NATURE AND THE NATURE RESEARCH JOURNALS PRESS RELEASE
For papers that will be published online on 11 November 2007
This press release is copyrighted to the Nature journals mentioned below.
This press release contains:
· Summaries of newsworthy papers:
Ocean carbon: The effects of acidification – Nature
Testing time – Nature Physics
A new virulence mechanism for MRSA – Nature Medicine
Genetic mutation in familial aortic aneurysm – Nature Genetics
Regulating immune suppression – Nature Immunology
Stalling chemotherapy damage – Nature Structural and Molecular Biology
Controlling protein stability in parasites – Nature Methods
· 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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PLEASE CITE THE SPECIFIC NATURE JOURNAL AND WEBSITE AS THE SOURCE OF THE FOLLOWING ITEMS. IF PUBLISHING ONLINE, PLEASE CARRY A HYPERLINK TO THE APPROPRIATE JOURNAL’S WEBSITE.
****************************************************NATURE************************************************
(http://www.nature.com/nature)
[1] Ocean carbon: The effects of acidification
DOI: 10.1038/nature06267
A new experiment carried out in the fjords of Norway gives insight into the effects on the oceans of rising atmospheric carbon dioxide levels over the next 150 years. The results show that, in an ocean with a greater acid content resulting from absorbance of atmospheric carbon, organisms such as plankton will potentially increase their growth and consumption rates, which could in turn influence climate processes.
The research shows the importance of biological systems in the changing oceans, say U. Riebesell and colleagues, who report the study in this week’s Nature. In their experiment, they sealed off areas of the Raune Fjord in southern Norway, and exposed the waters to air containing levels of carbon dioxide reflecting those of today, as well as those expected in 2100 and in 2150. Higher acidity led to increased consumption by plankton, as well as to changes in the chemical balances and mixing patterns of the waters.
Author contact:
Ulf Riebesell (Leibniz Institute of Marine Sciences, Kiel, Germany)
Tel: +49 431600 458; E-mail: [email protected]
Other papers from Nature to be published online at the same time and with the same embargo:
[2] The SRA protein Np95 mediates epigenetic inheritance by recruiting Dnmt1 to methylated DNA
DOI: 10.1038/nature06397
***********************************************NATURE PHYSICS*****************************************
(http://www.nature.com/naturephysics)
[3] Testing time
DOI: 10.1038/nphys778
The most precise test of time dilation so far is reported online this week in Nature Physics by Sascha Reinhardt and colleagues. Their results confirm the validity of Einstein’s special theory of relativity and provide important benchmarks for practical applications, such as the Global Positioning System (GPS).
Time dilation means that a clock that is in motion ticks more slowly than an identical clock at rest. For example, if one of two twins travelled at high speed through space, upon return to Earth he would be younger than his twin – this thought experiment is known as the Twin Paradox. Instead of twins, Reinhardt et al. use two atoms that they bring to speeds of around 10,000 km s–1 in an accelerator ring. The ‘age’ of the atoms can be determined with high precision by measuring their internal states using a laser-based method pioneered by one of the authors, 2005 Nobel laureate Theodor Hänsch.
The effect of time dilation has to be factored in to accurately determine location using GPS, which is based on satellites orbiting the Earth. GPS satellites in turn can be used to measure time dilation, but Reinhardt et al. claim that their experiment is the first time-dilation test that exceeds the sensitivity obtained from GPS data.
Author contact:
Gerald Gwinner (University of Manitoba, Winnipeg, Canada)
Tel: +1 204 474 9856; E-mail: [email protected]
Other papers from Nature Physics to be published online at the same time and with the same embargo:
[4] Observation of energetic electrons within magnetic islands
DOI: 10.1038/nphys777
[5] Coherent superposition of laser-driven soft-X-ray harmonics from successive sources
DOI: 10.1038/nphys775
*******************************************Nature MEDICINE********************************************
(http://www.nature.com/naturemedicine)
[6] A new virulence mechanism for MRSA
DOI: 10.1038/nm1656
Strains of methicillin-resistant staphylococcus aureus (MRSA) that are acquired in the community may be more virulent than hospital-associated strains because they secrete small peptides that disable immune cells, as reported this week in Nature Medicine.
