NATURE AND THE NATURE RESEARCH JOURNALS PRESS RELEASE
For papers that will be published online on 20 February 2011
This press release is copyrighted to the Nature journals mentioned below.
This press release contains:
Summaries of newsworthy papers:
Medicine: Detecting TB
Neuroscience: Understanding relapse
Immunology: Maintaining calm in the gut
Cell Biology: p53 mutations affect cancer cell metabolism
Cell Biology: Fine-tuning the DNA damage response for survival
And finally…Geoscience: Early Cretaceous warmth
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] Medicine: Detecting TB
DOI: 10.1038/nm.2299
An assay that can rapidly distinguish latent infection from active disease with Mycobacterium tuberculosis (Mtb) bacteria is reported this week in Nature Medicine. This new method could enable more timely clinical diagnosis and treatment of infected individuals with active tuberculosis disease.
Present assays for Mtb are time-consuming, and a correct diagnosis can take weeks. Giuseppe Pantaleo and colleagues show that using polychromatic flow cytometry—which is a technique for detecting cells labeled with five or more fluorochromes—latent infection can be distinguished from active disease in individuals based on the profile of their Mtb-specific CD4+ T immune cell responses. Individuals with latent disease show polyfunctional Mtb-specific CD4+ T cell responses, whereas individuals with active disease have largely monofunctional T cell responses.
The authors identify a cut-off value that can be used to predict infection status: individuals with more than 38.8% of T cells that are monofunctional are predicted to have active disease, whereas individuals with less than 38.8% of T cells showing a monofunctional profile are predicted to have latent disease.
Author contact:
Giuseppe Pantaleo (University of Lausanne, Switzerland)
Tel:+41 21 31 41063; E-mail: [email protected]
[2] Neuroscience: Understanding relapse
DOI: 10.1038/nn.2758
A study published this week in Nature Neuroscience provides causal evidence that the propensity to relapse back to heroin use is controlled by a small subset of medial prefrontal cortex (mPFC) neurons. These findings using rodent models of addiction could be important in understanding how to treat human addicts to lessen the likelihood of relapse.
Both rodents and humans form an association between addictive substance use and the context in which the addictive drugs were taken. Addicts are prone to relapse when re-exposed to the drug-associated contextual cues.
Yavin Shaham and colleagues show that a small group of neurons in mPFC exhibit higher activity when rats previously trained to self-administer heroin are re-introduced to the context in which drug was taken. By administrating a pharmacological agent that selectively disrupts these activated neurons, the scientists also show that inactivating these specific mPFC neurons can lessen the reinstatement of heroin-seeking behavior in relapsing rats.
Author contact:
Yavin Shaham (National Institute on Drug Abuse, Baltimore, MD, USA)
Tel: +1 442 740 2723; E-mail: [email protected]
[3] Immunology: Maintaining calm in the gut
DOI: 10.1038/ni.2002
The interplay between intestinal immune cells and gut microbes protects the intestine and prevents excessive tissue damage due to inflammatory immune responses, reports a study published online this week in Nature Immunology.
Although we are born with a sterile gut, beneficial bacteria and other microbes soon colonize, which necessitates a symbiotic relationship with these gut inhabitants. Gérard Eberl and colleagues show newborn or germ-free mice have innate immune cells that express abundant amounts of the immune molecule IL-22 in their gut. IL-22 induces the production of antimicrobial substances by cells lining the gut, a process that is blocked upon bacterial colonization by the production of another immune molecule, IL-25.
Intestinal damage, as can occur upon infection with gut pathogens or ingestion of toxic chemicals, activates IL-22 expression and production of antimicrobial proteins and speeds recovery to a ‘calm’ gut.
Author contact:
Gérard Eberl (Institut Pasteur, Paris, France)
Tel: +33 1 4438 9446; E-mail: [email protected]
[4] Cell Biology: p53 mutations affect cancer cell metabolism
DOI: 10.1038/ncb2172
The loss of the tumour suppressor protein p53 might underlie cancer cells' ability to undergo a metabolic switch that supports rapid proliferation in the face of limited availability of nutrients. This finding, reported online this week in Nature Cell Biology, reinforces the importance of p53 loss in the development of cancer.
p53 is known to modulate cancer cell metabolism by regulating gene transcription within the nucleus. Xiaolu Yang and colleagues recognized that cells lacking functional p53 consumed large quantities of glucose through the ox-PPP pathway, which supports the biosynthesis of new cellular building blocks from glucose and is critical for cancer cell proliferation.
