NATURE AND THE NATURE RESEARCH JOURNALS PRESS RELEASE
For papers that will be published online on 30 July 2006. This press release is copyrighted to the Nature journals mentioned below.
This press release contains:
* Summaries of newsworthy papers:
- Sensory receptors: Receptors in the mouse nose may be pheromone detectors - Nature
- Sulfation code for sugar chains - Nature Chemical Biology
- Genomic blueprint for oil slick cleanup bacterium - Nature Biotechnology
- Mouse model suggests treatment strategy for muscular dystrophy - Nature Genetics
- Inhibiting inflammation in multiple sclerosis - Nature Immunology
* 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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(<http://www.nature.com/nature>)
[1] Sensory receptors: Receptors in the mouse nose may be pheromone detectors
DOI: 10.1038/nature05066
Biologists have discovered a second set of olfactory receptors in the mouse nose, including ones that may detect pheromones and might therefore aid in the mating game. The genes that encode these receptors are also found in fish and humans, raising the tantalizing prospect that we may be on the brink of discovering a human pheromone receptor.
The receptors, which sit on the surface of unique subsets of cells in the nasal lining, are called trace amine-associated receptors (TAARs) and are distinct from the range of receptor molecules that sense odours. The discovery is unveiled by Stephen Liberles and Linda Buck in a study to be published online this week by Nature.
At least three different TAARs recognize separate compounds found in mouse urine, which suggests that they may have a role in detecting subtle chemical messages between individuals. One of the compounds is linked to stress, whereas the other two are generally more abundant in male than in female urine - and one of them is thought by biologists to be a mating signal.
Author contact:
Linda Buck (Howard Hughes Medical Institute - Fred Hutchinson Cancer Research Center, Seattle, WA, USA)
Tel: +1 206 667 6316; E-mail: [email protected]
**************************NATURE CHEMICAL BIOLOGY ***********************
(http://www.nature.com/nchembio, http://www.nature.com/natureneuroscience)
[2] Sulfation code for sugar chains
DOI: 10.1038/nchembio810
The importance of specific sugar chains in determining the function of neuronal growth factors is revealed in a study in the September issue of Nature Chemical Biology.
The role of particular sugar chains known as glycosaminoglycans (GAGs) has been elusive because they have such complex patterns. Gama and colleagues combine synthetic chemistry and microarrays with functional studies to show the existence of what they call a “sulfation code”. Comparing a number of computationally chosen GAG sugars, the authors found that the level of binding to two neuronal growth factors was dictated by the sequence and structure of the sugar. The GAGs best able to bind to the growth factors were the same as those that could promote the growth and development of neurons.
Much like the genetic code translates into functional information about proteins, the sulfation code translates into functional information about sugars.
Author contact:
Linda Hsieh-Wilson (California Institute of Technology and Howard Hughes Medical Institute, Pasadena, CA, USA)
Tel: +1 626 395 6101; E-mail: [email protected]
*******************************NATURE BIOTECHNOLOGY************************
(http://www.nature.com/naturebiotechnolgy)
[3] Genomic blueprint for oil slick cleanup bacterium
DOI: 10.1038/nbt1232
The complete genome sequence of an oil-eating bacterium that plays a key role in the cleanup of oil spills is reported in the August issue of Nature Biotechnology. The genome sequence of the bacterium, Alcanivorax borkumensis, provides the complete blueprint of biochemical functions and physiological adaptations that allow this bug to so efficiently biodegrade crude oil in the ocean.
Oil tanker accidents account for only a small percentage of the 1.3 million tons of petroleum released either accidentally or deliberately into the oceans annually. However, thanks to the appetite of some specialized marine bacteria for the hydrocarbons contained in oil, spills in our oceans can be slowly broken down.
Schneiker and colleagues have now sequenced the 3.1 Mb long genome of A. borkumensis. Among oil-eating bacteria, A. borkumensis stands out as one that almost exclusively degrades linear and branched organic compounds called alkanes, two major, resilient components of crude oil. The gene sequence of the bug contains 2,755 predicted open reading frames that include a wide range of alkane-degrading systems in addition to other functions, such as emulsifying compounds and exopolymers, which contribute to the formation of oil droplets that facilitate oil breakdown by A. borkumensis.
