NATURE AND THE NATURE RESEARCH JOURNALS PRESS RELEASE
For papers that will be published online on 05 August 2007
This press release is copyrighted to the Nature journals mentioned below.
This press release contains:
· Summaries of newsworthy papers:
Behaviour: Of mice and man-eaters – Nature
Cancer: Gene reduces severity of lung cancer – Nature
An unfolding antibiotics story – Nature Chemical Biology
How inflammatory lymphocytes develop – Nature Immunology
Seeing transcription in living colour – Nature Structural & Molecular Biology
Virus-based screen for ion channel modulators – 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] Behaviour: Of mice and man-eaters (N&V)
DOI: 10.1038/nature06089
The sexual behaviour of female mice can be altered dramatically by almost literally flicking a switch at the periphery of their brain. Disrupting the function of a sensory organ called the vomeronasal organ (VNO) causes female mice to display strikingly masculine sexual behaviours – such as mounting, pelvic thrust and solicitation.
It is thought that sex differences in mammalian behaviour arise as a result of exposure to hormones in the womb, which shape the development of either male- or female-specific neural circuits. The evidence Catherine Dulac and colleagues present in a study online in Nature this week suggests otherwise. They observed the behaviour of female mice after genetic or physical lesion of the VNO, and report that the mice display sexual and courtship behaviours that are uniquely male. The authors report that the lesioned female mice also show a reduction in female-specific behaviours such as nesting.
These results suggest that, in mice at least, the neural circuitry underlying masculine behaviour surprisingly still exists in adult females. This implies a new model of sex differences in behaviour, in which male and female circuits co-exist in the brains of both sexes and are switched on or off by sensory input such as the pheromones detected by the VNO.
Author contact:
Catherine Dulac (Harvard University, Cambridge, MA, USA)
Tel: +1 617 495 7893; E-mail: [email protected]
Marc Breedlove (Michigan State University, East Lansing, MI, USA) N&V author
Tel: +1 517 355 1749; E-mail: [email protected]
[2] Cancer: Gene reduces severity of lung cancer
DOI: 10.1038/nature06030
A gene known to aid suppression of some tumours is shown to reduce the aggression of lung cancers along with the risk of metastasis. The research, published online this week in Nature, demonstrates that Lkb1 loss, combined with the mutation of another factor, Kras, in a mouse model, causes more aggressive tumours to arise.
LKB1 is a tumour suppressor gene and is often found to be mutated in patients with Peutz–Jeghers syndrome, who have an increased incidence of cancer. Kras mutation and p53 loss lead to lung cancer in a mouse model, but Kwok-Kin Wong and colleagues found that, when combined with Lkb1 mutation, not only were tumours more aggressive but they were more likely to develop into squamous and large-cell carcinomas of the lung. This report also identifies LKB1 mutations in human lung cancers classified as squamous carcinomas.
Thus, LKB1 loss may be a marker for predicting disease development and spread, and the pathways regulated by LKB1 represent possible therapeutic targets.
Author contact:
Kwok-Kin Wong (Dana Farber Cancer Institute, Boston, MA, USA)
Tel: +1 617 632 6084; E-mail: [email protected]
Other papers from Nature to be published online at the same time and with the same embargo:
[3] Dominant-negative mutations in the DNA-binding domain of STAT3 cause hyper-IgE syndrome
DOI: 10.1038/nature06096
*************************************NATURE CHEMICAL BIOLOGY ***********************************
(http://www.nature.com/nchembio)
[4] An unfolding antibiotics story
DOI: 10.1038/nchembio.2007.21
Scientists have identified the way an unusual antibiotic works, reports a paper published online this week in Nature Chemical Biology. Lactivicin and similar molecules are a class of antibiotics that are unique because they do not contain a beta-lactam ring. This is significant because antibiotic resistance is frequently tied to the beta-lactam rings of the more common antibiotics, like penicillin.
Now a team led by Christopher Schofield and colleagues specifically demonstrate that lactivicin is an effective antibiotic against penicillin-resistant bacteria isolated from human patients. In addition, the authors explain lactivicin’s unique behaviour by providing a crystal structure of the compound bound to its protein target, in which the two rings of the compound have been opened. This discovery will undoubtedly lead to the design of new effective antibiotics that can be applied to resistant bacteria.
Author contact:
Christopher Schofield (Chemistry Research Laboratory, Oxford, UK)
Tel: +44 1865 275 625, Email: [email protected]
Additional contact for comment on paper:
Andréa Dessen (IBS, Grenoble, France)
Tel: +33 4 38 78 95 50, E-mail: [email protected]
*******************************************NATURE IMMUNOLOGY ************************************
(http://www.nature.com/natureimmunology)
[5], [6] & [7] How inflammatory lymphocytes develop
DOI: 10.1038/ni1497
DOI: 10.1038/ni1496
DOI: 10.1038/ni1500
In the September issue of Nature Immunology three papers describe the development of a unique type of white blood cell and how this development is different in humans and mice. These cells are required for healthy gut biology but also, in other areas of the body such as the brain, are associated with dangerous inflammation.
