This press release contains:
• Summaries of newsworthy papers:
Materials: Imaging bacterial infections
Geoscience: Earth’s heat flux from radioactive decay
Chemical Biology: Inactivating Ras
Immunology: Assembling the turn-off valve
Chemical Biology: A new channel for Polo delocalization
Climate Change: Conflict of interest in IPCC assessment reports
• Mention of papers to be published at the same time
• 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: Imaging bacterial infections
DOI: 10.1038/nmat3074
A family of highly sensitive contrast agents that enable in vivo imaging of bacterial infections in rats is presented in a study published online this week in Nature Materials. Such contrast agents could aid in the early clinical detection of bacterial infections, which could help people to avoid medical complications such as tissue damage or sepsis.
Bacteria are an important cause of various illnesses and sometimes death worldwide. The main challenge in imaging bacterial infections is in developing contrast agents that enter bacteria specifically and quickly.
Niren Murthy and colleagues achieved this by chemically attaching a fluorescent side group, the part of the molecule that creates the imaging contrast, to a specific type of carbohydrates that plays an important role in the metabolism of many bacteria. The researchers found that Escherichia coli and other species rapidly take up these metabolic fluorescent imaging probes, and that infections could be imaged with 100-fold improved sensitivity compared with previous contrast agents.
Author contact:
Niren Murthy (Georgia Institute of Technology, Atlanta, GA, USA)
Tel: +1 404 385 5145, E-mail: [email protected]
[2] Geoscience: Earth’s heat flux from radioactive decay
DOI: 10.1038/ngeo1205
Heat generated by the decay of radiogenic isotopes inside the planet contributes about half of total flux of heat from Earth into space, reports a paper published online this week in Nature Geoscience. The findings imply that the supply of residual primordial heat, left over after Earth formed, has not yet been exhausted.
Itaru Shimizu and colleagues, as part of the KamLAND Collaboration, measured the flux of geoneutrinos — electrically neutral particles that are emitted during radioactive decay of isotopes and can pass through the Earth virtually unaffected — using a detector in Japan. The researchers find that the radioactive decay of the elements uranium-238 and thorium-232 together contribute about 20 terawatts to the Earth’s outgoing heat flux. This value represents only about half of the total outgoing heat, implying that the remainder of the heat flux results from continued cooling of the Earth since its birth.
Author contact:
Itaru Shimizu (Tohoku University, Research Centre for Neutrino Science, Miyagi, Japan)
Tel: +81 22 795 6727; E-mail: [email protected]
[3] Chemical Biology: Inactivating Ras
DOI: 10.1038/nchembio.612
A peptide inhibitor that interferes with the activation of and signaling with Ras protein, a central component of many growth-promoting pathways in cells that can be hyperactivated in cancer or other diseases, is reported this week in Nature Chemical Biology. Strategies to inactivate or inhibit Ras-dependent signaling have proved elusive but would be beneficial for the treatment of many disorders.
The activity of Ras depends on protein-protein interactions with Sos, which converts Ras from an inactive to an active state. Sos is known to interact with Ras via a structural motif called an alpha helix. Synthetic mimics of the alpha helices on protein surfaces have emerged as a strategy for antagonizing protein-protein interactions.
Paramjit Arora, Dafna Bar-Sagi and colleagues engineered a peptide inhibitor, based on the Sos alpha helix, that interfered with Ras activation by Sos and blocked Ras-dependent signaling in cells. This study lends support to the notion that helical mimics are a viable approach for targeting protein-protein interaction interfaces and could provide the foundation for the development of Ras inhibitors for treatment of a variety of diseases.
Author contacts:
Paramjit Arora (New York University, NY, USA)
Tel: +1 212 998 8470; E-mail: [email protected]
Dafna Bar-Sagi (New York University, NY, USA)
Tel: +1 212 263 0637; E-mail: [email protected]
[4] Immunology: Assembling the turn-off valve
DOI: 10.1038/ni.2066
How immune cells turn off proinflammatory signaling is described in an online paper in Nature Immunology. These findings have implications in understanding the molecular basis by which the cancer-causing virus HTLV-1 can trigger T cell leukemia.