They found that p53 interacts with a key enzyme in the ox-PPP pathway outside of the nucleus. The authors conclude that p53 normally inhibits this enzyme to block the ox-PPP pathway, but that loss of p53 removes this block and activates the pathway. In an accompanying News & Views article, Eyal Gottlieb notes that this "effect of p53…is intriguing as it proposes a catalytic (enzymatic) role for p53 in the cytosol."
Author contact:
Xiaolu Yang (University of Pennsylvania School of Medicine, Philadelphia, PA, USA)
Tel: +1 215 573 6739; E-mail: [email protected]
Eyal Gottlieb (The Beatson Institute for Cancer Research, Glasgow, UK) N&V author
Tel: +44 141 3303981; E-mail: [email protected]
[5] Cell Biology: Fine-tuning the DNA damage response for survival
DOI: 10.1038/ncb2170
Specialised large regions of inactive DNA and protein complexes may provide a sophisticated mechanism for defective cells to survive, reports a paper published online this week in Nature Cell Biology. These findings could have potential implications in cancer.
DNA damage triggers cells to die, or to stop dividing but remain alive in a dormant state known as cellular senescence. Senescent cells are marked by large-scale inactive DNA and protein complexes, known as Senescence-associated heterochromatic foci (SAHF), the function of which has remained unclear.
Fabrizio d’Adda di Fagagna and colleagues find that SAHF controls the level of the cell’s response to DNA damage. The presence of SAHF dampens the response to damaged DNA to sublethal levels, permitting cells to stop dividing and become senescent rather than die. The implication is that such cells could acquire additional changes over time, allowing them to bypass the proliferative arrest of senescence and to resume cell division, leading to cancer.
In accordance with this idea, SAHF is found in human cancers and a compound that removes SAHF from cancer cells also potentiates the DNA damage response and increases cell death. The researchers propose that these findings may prove important for cancer research, as they could be therapeutically exploited.
Author contact:
Fabrizio d’Adda di Fagagna (IFOM Foundation - FIRC Institute of Molecular Oncology Foundation, Milan, Italy)
Tel: +39 02 574303 227; E-mail: [email protected]
[6] And finally…Geoscience: Early Cretaceous warmth
DOI: 10.1038/ngeo1081
Sea surface temperatures during the early Cretaceous period, about 142–128 million years ago, were warmer than previously thought, and at least five degrees Celsius warmer than today, according to a paper published online this week in Nature Geoscience.
Kate Littler and colleagues used organic compounds preserved in marine sediments to reconstruct sea surface temperatures from sites in the North Atlantic and Indian oceans. They found that temperatures were generally warm and stable throughout the 14-million-year period. Moreover, the temperature difference between the mid- and low-latitudes was minimal, relative to that found today. This was mostly the result of unusual warmth in the North Atlantic, with temperatures about 16 degrees Celsius warmer than at present.
