NATURE AND THE NATURE RESEARCH JOURNALS PRESS RELEASE
For papers that will be published online on 14 February 2010
This press release is copyrighted to the Nature journals mentioned below.
This press release contains:
· Summaries of newsworthy papers:
Materials: Full solar-cell performance with only one percent of material used
Genetics: Variants associated with dementia
Nature: Makeover to yield designer proteins?
Geoscience: Unprecedented pressure from ocean acidification
Neuroscience: A new villain in multiple sclerosis
Genetics: Deletion associated with childhood developmental delay
Geoscience: Melting glaciers in Greenland fjords
· 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] Materials: Full solar-cell performance with only one percent of material used
DOI: 10.1038/nmat2635
A flexible solar-cell design is reported online this week in Nature Materials that uses only one percent of the material used in conventional devices. Unlike many other flexible solar-cell designs, this new design achieves a high light-conversion efficiency. The possible applications for such lightweight, yet efficient solar cells could range from car sunroofs to devices that can be placed on clothing.
To achieve such high levels of light absorption while employing significantly less of the costly semiconductor material, Harry Atwater and colleagues use small micrometre-sized rods of silicon in their device. Incoming light bounces back and forth multiple times between the rods in the devise until it is absorbed. In order to ensure that the light is guided more efficiently, the researchers use small alumina nanoparticle reflectors placed between the rods. The overall result is that up to 85% of usable incident sunlight is absorbed.
Author contact:
Harry Atwater (California Institute of Technology, Pasadena, CA, USA)
Tel: +1 626 395 2197; E-mail: [email protected]
[2] Genetics: Variants associated with dementia
DOI: 10.1038/ng.536
A common genetic variant is associated with frontotemporal lobar degeneration (FTLD), a common cause of dementia, according to a study published online this week in Nature Genetics.
FTLD is characterized by the progressive degeneration of specific areas of the brain, along with progressive deficits in behavior and language. Fifty-percent of patients diagnosed with this disease have a specific form called FTLD-TDP, which is characterized by the presence of neuronal aggregates of TDP-43 protein.
Vivianna Van Deerlin and colleagues analyzed approximately 600 post-mortem cases of FTLD-TDP, with confirmed neuropathological evidence of TDP-43 aggregates. The scientists find that a common genetic variant at chromosome 7p21 is associated with increased risk of FTLD-TDP.
Author contact:
Vivianna Maia Van Deerlin (University of Pennsylvania, Philadelphia, PA, USA)
Tel: +1 215 662 6957; E-mail: [email protected]
[3] Nature: Makeover to yield designer proteins?
DOI: 10.1038/nature08817
The prospect of genetically encoded designer proteins takes a step forwards with the development of a new cellular system that can incorporate multiple unnatural amino acids into proteins. The process is described in this week’s Nature.
The new system, created by Jason W. Chin and colleagues, utilises a genetically engineered protein-making machinery that decodes messenger RNA in groups of 4 rather than 3 nucleotides. Consequently instead of the 22 amino acids allowed by the standard genetic code, this new approach makes it possible to encode more than 200 amino acids in recombinant proteins.
Although chemists can devise new amino acids with desirable properties, only a limited number have been successfully introduced into proteins by the cellular machinery. And even then, only one type of unnatural amino acid could be added to a protein. This system, incorporating various unnatural amino acids at defined positions, offers the promise of proteins tailored with molecular precision.
Jason W. Chin (Cambridge University, UK)
Tel: +44 122 340 2115; E-mail: [email protected]
[4] Geoscience: Unprecedented pressure from ocean acidification
DOI: 10.1038/ngeo755
Rates of ocean acidification not seen for the past 65 million years could result in unprecedented pressure on marine organisms with carbonate shells and body parts, according to a study published online this week in Nature Geoscience.
Andy Ridgwell and colleagues used an Earth-system model to compare past and future changes in ocean acidity. According to their simulations, the surface of the ocean is set to acidify more quickly than it did during a well-documented greenhouse warming event 55.5 million years ago. Equally unprecedented changes in the chemistry of the deep ocean are also expected. The scientists warn that future changes in ocean chemistry threaten both surface- and bottom-dwelling organisms.
Author contact:
Andy Ridgwell (University of Bristol, UK)
Tel: +44 117 954 6858; E-mail: [email protected]
[5] Neuroscience: A new villain in multiple sclerosis
DOI: 10.1038/nn.2491
The experimental chemical cuprizone destroys myelin via an unexpected mechanism. As reported in a study published online this week in Nature Neuroscience, cuprizone induces neutrophils—a specific population of white blood cell—to enter the central nervous system and kill oligodendrocytes (OLs), the myelin-forming cells. These blood cells could be targets for the development of new multiple sclerosis drugs.
