NATURE AND THE NATURE RESEARCH JOURNALS PRESS RELEASE
For papers that will be published online on 28 February 2010
This press release is copyrighted to the Nature journals mentioned below.
This press release contains:
· Summaries of newsworthy papers:
Biotechnology: Hope for spinal muscular atrophy
Genetics: Genetic variants influence risk of coeliac disease
Geoscience: Small creatures, big extinction
Immunology: Tragic ending for mutant immune cells
Chemical Biology: Pass the sugar, please
Immunology: “Licensed” to cross-prime
Methods: Protein dynamics in a living cell
And finally…Neuroscience: Getting through the night without a drink
· 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] Biotechnology: Hope for spinal muscular atrophy
DOI: 10.1038/nbt.1610
A new therapeutic approach for spinal muscular atrophy is demonstrated in a mouse model in this week’s Nature Biotechnology. Although further research is needed to determine whether the approach will be viable in human infants, the results are considered promising by spinal muscular atrophy experts.
Spinal muscular atrophy, a genetic disorder of infants, is caused by reduced function of the ‘survival motor neuron’ protein in nerve cells and leads to progressive muscle weakness and early death. Brian Kaspar and colleagues previously showed that a gene can be delivered to spinal motor nerve cells in newborn mice simply by injecting a specific engineered virus carrying the gene into the blood. Now, working with spinal muscular atrophy researcher Arthur Burghes, the Kaspar team has used the engineered virus to deliver the survival motor neuron gene to a strain of mouse that is used as a model of spinal muscular atrophy. Without treatment, these mice die within about 15 days, and previous experimental therapies had increased their survival to only about 45 days. In contrast, the new gene therapy outlined in this paper kept the mice alive for more than 250 days and substantially improved their muscle function.
As a first step in evaluating whether this approach could be translated to human infants, the authors injected the engineered virus carrying a fluorescent ‘reporter’ gene—which is easy to track—into a newborn cynomolgus monkey. They found that the fluorescent gene was successfully delivered to spinal motor nerve cells, suggesting that the therapy could work in non-human primates and, possibly, in humans.
Author contacts:
Brian Kaspar (The Ohio State University, Columbus, OH, USA)
Tel: +1 614 722 5085; E-mail: [email protected]
Arthur Burghes (The Ohio State University, Columbus, OH, USA)
Tel: +1 614 688 4957; E-mail: [email protected]
Alex MacKenzie (Childrens Hospital of Eastern Ontario, Ottawa, Canada) N&V author
Tel: +1 613 737 2772; E-mail: [email protected]
[2] Genetics: Genetic variants influence risk of coeliac disease
DOI: 10.1038/ng.543
Thirteen new genetic variants associated with increased risk of coeliac disease are reported online this week in Nature Genetics. This study doubles the number of common genetic variants that have been found to be associated with coeliac disease.
Coeliac disease is an inherited autoimmune condition in which the lining of the small intestine is damaged by dietary gluten and other proteins contained in wheat, barley and rye. The prevalence of coeliac disease is approximately 1% worldwide, and the only effective treatment is following a gluten-free diet.
David van Heel and colleagues scanned the genomes of 9,451 patients with coeliac disease and report 13 genetic regions that are associated with increased risk of the disease. Most of the associated genetic regions contain genes with known functions in the immune system. Eighteen of the 27 known genetic risk variants for coeliac disease are also associated with other immune-related diseases, including type 1 diabetes and rheumatoid arthritis.
Author contact:
David Van Heel (Queen Mary University, London, UK)
Tel: +44 207 882 2330; E-mail: [email protected]
[3] Geoscience: Small creatures, big extinction
DOI: 10.1038/ngeo775
Tiny phytoplankton in the oceans of the Northern Hemisphere had far larger extinction rates during the mass extinction event 65 million years ago than those living in the Southern Hemisphere, according to a paper published online this week in Nature Geoscience. The recovery of the Northern Hemisphere phytoplankton also occurred significantly later than recovery in the southern oceans.
Populations of phytoplankton smaller than 20 micrometres were decimated during the Cretaceous/Tertiary mass extinction, which is linked to an impact event. Timothy Bralower and colleagues propose that the clouds of debris from the impact — which would have blocked the sunlight that these phytoplankton needed to grow, and poisoned them as the metal-laden dust fell to the ocean surface — were concentrated in the Northern Hemisphere, leading to the higher extinction rates. The team also suggests that the recovery of marine diversity in the north may have been hindered by the phytoplankton’s slower start in this region.