Author contact:
Kate Littler (University College London, UK)
Tel: +44 77 2500 0894; 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 CELL BIOLOGY (http://www.nature.com/naturecellbiology)
[7] How APC/C–Cdc20 changes its substrate specificity in mitosis
DOI: 10.1038/ncb2165
[8] Calcineurin ensures a link between the DNA replication checkpoint and microtubule-dependent polarized growth
DOI: 10.1038/ncb2166
[9] Klotho suppresses RIG-I-mediated senescence-associated inflammation
DOI: 10.1038/ncb2167
[10] Inactivation of Rheb by PRAK-mediated phosphorylation is essential for
energy-depletion-induced suppression of mTORC1
DOI: 10.1038/ncb2168
[11] Oncogenic Ras abrogates MEK SUMOylation that suppresses the ERK pathway and cell transformation
DOI: 10.1038/ncb2169
[12] Stat3 controls lysosomal-mediated cell death in vivo
DOI: 10.1038/ncb2171
[13] p53 regulates epithelial–mesenchymal transition and stem cell properties through modulating miRNAs
DOI: 10.1038/ncb2173
[14] A non-genetic route to aneuploidy in human cancers
DOI: 10.1038/ncb2174
[15] Developmental roles for Srf, cortical cytoskeleton and cell shape in epidermal spindle orientation
DOI: 10.1038/ncb2163
NATURE CHEMICAL BIOLOGY (http://www.nature.com/nchembio)
[16] Navigating the kinome
DOI: 10.1038/nchembio.530
[17] Glycolytic intermediates induce amorphous calcium carbonate formation in crustaceans
DOI: 10.1038/nchembio.532
NATURE CHEMISTRY (http://www.nature.com/nchem)
[18] The role of long-lived reactive oxygen intermediates in the reaction of ozone with aerosol particles
DOI: 10.1038/nchem.988
[19] A renewable amine for photochemical reduction of CO2
DOI: 10.1038/nchem.1000
NATURE GENETICS (http://www.nature.com/naturegenetics)
[20] Association of a functional variant downstream of TNFAIP3 with systemic lupus erythematosus
DOI: 10.1038/ng.766
[21] The draft genome of the parasitic nematode Trichinella spiralis
DOI: 10.1038/ng.769
NATURE GEOSCIENCE (http://www.nature.com/ngeo)
[22] Haematite pseudomicrofossils present in the 3.5-billion-year-old Apex Chert
DOI: 10.1038/ngeo1084
[23] Reconciling the hemispherical structure of Earth’s inner core with its super-rotation
DOI: 10.1038/ngeo1083
[24] Metal flux from hydrothermal vents increased by organic complexation
DOI: 10.1038/ngeo1088
NATURE MATERIALS (http://www.nature.com/naturematerials)
[25] Interbilayer-crosslinked multilamellar vesicles as synthetic vaccines for potent humoral and cellular immune responses
DOI: 10.1038/nmat2960
[26] Observation of the intrinsic pinning of a magnetic domain wall in a ferromagnetic nanowire
DOI: 10.1038/nmat2961
NATURE MEDICINE (http://www.nature.com/naturemedicine)
[27] Assessment of atherosclerotic plaque burden with an elastin-specific magnetic resonance contrast agent
DOI: 10.1038/nm.2310
[28] Mutant huntingtin binds the mitochondrial fission GTPase dynamin-related protein-1 and increases its enzymatic activity
DOI: 10.1038/nm.2313
NATURE METHODS (http://www.nature.com/nmeth)
[29] Ultra-high resolution optical trap with single fluorophore sensitivity
DOI: 10.1038/nmeth.1574
NATURE NANOTECHNOLOGY (http://www.nature.com/nnano)
[30] Giant magnetoresistance through a single molecule
DOI: 10.1038/nnano.2011.11
[31] Controlling protein translocation through nanopores with bio-inspired fluid walls
DOI: 10.1038/nnano.2011.12
[32] Nanoporous metal/oxide hybrid electrodes for electrochemical supercapacitors
DOI: 10.1038/nnano.2011.13
[33] Controlling single-molecule conductance through lateral coupling of pi orbitals
DOI: 10.1038/nnano.2011.20
NATURE NEUROSCIENCE (http://www.nature.com/natureneuroscience)
[34] Cocaine inverts rules for synaptic plasticity of glutamate transmission in the VTA
DOI: 10.1038/nn.2763
[35] Transfection via whole-cell recording in vivo: Bridging single-cell physiology, genetics and connectomics
DOI: 10.1038/nn.2765
[36] Lasting synaptic changes underlie attention deficits caused by nicotine exposure during adolescence
DOI: 10.1038/nn.2770
NATURE PHOTONICS (http://www.nature.com/nphoton)
[37] Lensless X-ray imaging in reflection geometry
DOI: 10.1038/nphoton.2011.11
[38] Full-colour quantum dot displays fabricated by transfer printing
DOI: 10.1038/nphoton.2011.12
[39] Hybrid semiconductor-atomic interface: slowing down single photons from a quantum dot
DOI: 10.1038/nphoton.2011.16
NATURE PHYSICS (http://www.nature.com/naturephysics)
[40] Leidenfrost on a ratchet
DOI: 10.1038/nphys1925
[41] Frustrated nematic order in spherical geometries
DOI: 10.1038/nphys1920
[42] Quantum simulation of the wavefunction to probe frustrated Heisenberg spin systems
DOI: 10.1038/nphys1919
[43] Current quantization in an optically driven electron pump based on self-assembled quantum dots
DOI: 10.1038/nphys1918
NATURE STRUCTURAL & MOLECULAR BIOLOGY (http://www.nature.com/natstructmolbiol)
[44] Structural basis for allosteric regulation of human ribonucleotide reductase by nucleotide-induced oligomerization
DOI: 10.1038/nsmb.2007
[45] Structural basis of signal-sequence recognition by the signal recognition particle
DOI: 10.1038/nsmb.1994
[46] Mapping of INS promoter interactions reveals its role in long-range regulation of SYT8 transcription
DOI: 10.1038/nsmb.1993
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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.
