 45
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 Chemistry (London)
Stuart Cantrill
Tel: +44 20 7014 4018; 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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