Inflammatory signaling pathways are tightly regulated as prolonged activation can cause tissue damage and is linked to the development of autoimmune diseases, such as rheumatoid arthritis, and some cancers, including colon cancers.
Edward Harhaj and colleagues show that the protein TAX1BP1 is crucial for formation of an intracellular protein complex that acts as a shut-off valve, stopping production of inflammatory mediators. The off-switch is triggered by kinase IKKalpha phosphorylation of TAX1BP1, which allows for the protein’s interaction with other components of the A20 editing complex that act to dissemble proinflammatory signaling platform.
Author contact:
Edward Harhaj (University of Miami, FL, USA)
Tel: +1 305 243 7893; E-mail: [email protected]
[5] Chemical Biology: A new channel for Polo delocalization
DOI: 10.1038/nchembio.614
Chemical modifications that create an inhibitor with high affinity for Polo-like kinase-1 (Plk1), an important molecule for the regulation of cell growth and proliferation, are reported this week in Nature Chemical Biology. Since PlK1 is a potential target for cancer treatment, these finding could have important clinical application.
Specifically targeting Plk1 has proven challenging, as there are hundreds of human kinases and they all share similar structural features. In addition to features shared among kinases, Plk1 has some unique domains important for functional interaction with other proteins. One of these domains, called a polo-box domain (PBD), is necessary for the proper localization of Plk1 inside of a cell. Previous studies have shown that displacing Plk1 from its proper site is sufficient to interfere with cell proliferation.
Terrence Burke and colleagues identified an inhibitor for Plk1 that interferes with the protein-protein interactions with PBD. Structural analysis revealed that the inhibitor exposed a new binding channel on the kinase. Identification of this new channel could inspire the design of new inhibitors for cancer treatment that selectively target Plk1.
Author contact:
Terrence Burke (National Cancer Institute, Frederick, MD, USA)
Tel: +1 301 846 5906; E-mail: [email protected]
[6] & [7] Climate Change: Conflict of interest in IPCC assessment reports
DOI: 10.1038/nclimate1177
DOI: 10.1038/nclimate1178
The publication in June of the Intergovernmental Panel on Climate Change (IPCC)’s Special Report on Renewable Energy Sources and Climate Change Mitigation (SRREN) was greeted by claims that it was biased because of a conflict of interest in the panel assessing the data. Two opinion articles published online this week in Nature Climate Change argue the case, and look ahead at the implementation of a new policy regulating assessment transparency and fairness in the IPCC.
UK-based climate change commentator and author Mark Lynas asserts that the involvement of Sven Teske, a Greenpeace campaigner, in the panel that assessed data — including Greenpeace reports — for inclusion in the SRREN report "gave the appearance that he might have had an unfair influence over the content of the report." The bias issue chips away at the credibility of the SRREN report, Lynas argues.
In response, Ottmar Edenhofer — who is Co-Chair of Working Group III, which produced the SRREN report — says that including Teske helps reflect the wide range of scientifically credible views on the topics it assesses. Edenhofer says that IPCC's experts consider large bodies of literature that "will often include some of their own work as leading experts in an area will have contributed to the relevant literature." This does not represent a conflict of interest, he says.
