NATURE RESEARCH JOURNALS PRESS RELEASE
This press release is copyrighted to the Nature journals mentioned below.
This press release contains:
· Summaries of newsworthy papers:
Genetics: Rare ‘de novo’ mutations contribute to schizophrenia risk
Nanotechnology: Cleaning up oil spills
Genetics: New prognostic marker for breast cancer
Cell Biology: Cellular senescence and ageing
Immunology: Fighting infection from an unlikely source
Chemical Biology: Vitamins on the move
Chemical Biology: Synthesis shuts down power
Geoscience: Warm and salty Cretaceous oceans
Immunology: Multi-part bacterial sensor
Structural & Molecular Biology: Preventing amyloid formation
· 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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[1] Genetics: Rare ‘de novo’ mutations contribute to schizophrenia risk
DOI: 10.1038/ng.162
Individuals who have a non-familial form of schizophrenia are approximately eight times more likely than those without the disease to harbour copy number mutations in their genomes, reports a paper online this week in Nature Genetics. These newly occurring (de novo) mutations are not present in the unaffected parents, and may explain a significant portion of the occurrence of schizophrenia in individuals with no strong family history of the disease.
Maria Karayiorgou, Joseph Gogos and colleagues scanned the genomes of 152 individuals with schizophrenia and their unaffected parents for changes in copy number, and compared the results to a genome scan of 159 individuals without schizophrenia. They found copy number mutations in 15 of the 152 individuals with schizophrenia, but only in 2 of the 159 unaffected individuals. The mutations include deletions of a region on chromosome 22—previously implicated in schizophrenia—but also involve changes in copy number on several other chromosomes, which reflects the genetic heterogeneity of the disease. These regions are somewhat enriched in genes affecting neural development, and some contain good individual candidate genes that warrant further scrutiny.
Finally, the authors note that the significant number of de novo mutations may explain why schizophrenia persists in the population despite the low rates of fertility and fecundity in individuals with the disease.
Author contacts:
Maria Karayiorgou (Columbia University Medical Center, New York, NY, USA)
Tel: +1 212 568 4189; E-mail: [email protected]
Joseph Gogos (Columbia University Medical Center, New York, NY, USA)
Tel: +1 212 305 0744; E-mail: [email protected]
[2] Nanotechnology: Cleaning up oil spills
DOI: 10.1038/nnano.2008.136
Membranes made from a mesh of nanowires could be used to clean up oil spills according to a paper published online this week in Nature Nanotechnology.
It is estimated that almost 200,000 tonnes of oil has been spilled at sea in accidents since the start of the decade, so there is a clear need for materials that can remove oil from marine environments quickly and effectively.
Francesco Stellacci and co-workers constructed a membrane that can absorb up to 20 times its own weight of oil or other organic contaminants from water mixtures. The membrane, which is highly porous and about as thick as a sheet of paper, consists of a network of manganese oxide nanowires that are each about 20 nanometres in diameter and assemble into micrometre-length bundles. The team modified the surface of the nanowires to make them attract oil and repel water, and show that this property, combined with the highly porous nature of the membrane, results in selective absorption of organic pollutants such as toluene and motor oil from water mixtures.
In an accompanying News & Views article, Joerg Lahann writes that the membrane ‘provides a blueprint that can guide the design of future nanomaterials for environmental applications’.
Author contact:
Francesco Stellacci (Massachusetts Institute of Technology, Cambridge, MA, USA)
Tel: +1 617 452 3704; E-mail: [email protected]
Additional contact for comment on paper:
Joerg Lahann (University of Michigan, Ann Arbor, MI, USA)
Tel: +1 734 763 7543; E-mail: [email protected]
[3] Genetics: New prognostic marker for breast cancer
DOI: 10.1038/ng.155
Scientists have identified a genetic variant that strongly predicts poor survival among women with breast cancer, particularly after treatment with a commonly used form of chemotherapy, according to a study published online this week in Nature Genetics.