Multiple sclerosis (MS) is primarily an autoimmune attack on myelin, the crucial insulation of nerve tracts. The most severe damage in MS, however, is thought to be caused by a combination of autoimmune and toxic mechanisms. In mice, the chemical cuprizone causes this type of severe myelin damage. Richard Ransohoff and colleagues report that cuprizone does not kill OLs in mice that lack CXCR2, the receptor for an inflammation-promoting peptide. With a series of bone marrow transplantation experiments between normal and CXCR2-deficient mice, the researchers determined that CXCR2 had to be present on blood cells, not brain cells, for cuprizone to be toxic to OLs. Removing neutrophils, the only CXCR2-expressing blood cells, from the circulation of normal mice rendered them resistant to the toxic effects of cuprizone.
Cuprizone itself has not been linked to human MS, but other environmental toxins might trigger similar cellular mechanisms. If so, therapeutic approaches targeting neutrophils should be investigated.
Author contact:
Richard Ransohoff (Lerner Research Institute, Cleveland, OH, USA)
Tel: +1 216 444 0627; E-mail: [email protected]
[6] Genetics: Deletion associated with childhood developmental delay
DOI: 10.1038/ng.534
Deletion of a genetic region at chromosome 16p12.1 is found in some children with intellectual disability/developmental delay (ID/DD) and congenital malformations, according to a study published online this week in Nature Genetics. These results support a two-hit model in which a deletion at 16p12.1 acts as a risk factor for ID/DD and a secondary mutation results in more severe clinical problems.
Developmental delays, such as failing to sit, walk, and talk, at the average age, is a common symptom of mental retardation, cerebral palsy, autism spectrum disorder, Down syndrome, as well as other disorders.
Evan Eichler and colleagues analysed the genomes of over 21,000 children with intellectual disability/developmental delay. The scientists find that in 42 of the children, there is a deletion at chromosome 16p12.1, compared to 8 of 14,839 controls. Children carrying both the 16p12.1 deletion and an additional chromosomal abnormality exhibited more severe symptoms than children carrying only the additional mutation.
Author contact:
Evan Eichler (University of Washington, Seattle, WA, USA)
Tel: +1 206 685 7336; E-mail: [email protected]
[7] & [8] Geoscience: Melting glaciers in Greenland fjords
DOI: 10.1038/ngeo764
DOI: 10.1038/ngeo765
Marine melting in Greenland’s fjords represents a key influence on the stability of the Greenland ice sheet, according to two studies published online this week in Nature Geoscience. Oceanographic measurements from several fjords outline how warm waters from the open ocean enter the fjords and melt the outlet glaciers on the edge of the ice sheet.
Fiammetta Straneo and colleagues measured the water properties in the fjord that connects Helheim Glacier, one of East Greenland’s largest outlet glaciers, with the ocean. They report an active exchange between subtropical waters on the shelf and fjord waters, and suggest that the recent acceleration of the glacier could have been triggered by oceanic and atmospheric changes at a distance.
Eric Rignot and colleagues studied three glacial fjords in West Greenland, and found that ice loss through submarine melting is on the same order of magnitude as loss to icebergs breaking off, with high variability between the glaciers.
In an accompanying News & Views, Paul Holland writes, “The studies by Straneo and Rignot and their colleagues are vital steps towards an understanding of Greenland’s ice loss into fjords.”