Author contacts:
Mark Lynas (Journalist, Oxford, UK) Author paper [6]
Tel: +44 7811 456824; E-mail: [email protected]
Ottmar Edenhofer (Potsdam Institute of Climate Impact Research, Potsdam, Germany) Author paper [7]
Tel: +49 331 288 2565; E-mail: [email protected]
Items from other Nature journals to be published online at the same time
Nature (http://www.nature.com/nature)
[8] The crystal structure of GXGD membrane protease FlaK
DOI: 10.1038/nature10218
[9] A two-step chemical mechanism for ribosome-catalysed peptide bond formation
DOI: 10.1038/nature10248
[10] Photoentrainment and pupillary light reflex are mediated by distinct populations of ipRGCs
DOI: 10.1038/nature10206
[11] Control of TH17 cells occurs in the small intestine
DOI: 10.1038/nature10228
NATURE BIOTECHNOLOGY (http://www.nature.com/naturebiotechnology)
[12] Bright and stable near-infrared fluorescent protein for in vivo imaging
DOI: 10.1038/nbt.1918
NATURE CELL BIOLOGY (http://www.nature.com/naturecellbiology)
[13] A role for CSLD3 during cell-wall synthesis in apical plasma membranes of tip-growing root-hair cells
DOI: 10.1038/ncb2294
NATURE CHEMICAL BIOLOGY (http://www.nature.com/nchembio)
[14] Chemical genetics identify eIF2alpha kinase heme-regulated inhibitor as an anti-cancer target
DOI: 10.1038/nchembio.613
NATURE CHEMISTRY (http://www.nature.com/nchem)
[15] Tirandamycin biosynthesis is mediated by co-dependent oxidative enzymes
DOI: 10.1038/nchem.1087
NATURE GENETICS (http://www.nature.com/naturegenetics)
[16] NBEAL2 is mutated in gray platelet syndrome and is required for biogenesis of platelet alpha-granules
DOI: 10.1038/ng.883
[17] Exome sequencing identifies NBEAL2 as the causative gene for gray platelet syndrome
DOI: 10.1038/ng.885
[18] Mutations in NBEAL2, encoding a BEACH protein, cause gray platelet syndrome
DOI: 10.1038/ng.884
NATURE GEOSCIENCE (http://www.nature.com/ngeo)
[19] Magmatic breakup as an explanation for magnetic anomalies at magma-poor rifted margins
DOI: 10.1038/ngeo1201
NATURE IMMUNOLOGY (http://www.nature.com/natureimmunology)
[20] The tumor suppressor Tsc1 enforces quiescence of naive T cells to promote immune homeostasis and function
DOI:10.1038/ni.2068
NATURE MATERIALS (http://www.nature.com/naturematerials)
[21] Nanoscale surfaces for the long-term maintenance of mesenchymal stem cell phenotype and multipotency
DOI: 10.1038/nmat3058
[22] Kinetics of non-equilibrium lithium incorporation in LiFePO4
DOI: 10.1038/nmat3065
[23] Tailoring hot-exciton emission and lifetimes in semiconducting nanowires via whispering-gallery nanocavity plasmons
DOI: 10.1038/nmat3067
Nature MEDICINE (http://www.nature.com/naturemedicine)
[24] DNA released from dying host cells mediates aluminum adjuvant activity
DOI: 10.1038/nm.2403
[25] Protective HIV-specific CD8+ T cells evade Treg cell suppression
DOI: 10.1038/nm.2422
NATURE METHODS (http://www.nature.com/nmeth)
[26] Bayesian community-wide culture-independent microbial source tracking
DOI: 10.1038/nmeth.1650
[27] Deep and fast live imaging with two-photon scanned light-sheet microscopy
DOI: 10.1038/nmeth.1652
[28] High frequency genome editing using ssDNA oligonucleotides with zinc finger nucleases
DOI: 10.1038/nmeth.1653
NATURE NANOTECHNOLOGY (http://www.nature.com/nnano)
[29] Cell-surface sensors for real-time probing of cellular environments
DOI: 10.1038/nnano.2011.101
Nature NEUROSCIENCE (http://www.nature.com/natureneuroscience)
[30] Adaptation of the simple or complex nature of V1 receptive fields to visual statistics
DOI: 10.1038/nn.2861
[31] Generalized associative representations in parietal cortex
DOI: 10.1038/nn.2878
[32] Loss of activity-induced phosphorylation of MeCP2 enhances synaptogenesis, LTP, and spatial memory
DOI: 10.1038/nn.2866