Author contact:
Timothy Bralower (Pennsylvania State University, University Park, PA, USA)
Tel: +1 814 863 1240; E-mail: [email protected]
[4] Immunology: Tragic ending for mutant immune cells
DOI: 10.1038/ni.1847
A new mutant mouse that cannot sustain immune responses is described in a study published online this week in Nature Immunology.
“Elektra” mice are a special mutant strain that readily succumb to bacterial and viral infections. Immune cells in Elektra mice develop normally and become activated upon infection; however, unlike immune cells in normal mice, Elektra immune cells die soon after their activation. As a result, Elektra mice are immunodeficient, and die from any infection.
Bruce Beutler and colleagues identify a mutation in the gene called Schlafen-2 as responsible for the immune defect seen in Elektra mice. How the protein encoded by Schlafen-2 promotes survival of activated immune cells is not yet known. The scientists note, however, that several pox viruses encode Schlafen-like genes, suggesting that viruses might have appropriated a similar activity to perpetuate survival of viral-infected host cells.
Author contact:
Bruce Beutler (The Scripps Research Institute, La Jolla, CA, USA)
Tel: +1 858 784 8610; E-mail: [email protected]
[5] Chemical Biology: Pass the sugar, please
DOI: 10.1038/nchembio.314
A new way to attach sugars to proteins is reported online this week in Nature Chemical Biology. As these particular sugar/protein combinations are key to controlling viral infections and are involved in numerous diseases, such as muscular dystrophy, this work has immediate practical applications in biopharma and glycoprotein research.
It is typically much easier to use bacterial cells to produce large quantities of a desired protein than mammalian cells. However, some proteins, called glycoproteins, also need to have a sugar chain attached to the protein sequence in order to be fully functional. The sugars that can be attached using bacterial cells are significantly different than those found in mammalian cells, therefore limiting the extent to which these helpful bacterial cell cultures can be used to make natural mammalian glycoproteins.
Now Lai-Xi Wang, Markus Aebi and colleagues have created a hybrid E. coli that contains genes from C. jejuni – another kind of bacteria. These genes work together with normal E. coli genes to create the first sugar link present in mammalian glycoproteins. Though additional, unnecessary sugars are also placed on the sugar chain in cell culture, the team demonstrates that it is easy to use known methods in the lab to take off these extra sugars and replace them with others.
This combined methodology now makes it possible to create a large quantity of correctly-modified glycoproteins for further biological studies or for pharmaceutical preparations.
Author contacts:
Lai-Xi Wang (University of Maryland School of Medicine, Baltimore, MD, USA)
Tel: +1 410 706 4982; E-mail: [email protected]
Markus Aebi (Swiss Institute of Technology, Zurich, Switzerland)
Tel: +41 44 632 64 13; E-mail: [email protected]
[6] Immunology: “Licensed” to cross-prime
DOI: 10.1038/ni.1848
NKT cells play an important role in cross priming – a process whereby infectious agents outside the cell are taken up, processed, and presented to a certain type of T cell in order to create an immune response which is effective against tumours. The work, published online in Nature Immunology this week, suggests that NKT cells could potentially be an important new player in vaccine design.
Cross-priming critically depends on three cell types coming together: dendritic cells, a licensing cell, and a cytotoxic T cell (CTL). Normally, dendritic cells cross-prime infectious agents via the intervention of T helper cells – which are licensing cells. However Christian Kurts and colleagues have revealed a novel mechanism where this process is instead triggered by another cell type entirely — the NKT cell. Following interaction with NKT cells, dendritic cells secrete a chemical signal, which specifically attracts certain CTLs to them, where they can then be activated.
Until now it has been puzzling how the three rare cell types needed in order for cross-priming to occur can all interact in time and space. The NKT-elicited release of a chemical signal from dendritic cells provides a neat solution to this puzzle. The importance of NKT cells revealed by this study suggests that any future vaccine may be more effective if these cells are factored into their design.
Author contact:
Christian Kurts (Friedrich-Wilhelms-Universität, Bonn, Germany)
Tel: +49 228 287 11031; E-mail: [email protected]
[7] Methods: Protein dynamics in a living cell
DOI 10.1038/nmeth.1435
A method for monitoring the folding and stability of proteins in single living cells is reported in a paper published online this week in Nature Methods. The method will allow more detailed understanding of protein function within cells.
The stability and dynamics of proteins are directly tied to their biological functions. However, most studies investigating protein dynamics are carried out on isolated proteins in dilute solutions, outside of the cell. In contrast, the interior of a cell is a very crowded environment where proteins can interact with many other biomolecules. To truly understand protein function, therefore, it must be studied within the confines of the cellular environment. Martin Gruebele and colleagues now report an approach to do so.