Author contacts:
Fiammetta Straneo (Woods Hole Oceanographic Institution, MA, USA) Author paper [7]
Tel: +1 508 289 2914; E-mail: [email protected]
Eric Rignot (University of California Irvine, CA, USA) Author paper [8]
Tel: +1 949 824 3739; E-mail: [email protected]
Paul Holland (British Antarctic Survey, Cambridge, UK) N&V author
Tel: +44 1223 221444; E-mail: [email protected]
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Items from other Nature journals to be published online at the same time and with the same embargo:
Nature (http://www.nature.com/nature)
[9] Blood stem cells emerge from aortic endothelium by a novel type of cell transition
DOI: 10.1038/nature08761
[10] In vivo imaging of haematopoietic cells emerging from the mouse aortic endothelium
DOI: 10.1038/nature08764
[11] Haematopoietic stem cells derive directly from aortic endothelium during development
DOI: 10.1038/nature08738
[12] Neurogenic radial glia in the outer subventricular zone of human neocortex
DOI: 10.1038/nature08845
NATURE BIOTECHNOLOGY (http://www.nature.com/naturebiotechnology)
[13] Nutrient-sensitized screening for drugs that shift energy metabolism from mitochondrial respiration to glycolysis
DOI: 10.1038/nbt.1606
[14] Induction of cell cycle entry eliminates human leukemia stem cells in a mouse model of AML
DOI: 10.1038/nbt.1607
NATURE CELL BIOLOGY (http://www.nature.com/naturecellbiology)
[15] The peroxisomal importomer constitutes a large and highly dynamic pore
DOI: 10.1038/ncb2027
[16] TGF-beta-mediated phosphorylation of hnRNP E1 induces EMT via transcript-selective translational induction of Dab2 and ILEI
DOI: 10.1038/ncb2029
[17] Identification of the cell lineage at the origin of basal cell carcinoma
DOI: 10.1038/ncb2031
NATURE GENETICS (http://www.nature.com/naturegenetics)
[18] Germline mutations in TMEM127 confer susceptibility to pheochromocytoma
DOI: 10.1038/ng.533
NATURE IMMUNOLOGY (http://www.nature.com/natureimmunology)
[19] An essential role for the transcription factor HEB in thymocyte survival, Tcra rearrangement and the development of natural killer T cells
DOI: 10.1038/ni.1845
[20] Regulation of IL-9 expression by IL-25 signaling
DOI: 10.1038/ni.1846
NATURE MATERIALS (http://www.nature.com/naturematerials)
[21] Isotope effect in spin response of pi-conjugated polymer films and devices
DOI: 10.1038/nmat2633
[22] A homologous series of structures on the surface of SrTiO3(110)
DOI: 10.1038/nmat2636
[23] Insulating interlocked ferroelectric and structural antiphase domain walls in multiferroic YMnO3
DOI: 10.1038/nmat2632
Nature MEDICINE (http://www.nature.com/naturemedicine)
[24] An oncogene–tumor suppressor cascade drives metastatic prostate cancer by coordinately activating Ras and nuclear factor-kB
DOI: 10.1038/nm.2100
[25] Pharmacological correction of a defect in PPAR-gamma signaling ameliorates disease severity in Cftr-deficient mice
DOI: 10.1038/nm.2101
[26] Innate immune lectins kill bacteria expressing blood group antigen
DOI: 10.1038/nm.2103
NATURE METHODS (http://www.nature.com/nmeth)
[27] Organelle-Specific, Rapid Induction of Molecular Activities and Membrane Tethering
DOI: 10.1038/nmeth.1428
[28] Temporal Pixel Multiplexing for simultaneous high-speed high-resolution imaging
DOI: 10.1038/nmeth.1429
[29] Exploring the sequence determinants of amyloid structure using position-specific scoring matrices
DOI: 10.1038/nmeth.1432
NATURE NANOTECHNOLOGY (http://www.nature.com/nnano)
[30] Cold welding of ultrathin gold nanowires
DOI: 10.1038/nnano.2010.4
[31] High-speed atomic force microscopy shows dynamic molecular processes in photoactivated bacteriorhodopsin
DOI: 10.1038/nnano.2010.7
[32] Graphene nanomesh
DOI: 10.1038/nnano.2010.8
[33] A diamond nanowire single-photon source
DOI: 10.1038/nnano.2010.6
Nature NEUROSCIENCE (http://www.nature.com/natureneuroscience)
