NATURE RESEARCH JOURNALS PRESS RELEASE
For papers that will be published online on 03 December 2006
This press release is copyrighted to the Nature journals mentioned below.
This press release contains:
· Summaries of newsworthy papers:
New antibacterial targets? – Nature Chemical Biology
Mycobacterium tuberculosis copper regulator found – Nature Chemical Biology
Key to relapsing multiple sclerosis – Nature Immunology
Fast 3D imaging of brain cell networks – 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 CHEMICAL BIOLOGY **********************
(http://www.nature.com/nchembio)
[1] New antibacterial targets?
DOI: 10.1038/nchembio842
Small molecules that bind to segments of RNA called riboswitches could represent a novel class of antibiotics according to a report in the January issue of Nature Chemical Biology.
Small segments of RNA called riboswitches can control gene expression in response to the presence of bacterial metabolic products. The lysine riboswitch controls the biosynthesis of lysine, an essential amino acid for bacteria. Ronald Breaker and colleagues created small molecules that are chemically similar to lysine. They found that some of these lysine ‘analogs’ bind to the lysine riboswitch and as a result prevent lysine biosynthesis thereby stopping bacterial growth. The authors suggest that rationally targeting riboswitches – which are involved in sensing many critical bacterial metabolites – could provide a new class of antibiotics.
Author contact:
Ronald R Breaker (Yale University, New Haven, CT, USA)
Tel: +1 203 432 9389; E-mail: [email protected]
[2] Mycobacterium tuberculosis copper regulator found
DOI: 10.1038/nchembio844
Scientists have discovered a protein that controls gene expression in response to copper in the bacterium that causes most cases of tuberculosis and potentially a wide variety of other bacteria. These findings, reported in the January issue of Nature Chemical Biology, explain how many bacteria control copper concentrations within cells and this understanding could help in the design of new treatments for tuberculosis.
Copper is an essential element, but the levels within a cell must be carefully controlled as too much can cause cell death. Copper ions are prevented from damaging the cell by regulatory proteins that trap the metal. However, a mechanism for controlling the expression of these proteins had not previously been identified in many bacteria. Giedroc and colleagues have discovered a protein – CsoR – that regulates the expression of the copper-binding proteins and is present in many types of bacteria.
The discovery of a common copper-sensitive repressor helps scientists to understand how bacteria control concentrations of metals, and may provide a novel target for designing antibiotics to treat diseases including tuberculosis.
Author contact:
David Giedroc (Texas A&M University, College Station, TX, USA)
Tel: +1 979 845 4231; E-mail: [email protected]
**************************NATURE IMMUNOLOGY ***************
(http://www.nature.com/natureimmunology)
[3] Key to relapsing multiple sclerosis
DOI: 10.1038/ni1415
Insights into the pathology of relapsing multiple sclerosis are provided in a study in the January issue of Nature Immunology. This research shows that the molecule osteopontin, an inflammatory mediator, extends the lifetime of auto-aggressive immune cells and thus contributes to disease progression.
Larry Steinman and colleagues studied mice lacking osteopontin, in an animal model of relapsing multiple sclerosis, which develop a less severe form of the disease. Auto-aggressive immune cells were less likely to survive in the brains of osteopontin-deficient mice compared to their normal littermates; an observation that correlated with disease remission. In contrast, mice given osteopontin developed severe disease, ultimately leading to their death.
Using this information the authors were also able to show that osteopontin increased the lifespan of auto-aggressive immune cells grown in the lab, altering the expression of several genes that regulate cell survival and division. These findings suggest treatments targeting osteopontin might benefit multiple sclerosis patients.
Author contact:
Lawrence Steinman (Stanford University, CA, USA)
Tel: +1 650 725 6401; E-mail: [email protected]
Additional contact for comment on the paper:
Joan Goverman (University of Washington, Seattle, WA, USA)
Tel: +1 206 685 7604; E-mail: [email protected]
Other papers from Nature Immunology to be published online at the same time and with the same embargo:
[4] HLA-DM targets the hydrogen bond between the histidine at position beta81 and peptide to dissociate HLA-DR–peptide complexes
DOI: 10.1038/ni1414
[5] Kinase MEKK1 is required for CD40-dependent activation of the kinases Jnk and p38, germinal center formation, B cell proliferation and antibody production
DOI: 10.1038/ni1421
*******************NATURE METHODS****************************
[6] Fast 3D imaging of brain cell networks
DOI: 10.1038/nmeth989
A method of fast scanning microscopy that allows in vivo imaging of signalling in neuronal and glial cell networks is reported in the January issue of Nature Methods. This opens the way to studies of the complex cellular networks involved in information processing in the brain.
Processing of information in the brain involves complex patterns of communication between neural cells within large interconnected groups. Recent research has also highlighted the possible importance of brain support cells, or glia, in regulating this process. Technological limitations, however, have previously made the study of these complex interconnected signalling networks difficult.