The enzyme NQO1 protects cells from the damaging effects of oxidative stress. A common variant of NQO1 called NQO1*2, present in 4–20% of the human population, effectively eliminates production of the enzyme. Jiri Bartek, Heli Nevanlinna and colleagues carried out the first study investigating the NQO1*2 as a predictive factor for treatment in breast cancer by genotyping over 2,000 women with breast cancer in Finland and following the outcome of their disease and treatment.
Women with two copies of NQO1*2 who were treated with the drug epirubicin had a survival rate of only 17%, compared to 75% for women who had no copies or one copy of the NQO1*2 variant. The presence of NQO1*2 also had a significant effect on survival after metastasis. Given the large number of individuals who carry NQO1*2—up to 20% in Asian populations—the authors suggest that NQO1 genotype could be an important predictive factor for treatment. They call for a randomized prospective clinical trial comparing epirubicin treatment with alternatives to validate the predictive potential of NQO1*2.
Author contacts:
Jiri Bartek (Danish Cancer Society, Copenhagen, Denmark)
Tel: +45 35 25 73 57; E-mail: [email protected]
Heli Nevanlinna (Helsinki University Central Hospital, Finland)
Tel: +358 9 471 71750; E-mail: [email protected]
[4] Cell Biology: Cellular senescence and ageing
DOI: 10.1038/ncb1744
Two tumour suppressor genes with crucial effects on the ability of cells to divide and replicate have been found to affect the ageing process in mice. A report online this week in Nature Cell Biology demonstrates for the first time a direct link between the mechanisms of cellular senescence – the irreversible ceasing of cell replication – and ageing of the whole organism.
Mutant mice expressing low levels of the cell division protein BubR1 have been shown to undergo premature ageing characterized by a shorter lifespan, muscle atrophy and loss of fat. Of the tissues affected, skeletal muscle and fat accumulate high levels of the proteins p16Ink4a and p19Arf. Jan van Deursen and colleagues investigated the role of p16Ink4a and p19Arf genes in ageing by studying the consequences of their inactivation in BubR1-deficient mice. They found that elimination of p16Ink4a reduces both cellular senescence and premature ageing, whereas, in contrast, inactivation of p19Arf exacerbates these effects.
A role for the tumour suppressor genes p16Ink4a and p19Arf in ageing was previously suspected on the basis of findings that their expression increases with age; however, a direct involvement in the ageing process was never proven because mice lacking these genes die early of tumours.
Author contact:
Jan van Deursen (Mayo Clinic, Rochester, MN, USA)
Tel: +1 507 284 2524; E-mail: [email protected]
[5] Immunology: Fighting infection from an unlikely source
DOI: 10.1038/ni.1621
A rare type of white blood cell has been shown to play an important role in long term immunity to infections. A new study, online this week in Nature Immunology, shows that basophils, which constitute less than one percent of total white blood cells circulating throughout the body, could play a key role in the prevention of streptococcus infections. Basophils are mainly associated with release of histamine and other factors linked to allergic reactions and to defence against parasites.
Matthias Mack and co-workers find that basophils detect foreign molecules produced by pathogens. During subsequent infections basophils ‘remember’ the previous pathogen encounter and then release chemical mediators called interleukin 4 and interleukin 6. These factors help other immune cells called B lymphocytes produce antibodies that attack and destroy the pathogen. Mice with reduced numbers of basophils, for example, are significantly more susceptible to streptococcus infection, which causes meningitis, pneumonia and ‘flesh-eating’ diseases.
Although previous work had shown the importance of interleukins 4 and 6 for antibody production, the source of these signalling molecules was not heretofore attributed to this least common of the leukocytes—the basophil.
Author contact:
Matthias Mack (University of Munich, Germany)
Tel: +49 89 5996 846; E-mail: [email protected]
[6] Chemical Biology: Vitamins on the move
DOI: 10.1038/nchembio.93
Scientists have discovered a surprising step in enzyme catalysis by significantly expanding the utility of a standard biochemical method, according to a paper to be published online this week in Nature Chemical Biology. This advance will have major implications in understanding enzyme action and drug design.
Enzymes, or catalytic proteins, are finely tuned to help a specific chemical reaction occur very quickly. This usually means that it is hard or impossible to ‘see’ what is happening to the chemical during the catalytic steps. It is particularly difficult to see these chemical ‘intermediates’ in cases where the enzyme itself is very large, as that normally limits the range of techniques that can be used.