Two groups, one led by Rene Waal de Malefyt and the other by Federica Sallusto, evaluated how human T cells develop into TH-17 cells, which make several inflammatory immune proteins associated with inflammation and with fighting certain microbial infections. Both groups found that the requirements for TH-17 cell development in humans and mice are different, a surprising finding that has great significance because mice are commonly used to study human disease. A third study led by Michael Lohoff evaluated TH-17 cells in mice only, and found that a specific cellular protein called interferon regulatory factor 4 is absolutely required for their development.
These three studies provide considerable insight into how TH-17 inflammatory cells are produced in both mice and humans. Understanding the unique developmental requirements for these inflammatory T cells may help to explain the cause of inflammatory diseases of the brain and gut in humans.
Author contacts:
Rene Waal de Malefyt (Schering-Plough Biopharma, Palo Alto, CA, USA)
Tel: +1 650 496 1164; E-mail: [email protected] Author paper [5]
Federica Sallusto (Institute for Research in Biomedicine, Bellinzona, Switzerland)
Tel: +41 91 820 0315; E-mail: [email protected] Author paper [6]
Michael Lohoff (Marburg University, Germany) Author paper [7]
Tel: +49 6421 286 6455; E-mail: [email protected]
**********************NATURE STRUCTURAL AND MOLECULAR BIOLOGY************************
(http://www.nature.com/natstructmolbiol)
[8] Seeing transcription in living colour
DOI: 10.1038/nsmb1280
A closer look is taken at gene transcription in living organisms in a paper published online this week by Nature Structural & Molecular Biology. Transcription by RNA polymerase II, the enzyme that transcribes DNA into messenger RNAs, is at the core of gene expression and is a major focus of biological regulatory mechanisms. Much of what is known about transcription comes from test tube experiments (in vitro) with purified components but little is known about how RNA polymerase works in vivo.
Robert Singer and co-workers have now taken the analysis of the mechanism of gene transcription in higher organisms to a new level by using advanced fluorescence imaging techniques to measure quantitatively the kinetics of gene transcription by RNA polymerase II in living mammalian cells. The ultimate goal of this work is a quantitative model of gene transcription in vivo. They find several novel and unexpected features concerning the nature of the in vivo transcription.
First, they conclude that only a surprisingly small fraction of RNA polymerases that bind to the start of a gene, amounting to about 1%, actually go on to transcribe the gene and produce a messenger RNA. Second, they find that RNA polymerases transcribe more rapidly than previously thought, often pausing for prolonged periods. This study represents a critical milestone on the way to building a quantitative understanding of the mechanism of transcription in single live cells.
Author contact:
Robert Singer (Albert Einstein College of Medicine, New York, NY, USA)
Tel: + 1 718 430 8646; E-mail: [email protected]
Other papers from Nature Structural & Molecular Biology to be published online at the same time and with the same embargo:
[9] The Arabidopsis chromodomain-containing protein LHP1 colocalizes with histone H3 Lys27 trimethylation
DOI: 10.1038/nsmb1283
[10] The refined structure of nascent HDL reveals a key functional domain for particle maturation and dysfunction
DOI: 10.1038/nsmb1284
********************************************NATURE METHODS******************************************
[11] Virus-based screen for ion channel modulators
DOI: 10.1038/nmeth1077
A virus-based method that screens for chemical or genetically-encoded inhibitors of ion channels is described online this week in Nature Methods. Ion channels are cell membrane-spanning proteins that, when activated, allow the influx of ions. They encompass a large family of over 400 proteins and play key roles in maintaining cellular function. While blocking their activity has proven useful for certain medical applications, these drugs usually elicit severe side effects due to their wide range action and lack of selectivity for the intended cell alone.
Joseph Glorioso and colleagues wanted to find more specific channel modulators and set up a virus-based screen in which the virus level is an indicator for inhibitor efficacy. They reasoned that overexpression of an ion channel in cells via a virus would be detrimental to the cell and consequently impede viral replication; while the presence of an inhibitor of channel function would keep the cells healthy and allow replication. The advance over other screens for channel inhibitors is that the technique can easily be adapted to screen for genetically-encoded inhibitors by coinfection of a second virus that encodes the inhibitor. The inhibitor’s DNA can then be easily retrieved from the viral genome.
This method can easily be scaled up to screen whole DNA libraries that express a wide range of potential channel modulators. These genetically encoded inhibitors will help reveal the biology behind channel regulation and are likely to lead to more specific inhibitors.