[34] Active flight increases the gain of visual motion processing in Drosophila
DOI: 10.1038/nn.2492
[35] Regulation of neuronal activity by Cav3-Kv4 channel signaling complexes
DOI: 10.1038/nn.2493
NATURE PHOTONICS (http://www.nature.com/nphoton)
[36] Exploiting disorder for perfect focusing
DOI: 10.1038/nphoton.2010.3
[37] Quantum-optical state engineering up to the two-photon level
DOI: 10.1038/nphoton.2010.6
Nature PHYSICS (http://www.nature.com/naturephysics)
[38] Analog information processing at the quantum limit with a Josephson ring modulator
DOI: 10.1038/nphys1516
Nature STRUCTURAL & MOLECULAR BIOLOGY (http://www.nature.com/natstructmolbiol)
[39] Mechanism of error-free and semitargeted mutagenic bypass of an aromatic amine lesion by Y-family polymerase Dpo4
DOI: 10.1038/nsmb.1771
[40] A PP4 phosphatase complex dephosphorylates RPA2 to facilitate DNA repair via homologous recombination
DOI: 10.1038/nsmb.1769
[41] The structure of the catalytic subunit FANCL of the Fanconi anemia core complex
DOI: 10.1038/nsmb.1759
[42] Munc13 C2B domain is an activity-dependent Ca2+ regulator of synaptic exocytosis
DOI: 10.1038/nsmb.1758
[43] Mediator Head module structure and functional interactions
DOI: 10.1038/nsmb.1757
[44] The structures of the anti-tuberculosis antibiotics viomycin and capreomycin bound to the 70S ribosome
DOI: 10.1038/nsmb.1755
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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: 6
Melbourne: 2
New South Wales: 2
Sydney: 2
BELGIUM
Antwerp: 2
Brussels: 17, 29
BRAZIL
Sao Paula: 18, 26
CANADA:
Calgary: 35, 37
London: 2
Quebec: 7
St John’s: 7
Toronto: 2
Vancouver: 2, 8
CHINA
Hefei: 21
FINLAND
Kuopio: 2
FRANCE
Paris: 2, 9, 37
GERMANY
Bochum: 15
Erlangen: 37
Garching: 33
Goettingen: 42
Heidelberg: 29
Munich: 2
Osnabruck: 15
Wurzburg: 2
GREENLAND
Nuuk: 7
INDIA
Kolkata: 16
ISRAEL
Haifa: 21
ITALY
Padova: 18
Troina: 6
JAPAN
Nagoya: 31
Tokyo: 14, 31
Yokohama: 14, 20
NETHERLANDS
Amsterdam: 36
Enschede: 36
Rotterdam: 2, 10
NEW ZEALAND
Auckland: 6
SPAIN
Barcelona: 2, 29
Navarra: 2
SWEDEN
Stockholm: 2
Uppsala: 2
SWITZERLAND
Zurich: 2, 36
THAILAND
Pathum-than: 20
UNITED KINGDOM
Birmingham: 2
Bristol: 4
Cambridge: 2, 3, 15
Durham: 2
Falmer: 29
London: 41
Manchester: 2
Oxford: 28
Sheffield: 2
UNITED STATES OF AMERICA
Arizona
Phoenix: 2
Scottsdale: 2
Sun City: 2
California
Berkeley: 38
Irvine: 2, 5, 8
La Jolla: 6, 11, 19, 25, 43
Los Angeles: 2, 32
Pasadena: 1, 8, 34
Sacramento: 2
San Diego: 2
San Francisco: 11, 12
Stanford: 42
Connecticut
New Haven: 38, 40, 44
Georgia
Atlanta: 2, 26
Illinois
Chicago: 2
Indiana
Indianapolis: 2, 6, 43
Kansas
Lawrence: 7
Kentucky
Louisville: 6
Louisiana
New Orleans: 6
Maine
Bar Harbor: 14
Orono: 7
Maryland
Baltimore: 2, 27
Bethesda: 2, 44
Massachusetts
Bedford: 2
Belmont: 6
Boston: 2, 6, 13, 18, 24, 40
Brockton: 6
Cambridge: 13, 24, 33
Charlestown: 13
Woods Hole: 7
Worcester: 18
Michigan
Ann Arbor: 2
Minnesota
Rochester: 2
Missouri
Columbia: 6
St Louis: 2
Montana
Helena: 6
New Jersey
Piscataway: 23
Rahway: 42
New Mexico
Albuquerque: 30
New York
Cold Spring Harbor: 6
New York: 2, 39, 40
Rochester: 13
North Carolina
Durham: 6
Ohio
Cleveland: 5, 16
Toledo: 6
Oregon
Portland: 2, 6
Pennsylvania
Danville: 6
Philadelphia: 2, 24
Pittsburgh: 2, 6
Rhode Island
Providence: 30
Texas
College Station: 33
Dallas: 2, 42
Galveston: 42
Houston: 20, 30, 42
San Antonio: 18
Utah
Salt Lake City: 21
Virginia
Charlottesville: 2
Washington
Seattle: 2, 6, 7
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 Biotechnology (New York)
Michael Francisco
Tel: +1 212 726 9284; E-mail: [email protected]
Nature Cell Biology (London)
Sowmya Swaminathan
Tel: +44 20 7843 4656; 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 Photonics (Tokyo)
Oliver Graydon
Tel: +81 3 3267 8776; 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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