The majority of infections seen in the emergency room in the US are due to community-associated (CA) MRSA. Some strains of CA-MRSA can be especially virulent, causing sepsis and skin infections. Michael Otto and colleagues found that CA-MRSA strains produce much higher levels of a cluster of small peptides — called phenol soluble modulins — than strains of bacteria acquired from hospitals. The authors showed that mutant bacteria that couldn’t make these peptides were much less virulent in mice.
The peptides seem to have several functions that allow the bacteria to cause severe disease: they contribute to activation of inflammation, and also kill neutrophils and red blood cells. As neutrophils are key immune cells involved in clearing bacterial infections, secretion of phenol soluble modulins seems to be one way that CA-MRSA evades elimination by the immune system
Author contact:
Michael Otto (NIAID, Hamilton, MT, USA)
Tel: +1 406 363 9283; E-mail: [email protected]
Other papers from Nature Medicine to be published online at the same time and with the same embargo:
[7] Acid-sensing ion channel-1 contributes to axonal degeneration in autoimmune inflammation of the central nervous system
DOI: 10.1038/nm1668
***********************************************NATURE GENETICS **************************************
(http://www.nature.com/naturegenetics)
[8] Genetic mutation in familial aortic aneurysm
DOI: 10.1038/ng.2007.6
Mutations in a gene expressed in smooth muscle cells account for about 14% of cases of hereditary thoracic aortic aneurysm, reports a paper published online this week in Nature Genetics. A thoracic aortic aneurysm is a widening of the wall of the aorta—the body’s largest artery—and can lead to heart attack and stroke.
About one in five of all individuals affected by thoracic aortic aneurysms and dissections (TAAD) have a family history of the disorder, suggesting a genetic predisposition. Only two genes have been implicated in familial cases of TAAD so far, and they account for only about 5% of such cases. Dianna Milewicz and colleagues mapped the gene causing a novel form of TAAD in a large family, and identified mutations in ACTA2, encoding smooth muscle alpha-actin. Mutations in ACTA2 were also identified in individuals in 14 additional families affected by TAAD.
Smooth muscle alpha-actin is the most abundant protein found in smooth muscle cells, which are required for contraction of the aorta and other blood vessels in the regulation of blood pressure and flow. One of the other proteins associated with TAAD, MYH11, interacts with ACTA2 in regulating smooth muscle cell contraction, and the authors suggest that this process must be critical in maintaining the structural integrity of the aorta. It is not known whether mutations in ACTA2 are involved in non-familial cases of TAAD.
Author contact:
Dianna Milewicz (University of Texas Health Science Center, Houston, TX, USA)
Tel: +1 713 500 6715; E-mail: [email protected]
Other papers from Nature Genetics to be published online at the same time and with the same embargo:
[9] Mutations in LMF1 cause combined lipase deficiency and severe hypertriglyceridemia
DOI: 10.1038/ng.2007.24
[10] RNA polymerase is poised for activation across the genome
DOI: 10.1038/ng.2007.21
[11] RNA polymerase stalling at developmental control genes in the Drosophila melanogaster embryo
DOI: 10.1038/ng.2007.26
[12] PU.1 is a major downstream target of AML1 (RUNX1) in adult mouse hematopoiesis
DOI: 10.1038/ng.2007.7
*******************************************NATURE IMMUNOLOGY ************************************
(http://www.nature.com/natureimmunology)
[13], [14], [15], & [16] Regulating immune suppression
DOI: 10.1038/ni1537
DOI: 10.1038/ni1539
DOI: 10.1038/ni1540
DOI: 10.1038/ni1541
A quartet of papers in the December issue of Nature Immunology show how white blood cells produce interleukin 10, a chemical mediator that helps keep the immune response in check. This response is vital in fighting autoimmune conditions such as colitis, multiple sclerosis and arthritis.
Four separate groups led by Christopher Hunter, Daniel Cua, Abdolmohamad Rostami and Mohamed Oukka showed a certain type of lymphocyte can be stimulated by specific immune messenger molecules to produce the immune suppressive factor interleukin 10. The messenger molecules included either interleukin 27 or a combination of interleukin 6 and another type of messenger molecule called tumor growth factor beta. These results suggest that modulating these messenger molecules could increase interleukin 10 concentrations and temper over-active immune responses.
Many autoimmune conditions are exacerbated when immune suppressing factors such as interleukin 10 are lacking. The work described in the current four papers may provide directed means to intervene in these and other severe autoimmune diseases.