Fritjof Helmchen and colleagues describe a method of fast three-dimensional scanning fluorescence microscopy that detects signals from cells in the entire scanned volume over a very short period of time. They were able to achieve such fast scanning by vibrating the microscope lens up and down very quickly while scanning the illumination beam back and forth in a defined pattern at the same time. The authors verified the performance of the method by imaging calcium signals in neuronal and glial cell networks in the brain of anaesthetized rats.
Author contact:
Fritjof Helmchen (University of Zurich, Switzerland)
Tel: +41 44 635 33 40; E-mail: [email protected]
Other papers from Nature Methods to be published online at the same time and with the same embargo:
[7] Tomographic molecular imaging and 3D quantification within adult mouse organs
DOI: 10.1038/nmeth985
********************************************************************
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)
[8] Half-cycle cutoffs in harmonic spectra and robust carrier-envelope phase retrieval
DOI: 10.1038/nphys463
[9] Direct observation of the coherent precession of magnetic domain walls propagating along permalloy nanowires
DOI: 10.1038/nphys464
NATURE MATERIALS (http://www.nature.com/naturematerials)
[10] Polyarginine segments in block copolypeptides drive both vesicular assembly and intracellular delivery
DOI: 10.1038/nmat1794
[11] Hydrogen multicentre bonds
DOI: 10.1038/nmat1795
Nature MEDICINE (http://www.nature.com/naturemedicine)
[12] Epidermal RANKL controls regulatory T-cell numbers via activation of dendritic cells
DOI: 10.1038/nm1518
[13] Quantitative micro positron emission tomography (PET) imaging for the in vivo determination of pancreatic islet graft survival
DOI: 10.1038/nm1458
Nature BIOTECHNOLOGY (http://www.nature.com/naturebiotechnolgy)
[14] An essential role for Akt1 in dendritic cell function and tumor immunotherapy
DOI: 10.1038/nbt1262
NATURE GENETICS (http://www.nature.com/naturegenetics)
[15] Germline gain-of-function mutations in SOS1 cause Noonan syndrome
DOI: 10.1038/ng1926
[16] Gain-of-function SOS1 mutations cause a distinctive form of Noonan syndrome
DOI: 10.1038/ng1939
[17] Cdkn1a deletion improves stem cell function and lifespan of mice with dysfunctional telomeres without accelerating cancer formation
DOI: 10.1038/ng1937
[18] A viable allele of Mcm4 causes chromosome instability and mammary adenocarcinomas in mice
DOI: 10.1038/ng1936
[19] PDGF signaling specificity is mediated through multiple immediate early genes
DOI: 10.1038/ng1922
Nature NEUROSCIENCE (http://www.nature.com/natureneuroscience)
[20] Cdk5 regulates EphA4-mediated dendritic spine retraction through an ephexin1-dependent mechanism
DOI: 10.1038/nn1811
[21] IRS2-Akt pathway in midbrain dopamine neurons regulates behavioral and cellular responses to opiates
DOI: 10.1038/nn1812
NATURE CELL BIOLOGY (http://www.nature.com/naturecellbiology)
[22] PGC7/Stella protects against DNA demethylation in early embryogenesis
DOI: 10.1038/ncb1519
[23] Sharp boundaries of Dpp signalling trigger local cell death required for Drosophila leg morphogenesis
DOI: 10.1038/ncb1518
Nature STRUCTURAL & MOLECULAR BIOLOGY (http://www.nature.com/natstructmolbiol)
[24] A folding control element for tertiary collapse of a group II intron ribozyme
DOI: 10.1038/nsmb1181
****************************************************************************
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
Herston: 16
AUSTRIA
Vienna: 12, 24
CANADA:
Saskatchewan: 2
Vancouver: 13
CHINA
Hong Kong: 20
FRANCE
Nice: 23
GERMANY
Braunschweig: 17
Essen: 12
Hannover: 17
Heidelberg: 12, 17
Kiel: 12
Munster: 12
ITALY
Rome: 16
JAPAN
Osaka: 22
Saitama: 22
Tokyo: 17, 22
KOREA :
Seoul : 17
SPAIN
Barcelona: 7
Madrid: 23
Malaga: 16
SWEDEN
Umeå: 7
SWITZERLAND
Zurich: 6
UNITED KINGDOM
Edinburgh: 7
London: 8
Newcastle: 17
UNITED STATES OF AMERICA
California
Berkeley: 16
Fresno: 16
La Jolla: 5
Los Angeles: 10
San Jose: 9
Santa Barbara: 11
Stanford: 3, 9, 13
Walnut Creek: 16
Connecticut
New Haven: 1, 21, 24
Florida
Tallahasse : 21
Maine:
Bar Harbor: 18
Maryland
Baltimore: 4
Massachusetts
Boston: 15, 20
Minnesota
Minneapolis: 18
New Jersey: 5
Cranbury: 5
New York
Ithaca: 18
New York: 16
Texas
College Station: 2
Dallas: 21
Houston: 14
Washington:
Seattle: 19
Wisconsin
Madison: 2
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)
Maria Bellantone
Tel: +44 20 7843 4556; 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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