Proteins are very sensitive to temperature changes and will eventually unfold at high enough temperatures – ‘temperature jump’ experiments are often used for studying the folding and stability of isolated proteins in solution. To adapt the approach to look at proteins in single living cells, the team fitted a fluorescence microscope with an infrared laser that can be used to induce very rapid temperature jumps. By labeling the protein of interest in the cell with fluorescent probes, it is possible to watch how its structure rapidly changes as the temperature is ramped higher and higher. This reveals information about the stability of the protein within the cell as well as the protein’s unfolding kinetics.
Besides analyzing protein dynamics, the method could aid researchers studying other fast processes such as protein-protein interactions and heat-shock responses across populations of cells.
Author contact:
Martin Gruebele (University of Illinois, Urbana, IL, USA)
Tel: +1 217 333 1624; E-mail: [email protected]
[8] And finally…Neuroscience: Getting through the night without a drink
DOI: 10.1038/nn.2503
The changes which our body orchestrates that prevent dehydration at night, when we sleep are reported in a study published online this week in Nature Neuroscience.
The amount of water retained by the body is controlled by vasopressin, a hormone released by neurosecretory cells in a brain area known as the hypothalamus. These cells are activated by osmosensory cells, which track the concentration of water in blood. The hypothalamus also contains cells that form the suprachiasmatic nucleus, which is thought to contain a central body clock. Daily, rhythmic changes in the activity of the cells in this nucleus influences all of the body’s daily rhythms, from when we feel hungry to when we feel sleepy.
Eric Trudel and Charles Bourque studied the connection between these three groups of cells. They found that late at night, the connection between the water-sensing osmosensory cells and the vasopressin-releasing neurosecretory cells grows stronger, so that even slight dehydration results in a greater release of vasopressin. Also at this time of the night, activity in the suprachiasmatic nucleus reduces. The team artificially increased the firing of the suprachiasmatic nucleus cells and found that the connection between the osmosensory and neurosecretory cells grew weaker.
These results suggest that that activation of the suprachiasmatic nucleus weakens the connection between osmosensory and neurosecretory cells, acting like a ‘brake.’ During the day, we can remedy low water concentrations merely by drinking some water. However, when we sleep during the night, the activity in the suprachiasmatic nucleus reduces, releasing the ‘brake’, and allowing more water retention.
Author contacts:
Charles Bourque (Research Institute of the McGill University Health Centre, Quebec, Canada)
Tel: + 1 514 934 8094; E-mail: [email protected]
Eric Trudel (Research Institute of the McGill University Health Centre, Quebec, Canada)
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)
[9] Systems survey of endocytosis by multiparametric image analysis
DOI: 10.1038/nature08779
[10] Control of Arabidopsis apical–basal embryo polarity by antagonistic transcription factors
DOI: 10.1038/nature08843
NATURE BIOTECHNOLOGY (http://www.nature.com/naturebiotechnology)
[11] Harnessing chaperone-mediated autophagy for the selective degradation of mutant huntingtin protein
DOI: 10.1038/nbt.1608
[12] Directed evolution of a magnetic resonance imaging contrast agent for noninvasive imaging of dopamine
DOI: 10.1038/nbt.1609
NATURE CELL BIOLOGY (http://www.nature.com/naturecellbiology)
[13] A deneddylase encoded by Epstein–Barr virus promotes viral DNA replication by regulating the activity of cullin-RING ligases
DOI: 10.1038/ncb2035
[14] Genome-wide RNA-mediated interference screen identifies miR-19 targets in Notch-induced T-cell acute lymphoblastic leukaemia