ARGENTINA
Rosario: 20
AUSTRIA
Salzburg: 28
Vienna: 42
CANADA:
London: 20
Montreal: 28
Toronto: 18
Vancouver: 28
CHINA
Beijing: 9, 10
Hefei: 4
Nanjing: 4
Shanghai: 33
Xiaman: 10
COLOMBIA
Bogota: 20
FRANCE
Palaiseau: 40
Paris: 3, 34, 40
Strasbourg: 30
GERMANY
Berlin: 27
Bremen: 24
Dresden: 39
Hannover: 3
Heidelberg: 35
Karlsruhe: 30
Mainz: 18, 33
GREECE
Athens: 5
ITALY
Milan: 5
Turin: 12
JAPAN
Chiba: 30
Gunma: 17
Hiroshima: 8
Ibaraki: 17
Kanagawa: 26
Kyoto: 26
Nagoya: 11
Saitama: 26
Sendai: 32
Tokyo: 11, 17, 26
KOREA
Seoul: 20, 38
Yongin: 38
NETHERLANDS
Amsterdam: 5, 36
Delft: 39
Leiden: 41
NEW ZEALAND
Dunedin: 24
PUERTO RICO
San Juan: 20
SPAIN
Barcelona: 33
Granada: 20
SOUTH AFRICA
Cape Town: 1
SWEDEN
Stockholm: 44
Umea: 45
Uppsala: 20
SWITZERLAND
Bern: 18
Geneva: 34
Lausanne: 1
Villigen: 18, 43
Zurich: 43
TAIWAN
Taichung: 13
UNITED KINGDOM
Bristol: 6
Cardiff: 12, 19
Cambridge: 7, 12, 23, 38
London: 6, 8, 27, 35
Mill Hill: 35
UNITED STATES OF AMERICA
Alabama
Birmingham: 20
Arizona
Tempe: 33
Arkansas
Fayetteville: 31
California
Berkeley: 37
La Jolla: 10, 28
Los Angeles: 20
Menlo Park: 37
Palo Alto: 3
San Diego: 28, 31
San Francisco: 20
Stanford: 13
Colorado
Denver: 20
Connecticut
New Haven: 12
Florida
Orlando: 12, 28
Georgia
Atlanta: 41
Illinois
Abbott Park: 16
Chicago: 20
Urbana: 29
Kansas
Lawrence: 22
Maryland
Baltimore: 2, 20
Beltsville: 21
Bethesda: 46
Chevy Chase: 25
Gaithersburg: 44
Massachusetts
Boston: 5, 14, 25, 44
Cambridge: 25
North Billerica: 27
Michigan
Ann Arbor: 31
Missouri
St Louis: 21
New York
Ithaca: 21
Manhasset: 20
New York: 5, 14, 15, 35
North Carolina
Winston-Salem: 20
Ohio
Cincinnati: 20
Cleveland: 44
Oklahoma
Oklahoma City: 20
Pennsylvania
Philadelphia: 4
South Carolina
Charleston: 20
Tennessee
Knoxville: 44
Texas
Houston: 13, 20, 25
Washington
Pullman: 21
Seattle: 20
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)
Sowmya Swaminathan
Tel: +44 20 7843 4656; E-mail: [email protected]
Nature Chemical Biology (Boston)
Carrie Meggs
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 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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