Author contacts:
Christopher A. Hunter (University of Pennsylvania, Dept of Pathobiology Philadelphia, PA)
Tel: +1 215 573 7772; Email: [email protected]
Daniel Cua (Schering-Plough Biopharma, Palo Alto, MA, USA)
Tel: +1 650 496 1261; Email: [email protected]
Abdolmohamad Rostami (Thomas Jefferson University, Philadelphia, PA, USA)
Tel: +1 215 955 8100; Email: [email protected]
Mohamed Oukka (BRIGHAM and Women's/CND and Harvard Medical School, Boston, MA, USA)
Tel: +1 617 768 8629; Email: [email protected]
**********************NATURE STRUCTURAL AND MOLECULAR BIOLOGY************************
(http://www.nature.com/natstructmolbiol)
[17] Stalling chemotherapy damage
DOI: 10.1038/nsmb1314
The understanding of how healthy cells cope with damages caused by anti-cancer drugs is furthered by new findings online this week in Nature Structural & Molecular Biology.
Transcription is the process whereby genetic information is transferred from DNA to RNA, in most cases leading to production of a particular protein. DNA damage, such as that caused by some anticancer drugs, can lead to errors in the RNA produced during transcription, resulting in incorrect protein production that may be harmful to the cell.
Patrick Cramer and colleagues have investigated how transcription machinery avoids DNA lesions caused by cisplatin, a widely used chemotherapy drug. They found that the cisplatin lesion forces the transcription machinery to stop before it reaches the lesion. This transcriptional “stalling” triggers a DNA-repair pathway that can remove the toxic lesion.
Author contact:
Patrick Cramer (Gene Center Munich, Germany)
Tel: +49 89 2180 76965; e-mail: [email protected]
Other papers from Nature Structural & Molecular Biology to be published online at the same time and with the same embargo:
[18] Autotransporter structure reveals intra-barrel cleavage followed by conformational changes
DOI: 10.1038/nsmb1322
[19] Structure and dynamics of a molten globular enzyme
DOI: 10.1038/nsmb1325
[20] NC2 mobilizes TBP on core promoter TATA boxes
DOI: 10.1038/nsmb1328
********************************************NATURE METHODS******************************************
[21] & [22] Controlling protein stability in parasites
DOI: 10.1038/nmeth1134
DOI: 10.1038/nmeth1132
Methods to regulate protein expression in two hazardous parasites are described in two reports in this week’s Nature Methods, providing valuable tools for understanding disease development.
Toxoplasma gondii, a parasite that can cause encephalitis and neurological diseases, and Plasmodium falciparum, a malaria parasite, have both had their genome sequenced. Still lacking are methods to control protein expression on a large scale, so the effects of proteins on parasite biology and pathogenesis can be studied.
The research groups of Daniel Goldberg and Markus Meissner adapted a system, originally developed in mammalian cells, that allows them to trigger the degradation of any protein at will. The only pre-requisite is that the protein is coupled to a short peptide that makes protein stability dependent on the presence of another component, appropriately named Shield. If Shield is added to the parasites the targeted protein is stable, but if Shield is withdrawn, the protein is degraded and the effect of its loss on the parasite can be studied.
This fast and efficient method for regulating protein levels will allow a genome wide analysis of their roles in the parasite life cycle and the interaction with its host.
Author contacts:
Markus Meissner (University Hospital Heidelberg, Heidelberg, Germany)
Tel: +49 6221 566518; E-mail: [email protected]
Daniel Goldberg (Washington University School of Medicine, St. Louis, MO, USA)
Tel: +1 314 362 1514; E-mail: [email protected]
Other papers from Nature Methods to be published online at the same time and with the same embargo:
[23] Visualizing single DNA-bound proteins using DNA as a scanning probe
DOI: 10.1038/nmeth1126
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Items from other Nature journals to be published online at the same time and with the same embargo:
NATURE CHEMICAL BIOLOGY (http://www.nature.com/nchembio)
[24] Enzymatic catalysis on conducting graphite particles
DOI: NChemBio.2007.47
NATURE MATERIALS (http://www.nature.com/naturematerials)
[25] Controlled nanoscale doping of semiconductors via molecular monolayers
DOI: 10.1038/nmat2058
[26] Fabrication of a simultaneous red–green–blue reflector using single-pitched cholesteric liquid crystals
DOI: 10.1038/nmat2045
[27] Where are nature’s missing structures?