Tadhg Begley and colleagues have now determined the structure of three intermediates in the biosynthesis of a form of vitamin B6, by disrupting the structure of the very large enzyme Pdx1. This allowed them to see an unusual reaction step in which the chemical lost its attachment to the protein at one atom and reconnected using a different atom. The extension of this method to large proteins opens new doors in understanding other biosynthetic pathways and learning more about how drugs can and do act to change these processes.
Author contact:
Tadhg Begley, (Cornell University, Ithaca, NY, USA)
Tel: +1 607 255 7133, Email: [email protected]
[7] Chemical Biology: Synthesis shuts down power
DOI: 10.1038/nchembio.94
Scientists have discovered how two natural products stop cell growth, according to a paper to be published online this week in Nature Chemical Biology. This discovery will have major implications in applying these compounds as potential chemotherapy drugs.
Many natural products are potentially useful as drugs or to find out how a particular biological system works, but it is difficult to figure out what natural products ‘do’—what other molecules they bind to and what result that causes. In many cases, this is made more challenging because it is hard to obtain the natural product in sufficient quantities to perform the necessary tests for binding.
Sergey Kozmin and colleagues have developed new synthetic methods to make two natural products called neopeltolide and a simplified version of leucascandrolide A. With sufficient material in hand, they were able to determine that the compounds bind to the cytochrome bc1 complex, an important piece of the machinery that makes ATP and thus provides energy to the rest of the cell. This discovery provides important information about how these compounds act and will open new doors in the development of chemotherapy compounds.
Author contact:
Sergey Kozmin, (University of Chicago, Chicago, IL, USA)
Tel: +1 773 702 6886, Email: [email protected]
[8] Geoscience: Warm and salty Cretaceous oceans
DOI: 10.1038/ngeo217
The anomalously warm waters that bathed the sea floor 95 million years ago developed in shallow shelf seas in an ocean circulation pattern very different from today’s, according to research published online this week in Nature Geoscience.
Oliver Friedrich and colleagues studied the shells of bottom-dwelling micro-organisms collected in deep-sea drill cores in the region equivalent to the modern tropical North Atlantic Ocean. They found evidence of extremely warm water temperatures at intermediate depths associated with intervals of high salinity conditions. The team suggests that warm surface temperatures during this time led to high rates of evaporation in the shallow seas that lined the proto-North Atlantic. The remaining salty waters became increasingly dense and began to flow off the shelves and sink into the deep ocean.
Such a circulation pattern is markedly different from modern deep-water formation, in which water in the polar regions cools to freezing temperature before sinking and flowing towards lower latitudes.
Author contact:
Oliver Friedrich (National Oceanography Centre, Southampton, UK)
Tel: +44 2380 596 245; E-mail: [email protected]
[9] Immunology: Multi-part bacterial sensor
DOI: 10.1038/ni.1618
One process through which immune cells “sense” the presence of dangerous bacteria is revealed online this week in Nature Immunology. This could be particularly important in the treatment of some infections.
The receptor TLR2, which is expressed on the surface of immune cells, somehow detects and elicits defence responses to molecules, called lipopeptides, that decorate the outer layer of bacteria. Juana de Diego and co-workers showed that TLR2 does not work alone in this process. The serum protein vitronectin and the adhesion protein integrin beta3 are also required for immune responsiveness to bacterial lipopeptide.
Solidifying the clinical importance of this work, patients with the hematological disorder Glanzmann thrombasthenia—the result of a mutation in the gene encoding integrin beta3—showed impaired sensing of bacterial lipopeptide.
Author contact:
Juana de Diego (Max Planck Institute for Infection Biology, Berlin, Germany)
Tel: +49 302 846 0356; E-mail: [email protected]
[10] Structural & Molecular Biology: Preventing amyloid formation
DOI: 10.1038/nsmb.1437
Epigallocatechin gallate, an antioxidant popularly known as EGCG, can prevent the formation of amyloid fibrils, toxic protein aggregates associated with Alzheimer’s and Parkinson’s diseases. The findings, published online this week in Nature Structural & Molecular Biology, may pave the way for the development of more potent compounds designed to prevent amyloid formation associated with several neurodegenerative diseases.