DOI: 10.1038/ncb2037
NATURE CHEMICAL BIOLOGY (http://www.nature.com/nchembio)
[15] Combinatorial profiling of chromatin-binding modules reveals multi-site discrimination
DOI: 10.1038/nchembio.319
[16] Symbiotic streptomycetes provide antibiotic combination prophylaxis for wasp offspring
DOI: 10.1038/nchembio.331
[17] A chemical and phosphoproteomic characterization of dasatinib action in lung cancer
DOI: 10.1038/nchembio.332
NATURE CHEMISTRY (http://www.nature.com/nchem)
[18] Triflimide-catalysed sigmatropic rearrangement of N-allylhydrazones as an example of a traceless bond construction
DOI: 10.1038/nchem.576
[19] Stereoinduction by distortional asymmetry
DOI: 10.1038/nchem.577
[20] Quantum-induced symmetry breaking explains infrared spectra of CH5+ isotopologues
DOI: 10.1038/nchem.574
[21] Nanocrystalline intermetallics on mesoporous carbon for direct formic acid fuel cell anodes
DOI: 10.1038/nchem.553
NATURE GENETICS (http://www.nature.com/naturegenetics)
[22] Mutations in VIPAR cause an arthrogryposis, renal dysfunction, and cholestasis syndrome phenotype with defects in epithelial polarisation
DOI: 10.1038/ng.538
NATURE GEOSCIENCE (http://www.nature.com/ngeo)
[23] Insolation and CO2 contribution to interglacial warmth before and after the Mid-Brunhes Event
DOI: 10.1038/ngeo771
[24] Landslide erosion controlled by hillslope material
DOI: 10.1038/ngeo776
[25] Atmospheric nanoparticles formed from heterogeneous reactions of organics
DOI: 10.1038/ngeo778
NATURE IMMUNOLOGY (http://www.nature.com/natureimmunology)
[26] ‘Unlicensed’ natural killer cells dominate the response to cytomegalovirus infection
DOI: 10.1038/ni.1849
[27] Unique autoreactive T cells recognize insulin peptides generated within the islets of Langerhans in autoimmune diabetes
DOI: 10.1038/ni.1850
NATURE MATERIALS (http://www.nature.com/naturematerials)
[28] Ferroelastic switching for nanoscale non-volatile magnetoelectric devices
DOI: 10.1038/nmat2703
[29] Template engineering of Co-doped BaFe2As2 single-crystal thin films
DOI: 10.1038/nmat2721
[30] Atomic layers of hybridized boron nitride and graphene domains
DOI: 10.1038/nmat2711
[31] Plastic-deformation mechanism in complex solids
DOI: 10.1038/nmat2713
[32] A genetic algorithm for predicting the structures of interfaces in multicomponent systems
DOI: 10.1038/nmat2712
Nature MEDICINE (http://www.nature.com/naturemedicine)
[33] Kynurenine is an endothelium-derived relaxing factor produced during inflammation
DOI: 10.1038/nm.2092
[34] Down-regulation of the potassium-chloride cotransporter KCC2 contributes to spasticity after spinal cord injury
DOI: 10.1038/nm.2107
NATURE METHODS (http://www.nature.com/nmeth)
[35] Atomic accuracy in predicting and designing non-canonical RNA structure
DOI: 10.1038/nmeth.1433
NATURE NANOTECHNOLOGY (http://www.nature.com/nnano)
[36] Single-molecule chemical reactions on DNA origami
DOI: 10.1038/nnano.2010.5
[37] Nanostructured films from hierarchical self-assembly of amyloidogenic proteins
DOI: 10.1038/nnano.2010.26
[38] Lipid multilayer gratings
DOI: 10.1038/nnano.2010.17
[39] Proposal for an all-spin logic device with built-in memory
DOI: 10.1038/nnano.2010.31
Nature NEUROSCIENCE (http://www.nature.com/natureneuroscience)
[40] A fast rod photoreceptor signaling pathway in the mammalian retina
DOI: 10.1038/nn.2507
[41] Intention and Attention: Different functional roles for LIPd and LIPv
DOI: 10.1038/nn.2496
[42] Resistance to forgetting associated with hippocampus-mediated reactivation during new learning
DOI: 10.1038/nn.2498
[43] Observational fear learning involves affective pain system and Cav1.2 Ca2+ channels in ACC
DOI: 10.1038/nn.2504
NATURE PHOTONICS (http://www.nature.com/nphoton)
[44] Real-time full-field arbitrary optical waveform measurement
DOI: 10.1038/nphoton.2010.28
[45] Experimental realization of sub-shot-noise quantum imaging
DOI: 10.1038/nphoton.2010.29
Nature PHYSICS (http://www.nature.com/naturephysics)