DOI: 10.1038/nmat2057
Nature BIOTECHNOLOGY (http://www.nature.com/naturebiotechnology)
[28] A scorpion neurotoxin increases the potency of a fungal insecticide
DOI: 10.1038/nbt1357
Nature NEUROSCIENCE (http://www.nature.com/natureneuroscience)
[29] Homeostatic regulation of MeCP2 expression by a CREB-induced microRNA
DOI: 10.1038/nn2010
[30] Cortical interference effects in the cocktail party problem
DOI: 10.1038/nn2009
[31] Polyglutamine domain modulates the TBP-TFIIB interaction: implications for its normal function and neurodegeneration
DOI: 10.1038/nn2011
[32] Defining cortical frequency tuning with recurrent excitatory circuitry
DOI: 10.1038/nn2012
NATURE CELL BIOLOGY (http://www.nature.com/naturecellbiology)
[33] SNX4 coordinates endosomal sorting of TfnR with dynein-mediated transport into the endocytic recycling compartment
DOI: 10.1038/ncb1656
[34] Genome-scale RNAi profiling of cell division in human tissue culture cells
DOI: 10.1038/ncb1659
***************************************************************************************************************
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
Sydney: 8
Victoria: 8, 13
AUSTRIA
Wien: 5
BRAZIL:
Sao Paulo: 16
CANADA:
Alberta: 24
Toronto: 34
Winnipeg: 3
CHINA
Shanghai: 28
DENMARK
Aarhus: 7
GERMANY
Dresden: 34
Garching: 3, 4, 5
Heidelberg: 3, 21
Katlenburg-Lindau: 4
Kiel: 1
Mainz: 3
Muenster: 12, 20, 33
Munich: 17, 20
Tubingen: 6
Würzburg: 5
JAPAN
Kobe : 2
Kyoto: 12
Osaka : 2
Osawa : 4
Sendai : 2
Tokyo: 2, 26
Yokohama: 2, 26
NETHERLANDS
Amsterdam: 23
NORWAY
Bergen: 1
SINGAPORE
Nanyang: 19
SWEDEN
Uppsala: 4
SWITZERLAND
Zurich: 19
UNITED KINGDOM
Belfast: 8
Bristol: 33
Dorking: 4
London: 4, 33
Melbourn Science Park: 34
Nottingham: 15
Oxford: 7, 24
UNITED STATES OF AMERICA
California
Berkeley: 11, 25
Los Angeles: 9, 32
Palo Alto: 14
San Francisco: 9
Stanford: 21
Thousand Oaks: 13, 15
Connecticut
New Haven: 16
Georgia
Atlanta: 31
Illinois
Chicago: 34
Urbana: 20
Iowa
Iowa City: 7, 8
Maryland
Bethesda: 13, 18
College Park: 28
Massachusetts
Boston: 8, 12, 16, 30
Cambridge: 10, 11, 16
Missouri
Kansas City: 10, 11
St Louis: 22
Montana
Hamilton: 6
New Hampshire:
Durham: 4
Hanover: 12
New York
Buffalo: 30
New York: 12, 32
North Carolina
Durham: 10
Research Triangle: 10, 11
Ohio
Columbus: 8
Oregon
Portland: 29
Pennsylvania
Philadelphia: 13, 15
Rhode Island
Providence: 8
Texas
Houston: 8
Lubbock: 9
Utah
Provo: 27
Washington
Seattle: 6, 34
PRESS CONTACTS…
For media inquiries relating to embargo policy for all the Nature Research Journals:
Katherine Anderson (Nature London)
Tel: +44 20 7843 4502; E-mail: [email protected]
Ruth Francis (Senior Press Officer, 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)
Peter Hare
Tel: +1 212 726 9284; E-mail: [email protected]
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 Immunology (New York)
Laurie Dempsey
Tel: +1 212 726 9372; E-mail: [email protected]
Nature Materials (London)
Fabio Pulizzi
Tel: +44 20 7014 4024; E-mail: [email protected]
Nature Medicine (New York)
Juan Carlos Lopez
Tel: +1 212 726 9325; E-mail: [email protected]
Nature Methods (New York)
Allison Doerr
Tel: +1 212 726 9393; 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 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]
About Nature Publishing Group
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