The accumulation of amyloid fibrils in disorders such as Alzheimer’s and Parkinson’s are believed to be caused by the misfolding and aggregation of certain unfolded proteins, which can be toxic to cells and lead to neurodegeneration. Erich Wanker and colleagues show that EGCG, a compound found abundantly in green tea, can bind to these natively unfolded proteins and prevent their conversion to toxic amyloid species. Instead, EGCG directs them to ‘off-pathway’ aggregates that are non-harmful to cells.
Because the authors found that EGCG also binds to unfolded proteins not associated with these diseases, future work could be directed to design compounds that specifically recognize the proteins linked to amyloid formation.
Author contact:
Erich Wanker (Max Delbrueck Center for Molecular Medicine, Berlin, Germany)
Tel: +49 30 940 62157; E-mail: [email protected]
*************************************************************************************************************
Items from other Nature journals to be published online at the same time and with the same embargo:
NATURE CELL BIOLOGY (http://www.nature.com/naturecellbiology)
[11] WAVE and Arp2/3 jointly inhibit filopodium formation by entering into a complex with mDia2
DOI: 10.1038/ncb1745
NATURE CHEMICAL BIOLOGY (http://www.nature.com/nchembio)
[12] A mammalian functional nitrate reductase that regulates nitrite and nitric oxide homeostasis
DOI: 10.1038/nchembio.92
NATURE GENETICS (http://www.nature.com/naturegenetics)
[13] Age-related macular degeneration is associated with an unstable ARMS2 (LOC387715) mRNA
DOI: 10.1038/ng.170
NATURE GEOSCIENCE (http://www.nature.com/ngeo)
[14] Oceanic link between abrupt changes in the North Atlantic Ocean and the African monsoon
DOI: 10.1038/ngeo218
NATURE IMMUNOLOGY (http://www.nature.com/natureimmunology)
[15] An autonomous CDR3delta is sufficient for recognition of the nonclassical MHC class I molecules T10 and T22 by gamma delta T cells
DOI: 10.1038/ni.1620
[16] Regulation of humoral and cellular gut immunity by lamina propria dendritic cells expressing Toll-like receptor 5
DOI: 10.1038/ni.1622
NATURE MATERIALS (http://www.nature.com/naturematerials)
[17] In situ collagen assembly for integrating microfabricated three-dimensional cell-seeded matrices
DOI: 10.1038/nmat2203
Nature MEDICINE (http://www.nature.com/naturemedicine)
[18] SNO-hemoglobin is not essential for red blood cell–dependent hypoxic vasodilation
DOI: 10.1038/nm1771
[19] Leptin controls adipose tissue lipogenesis via central, signal transducer and activator of transcription-3–independent mechanisms
DOI: 10.1038/nm1775
[20] Aggravation of viral hepatitis by platelet-derived serotonin
DOI: 10.1038/nm1780
[21] Blocking TGF-beta–Smad2/3 innate immune signaling mitigates Alzheimer’s-like pathology
DOI: 10.1038/nm1781
NATURE METHODS (http://www.nature.com/nmeth)
[22] In vitro whole-organ imaging: Quantitative 4D analysis of growth and dynamic gene expression in mouse limb buds
DOI: 10.1038/nmeth.1219
NATURE NANOTECHNOLOGY (http://www.nature.com/nnano)
[23] Trophic transfer of nanoparticles in a simplified invertebrate food web
DOI: 10.1038/nnano.2008.110
[24] Selection of carbon nanotubes with specific chiralities using helical assemblies of flavin mononucleotide
DOI: 10.1038/nnano.2008.148
[25] Progress towards monodisperse single-walled carbon nanotubes
DOI: 10.1038/nnano.2008.135