Author contact:
Joseph Glorioso (University of Pittsburgh School of Medicine, PA, USA)
Tel: +1 412 648 8105; E-mail: [email protected]
Other papers from Nature Methods to be published online at the same time and with the same embargo:
[12] Genome-wide prediction of matrix attachment regions and use to increase gene expression in mammalian cells
DOI: 10.1038/nmeth1076
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Items from other Nature journals to be published online at the same time and with the same embargo:
Nature PHYSICS (http://www.nature.com/naturephysics)
[13] Flow diagram of the metal–insulator transition in two dimensions
DOI: 10.1038/nphys685
[14] Charge inversion accompanies DNA condensation by multivalent ions
DOI: 10.1038/nphys697
NATURE MATERIALS (http://www.nature.com/naturematerials)
[15] Surfactant-assisted fabrication of free-standing inorganic sheets covering an array of micrometre-sized holes
DOI: 10.1038/nmat1980
[16] High-resolution electrohydrodynamic jet printing
DOI: 10.1038/nmat1974
Nature MEDICINE (http://www.nature.com/naturemedicine)
[17] Type II monocytes modulate T cell–mediated central nervous system autoimmune disease
DOI: 10.1038/nm1620
[18] Increased serine protease activity and cathelicidin promotes skin inflammation in rosacea
DOI: 10.1038/nm1616
[19] A spatially and temporally restricted mouse model of soft tissue sarcoma
DOI: 10.1038/nm1602
Nature BIOTECHNOLOGY (http://www.nature.com/naturebiotechnology)
[20] Small antibody mimetics comprising two complementarity-determining regions and a framework region for tumor targeting
DOI: 10.1038/nbt1320
[21] Embryo-specific silencing of a transporter reduces phytic acid content of maize and soybean seeds
DOI: 10.1038/nbt1322
NATURE GENETICS (http://www.nature.com/naturegenetics)
[22] Large-scale genetic fine mapping and genotype-phenotype associations implicate polymorphism in the IL2RA region in type 1 diabetes
DOI: 10.1038/ng2102
[23] Recombination and linkage disequilibrium in Arabidopsis thaliana
DOI: 10.1038/ng2115
[24] Mutations in amphiphysin 2 (BIN1) disrupt interaction with dynamin 2 and cause autosomal recessive centronuclear myopathy
DOI: 10.1038/ng2086
Nature NEUROSCIENCE (http://www.nature.com/natureneuroscience)
[25] EP3 prostaglandin receptors in the median preoptic nucleus are critical for fever responses
DOI: 10.1038/nn1949
[26] Development of the declarative memory system in the human brain
DOI: 10.1038/nn1950
[27] Cell type–specific gating of perisomatic inhibition by cholecystokinin
DOI: 10.1038/nn1952
[28] Learning the value of information in an uncertain world
DOI: 10.1038/nn1954
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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.
BELGIUM
Liege: 4
CANADA:
Toronto: 7
CHINA
Chengdu: 20
FINLAND
Helsinki: 24
FRANCE
Grenoble: 4
Illkirch: 24
Paris: 8
Poitiers: 5
Strasbourg: 24
Toulouse: 18
Versailles: 9
GERMANY
Goettingen: 7
Jena: 7
Marburg: 7
Tubingen: 23
ISRAEL
Ramat Gan: 8
Rehovot: 13
JAPAN
Aichi: 3
Asahikawa: 18
Fukuoka: 3
Ibaraki: 15
Osaka: 25
Sapporo: 3
Sendai: 3
Tokyo: 3
KOREA
Daejon: 16
NETHERLANDS
Delft: 13, 14
SERBIA
Belgrade: 3
SWEDEN
Goteborg: 24
Stockholm: 24
SWITZERLAND
Bellinzona: 6
Epalinges: 12
Geneva: 12
Lausanne: 12
TURKEY
Ankara: 3
UNITED KINGDOM
Cambridge: 22, 23
Manchester: 24
Oxford: 4, 12, 28
UNITED STATES OF AMERICA
California
Berkeley: 26
Foster City: 5
Irvine: 27
La Jolla: 23
Los Altos: 8
Los Angeles: 9, 23
Palo Alto: 5
San Diego: 18
San Francisco: 17
Stanford: 17, 26
Florida
Gainesville: 22
Georgia
Athens: 9
Illinois
Urbana: 16
Iowa
Johnston: 21
Maryland
Chevy Chase: 19
Massachusetts
Boston: 2, 13, 19, 25
Cambridge: 1, 2, 19, 26
Charlestown: 19
North Grafton: 19
New York
Bronx: 8
New York: 13, 19, 26
North Carolina
Chapel Hill: 2
Durham: 19
Winston-Salem: 10, 25
Ohio
Cleveland: 10
Pennsylvania
Pittsburgh: 11
Tennessee
Memphis: 2
Texas
Dallas: 2, 17, 25
Virginia
Charlottesville: 9
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 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 Neuroscience (New York)
Sandra Aamodt (based in California)
Tel: +1 530 795 3256; 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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