[33] Mammalian glial cells missing genes induce Hes5 expression by active DNA demethylation and induce neural stem cells
DOI: 10.1038/nn.2875
[34] Precise olfactory responses tile the sniff cycle
DOI: 10.1038/nn.2877
[35] Differential tuning and population dynamics of excitatory and inhibitory neurons reflect differences in local intracortical connectivity
DOI: 10.1038/nn.2876
NATURE PHOTONICS (http://www.nature.com/nphoton)
[36] Past achievements and future challenges in the development of three-dimensional photonic metamaterials
DOI: 10.1038/nphoton.2011.154
Nature PHYSICS (http://www.nature.com/naturephysics)
[37] Visualizing the local optical response to extreme-ultraviolet radiation with a resolution of l /380
DOI: 10.1038/nphys2044
Nature STRUCTURAL & MOLECULAR BIOLOGY (http://www.nature.com/natstructmolbiol)
[38] Crystal structure of a chaperone-bound assembly intermediate of form I Rubisco
DOI: 10.1038/nsmb.2090
[39] Condensin structures chromosomal DNA through topological links
DOI: 10.1038/nsmb.2087
[40] A RING E3-substrate complex poised for ubiquitin-like protein transfer: structural insights into cullin-RING ligases
DOI: 10.1038/nsmb.2086
[41] Transcription Initiation Platforms and GTF recruitment at tissue specific enhancers and promoters
DOI: 10.1038/nsmb.2085
***The following paper was published electronically on Nature Biotechnology’s website on 07 July and is therefore no longer under embargo. The rest of the above articles on this release remain under embargo until 17 July at 1800 London time / 1300 US Eastern time ***
[42] Genetic engineering of human pluripotent cells using TALE nucleases
DOI: 10.1038/nbt.1927
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:
London: 35
Toronto: 18
DENMARK
Copenhagen: 28
FRANCE
Evry: 41
Gif-sur-Yvette: 30
Marseille: 17, 41
Orsay: 30
Palaiseau: 27
Paris: 17, 41
Pessac: 17
Strasbourg: 19
Villejuif: 17
GERMANY
Berlin: 11
Hamburg: 11
Heidelberg: 39
Karlsruhe: 36
Leipzig: 5
Martinsried: 38
Munich: 41
Munster: 16, 41
Potsdam: 7
GREECE
Crete: 36
ISRAEL
Haifa: 16
Naharia: 16
Tel-Aviv: 16
ITALY
Milan: 11
Rovereto: 31
JAPAN
Hyogo: 37
Nagoya: 37
Okazaki: 33
Osaka: 24
Saitama: 33, 37
Sendai: 2
Tokyo: 2, 11, 33
NETHERLANDS
Amsterdam: 2, 11, 17
NORWAY
Trondheim: 19
SPAIN
Barcelona: 41
SAUDI ARABIA
Riyadh: 21
TURKEY
Ankara: 16
UNITED KINGDOM
Cambridge: 17, 42
Glasgow: 21
Oxford: 6
Southampton: 21
UNITED STATES OF AMERICA
Alabama
Tuscaloosa: 2
California
Berkeley: 2
Los Angeles: 11, 22
Pasadena: 2, 27
Richmond: 42
San Diego: 26
San Francisco: 11, 15, 28
Stanford: 2
Colorado
Aurora: 18
Boulder: 26
Connecticut
New Haven: 8, 9, 11
Florida
Miami: 4
Georgia
Athens: 1
Atlanta: 1, 18
Hawaii
Honolulu: 2
Illinois
Argonne: 40
Evanston: 34
Chicago: 31
Iowa
Ames: 36
Iowa City: 18
Kansas
Manhattan: 2
Louisiana
New Orleans: 11
Maryland
Baltimore: 10, 35
Bethesda: 5, 10, 16
Chevy Chase: 26
Frederick: 5
Massachusetts
Boston: 11, 14, 29, 31
Cambridge: 5, 9, 22, 29
Michigan
Ann Arbor: 13, 15
East Lansing: 18
Minnesota
Minneapolis: 16
Missouri
St Louis: 28
New York
Albany: 9
Bronx: 12
Cold Spring Harbor: 34
New York: 3
North Carolina
Chapel Hill: 2, 11
Durham: 2
Ohio
Cleveland: 4
Oklahoma
Enid: 18
Pennsylvania
Hershey: 16
Philadelphia: 2, 23, 26
Tennessee
Knoxville: 2
Memphis: 20, 40
Utah
Salt Lake City: 18
Virginia
Ashburn: 34
Washington
Seattle: 25, 35
Wisconsin
Madison: 2, 18, 32
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)
Elissa Bolt
Tel: +1 617 475 9241, E-mail: [email protected]
Nature Chemistry (London)
Stuart Cantrill
Tel: +44 20 7014 4018; E-mail: [email protected]
Nature Climate Change (London)
Olive Heffernan
Tel: +44 20 7014 4009; 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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