Nature NEUROSCIENCE (http://www.nature.com/natureneuroscience)
[26] Outer hair cell somatic, not hair bundle, motility is the basis of the cochlear amplifier
DOI: 10.1038/nn.2129
[27] Spike timing–dependent long-term depression requires presynaptic NMDA receptors
DOI: 10.1038/nn.2125
[28] Critical role of TRPC6 channels in the formation of excitatory synapses
DOI: 10.1038/nn.2127
[29] Behavior-dependent short-term assembly dynamics in the medial prefrontal cortex
DOI: 10.1038/nn.2134
NATURE PHOTONICS (http://www.nature.com/nphoton)
[30] Waveguide-integrated, ultralow-energy GeSi electro-absorption modulators
DOI: 10.1038/nphoton.2008.99
[31] Blood-vessel closure using photosensitizers engineered for two-photon excitation
DOI: 10.1038/nphoton.2008.100
Nature PHYSICS (http://www.nature.com/naturephysics)
[32] Sharp peaks in the momentum distribution of bosons in optical lattices in the normal state
DOI: 10.1038/nphys983
[33] Attosecond angular streaking
DOI: 10.1038/nphys982
Nature STRUCTURAL & MOLECULAR BIOLOGY (http://www.nature.com/natstructmolbiol)
[34] The central unit within the 19S regulatory particle of the proteasome
DOI: 10.1038/nsmb.1427
[35] Long single alpha-helical tail domains bridge the gap between structure and function of myosin VI
DOI: 10.1038/nsmb.1429
[36] Nonprocessive methylation by Dot1 leads to functional redundancy of histone H3K79 methylation states
DOI: 10.1038/nsmb.1432
***************************************************************************************************************
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.
CANADA:
Ottawa: 33
Toronto: 20, 31
CHINA
Shanghai: 28
CZECH REPUBLIC
Olomouc: 3
DENMARK
Copenhagen: 3
FINLAND
Helsinki: 3
Kuopio: 3
Tampere: 3
Vaasa: 3
GERMANY
Berlin: 9, 10, 20
Bremen: 8
Dresden: 5
Düsseldorf: 9
Frankfurt: 11
Frankfurt am Main: 33
Goettingen: 20
Hannover: 5, 8
Regensburg: 5, 13
Tubingen: 5
Wurzburg: 13
ISRAEL
Haifa: 34
JAPAN
Chiba: 16, 32
Fukui: 16
Hyogo: 16
Ibaraki: 2
Osaka: 16
Saitama: 21
Tokyo: 16
NETHERLANDS
Amsterdam: 33, 36
De Bilt: 14
Delft: 14, 35
Plesmanlaan: 36
Utrecht: 36
SINGAPORE
Singapore: 2
SOUTH AFRICA
Pretoria: 1
SOUTH KOREA
Incheon: 16
SPAIN
Barcelona: 22, 33
Madrid: 22
Seville: 27
SWEDEN
Stockholm: 12
Uppsala: 3, 12
SWITZERLAND
St Gallen: 20
Zurich: 20, 33
UNITED KINGDOM
Brighton: 26
Edinburgh: 22
London: 10, 13, 31
Oxford: 27, 31
Southampton: 8
UNITED STATES OF AMERICA
Alabama
Birmingham: 5, 18
California
Los Angeles: 21
Stanford: 15, 35
Colorado
Fort Collins: 33
Connecticut
New Haven: 21
Storrs: 2, 24
Florida
Tampa: 21
Illinois
Chicago: 7, 15
Evanston: 25
Louisiana
Shreveport: 18
Maryland
Baltimore: 21
Bethesda: 19
Gaithersburg: 23
Massachusetts
Cambridge: 2, 30
Michigan
Ann Arbor: 21
Minnesota
Rochester: 4
Montana
Bozeman: 31
New Jersey
Newark: 29
Princeton: 14
Rahway: 19
New York
Bronx: 19
Ithaca: 6
New York: 1, 17, 19
Ohio
Columbus: 32
Oregon
Portland: 22
Pennsylvania
Pittsburgh: 29
Tennessee
Nashville: 1
Texas
College Station: 14
San Antonio: 34
Virginia
Manassas: 30
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]
Katherine Anderson (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)
Orli Bahcall
Tel: +1 212 726 9311; 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)
Alison Stoddart
Tel: +44 20 7843 4593; 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)
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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