[46] Quantum register based on coupled electron spins in a room-temperature solid
DOI: 10.1038/nphys1536
[47] Superconducting quantum interference proximity transistor
DOI: 10.1038/nphys1537
[48] Two-orbital SU(N) magnetism with ultracold alkaline-earth atoms
DOI: 10.1038/nphys1535
Nature STRUCTURAL & MOLECULAR BIOLOGY (http://www.nature.com/natstructmolbiol)
[49] T-cadherin structures reveal a novel adhesive binding mechanism
DOI: 10.1038/ nsmb.1781
[50] Two-step adhesive binding by classical cadherins
DOI: 10.1038/ nsmb.1784
****************************************************************************
***The following paper will be published electronically on Nature’s website on 23 February at 1800 London time / 1300 US Eastern time. This paper will be under embargo until this time. The rest of the articles on this release remain under embargo until 28 February at 1800 London time / 1300 US Eastern time ***
[51] RAF inhibitors transactivate RAF dimers and ERK signalling in cells with wild-type BRAF
DOI: 10.1038/nature08902
****************************************************************************
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
Clayton: 6
Parkville: 4, 6
Perth: 33
Sydney: 33, 46
AUSTRIA
Innsbruck: 48
Vienna: 17
BELGIUM
Louvain-la-Neuve: 23
CANADA:
Hamilton: 21
Montreal: 8
Vancouver: 21
Waterloo: 21
CHINA
Lanzhou: 30
Nanjing: 25
CROATIA
Zagreb: 22
DENMARK
Aarhus: 36
FINLAND
Aalto: 47
Helsinki: 2
Tampere: 2
FRANCE
Marseille: 4, 34
Strasbourg: 34
Talence: 34
GERMANY
Bochum: 20, 46
Bonn: 6
Cologne: 20
Dresden: 9
Düsseldorf: 6
Hamburg: 6
Heidelberg: 36
Jena: 16
Julich: 31
Karlsruhe: 38
Munich: 20
Munster: 38
Potsdam: 24
Regensburg: 16
Rostock: 22
Stuttgart: 46
Tubingen: 22
Wuppertal: 33
HUNGARY
Budapest: 2
Debrecen: 2
INDIA
Varanasi: 30
IRELAND
Dublin: 2
ISRAEL
Haifa: 22
ITALY
Foggia: 2
Genoa: 22
Milan: 2
Monza: 2
Naples: 2
Pisa: 47
Rome: 2
Turin: 45
JAPAN
Osaka: 4
Saitama: 11
Tokyo: 11
Tsukuba: 30
NETHERLANDS
Groningen: 2
Leiden: 2
Nieuwegein: 20
Utrecht: 2
POLAND
Warsaw: 2
RUSSIA
Moscow: 9
SLOVAKIA
Kosice: 34
SOUTH KOREA
Gwangju: 38
Seoul: 43
SPAIN
Madrid: 2
SWEDEN
Stockholm: 13
SWITZERLAND
Basel: 34
Davos: 24
Zurich: 5
TURKEY
Ankara: 22
Bursa: 22
UNITED KINGDOM
Ascot: 46
Birmingham: 22
Cambridge: 2, 37
London: 2, 22, 32, 50
UNITED STATES OF AMERICA
California
Berkeley: 28, 39, 51
Davis: 44
Duarte: 2
La Jolla: 4, 10, 34, 49
Los Angeles: 2
Pasadena: 12
Sacramento: 26
San Francisco: 9, 26, 51
Stanford: 35, 42
Colorado
Aurora: 51
Boulder: 48
Florida
Homestead: 1
Tallahassee: 29, 30, 38
Tampa: 17
Georgia
Augusta: 33
Illinois
Chicago: 40
Evanston: 18
Urbana: 7
Indiana
West Lafayette: 39
Kansas
Lawrence: 35
Maryland
Baltimore: 5
Bethesda: 22, 40
Gaithersburg: 48
Massachusetts
Boston: 6, 33, 43
Cambridge: 12, 48
Worcester: 33
Michigan
Ann Arbor: 28, 29
Minnesota
Rochester: 2
Missouri
St Louis: 27, 41
New Jersey
New Brunswick: 19
Princeton: 15
Rahway: 27
New York
Cold Spring Harbor: 14
Ithaca: 32
New York: 14, 49, 50, 51
North Carolina
Durham: 14
Ohio
Columbus: 1
Dayton: 1
Pennsylvania
Philadelphia: 22
University Park: 3, 28
Tennessee
Nashville: 34, 43
Texas
College Station: 25
Houston: 30
Prairie View: 30
Utah
Provo: 6
Salt Lake City: 9, 30
Washington
Seattle: 14, 24, 35
Wisconsin
Madison: 15, 28, 29
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 9288; E-mail: [email protected]
Nature Cell Biology (London)
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Tel: +44 20 7843 4656; E-mail: [email protected]
Nature Chemical Biology (Boston)
Sarah Daniels
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)
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Tel: +1 212 726 9325; E-mail: [email protected]
Nature Methods (New York)
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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)
Sabbi Lall
Tel: +1 212 726 9326; E-mail: [email protected]
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