Author contact:
Vitor AP Martins dos Santos (German Research Center for Biotechnology, Braunschweig, Germany)
Tel: +49 531 6181 422; E-mail: [email protected]
Other papers from Nature Biotechnology to be published online at the same time and with the same embargo:
[4] Gene targeting in vivo by adeno-associated virus vectors
DOI: 10.1038/nbt1231
****************************NATURE GENETICS ***************************
(<http://www.nature.com/naturegenetics>)
[5] Mouse model suggests treatment strategy for muscular dystrophy
DOI: 10.1038/ng1857
A reversible mouse model of myotonic dystrophy, the most common form of muscular dystrophy in adults, is reported in a study to be published in the September issue of Nature Genetics. The mouse model shows for the first time that at least some aspects of the disease might be fully reversible, and suggests that a potential therapy might be devised by targeting a particular kind of toxic molecule present in the diseased muscle.
Myotonic dystrophy occurs because of a large expansion in the number of ‘CTG’ repeats in a region flanking a gene called DMPK, and is associated with skeletal muscle loss, cardiac abnormalities, cataracts and insulin resistance. While there has been good evidence in favor of the idea that the expanded DMPK messenger RNA is toxic to cells in which it is expressed, and is the underlying cause of the disease, a definitive demonstration has been lacking. Mani Mahadevan and colleagues at the University of Virginia generated a mouse carrying an extra normal copy of the DMPK gene that could be turned on and off by adding (or removing) an antibiotic to the drinking water. Mice that expressed very high levels of this extra DMPK-and thus had more copies of the CTG repeat-showed all of the cardinal features of myotonic dystrophy. When expression of DMPK was turned off, normal skeletal and cardiac muscle function was restored in many of the mice. These results suggest that muscle damage in individuals with the disease might not be permanent, and that eliminating messenger RNAs carrying the extra CTG repeats might have therapeutic benefit.
Author contacts:
Mani Mahadevan (University of Virginia, Charlottesville, VA, USA)
Tel: +1 434 243 4816; E-mail: [email protected]
Ramesh Yadava (University of Virginia, Charlottesville, VA, USA)
Tel: +1 434 924 9816; E-mail: [email protected]
Additional contact for comment on paper:
Lubov Timchenko (Baylor College of Medicine, Houston, TX, USA)
Tel: +1 713 798 6911; E-mail: [email protected]
Other papers from Nature Genetics to be published online at the same time and with the same embargo:
[6] Characterization of the Drosophila melanogaster genome at the nuclear lamina
DOI: 10.1038/ng1852
[7] Augmentation of tumor angiogenesis by a Myc-activated microRNA cluster
DOI: 10.1038/ng1855
******************************NATURE IMMUNOLOGY ***************************
(<http://www.nature.com/natureimmunology>)
[8] Inhibiting inflammation in multiple sclerosis
DOI: 10.1038/ni1370
T cells, a type of immune cell, can impede the development and progression of multiple sclerosis in mice, according to a paper to be published in the September issue of Nature Immunology.
Many different types of T cells exist, each expressing a unique T cell receptor that helps the cell sense and react appropriately to its environment. J. Ludovic Croxford and colleagues show that a specific subset of T cells slows the onset and decreases the severity of a mouse version of human multiple sclerosis. The disease is worsened in the absence of these T cells, which block autoimmunity at least in part by triggering other immune cells to release chemical mediators that dampen the inflammatory response. Whether these T cells are involved in human autoimmune disease, and whether they can be harnessed for therapeutic intervention, remains to be determined.
Author contact:
J Ludovic Croxford (National Institute of Neuroscience and Immunology, Tokyo, Japan)
Tel: +81 42 341 2711; E-mail: [email protected] <mailto:[email protected]>
Other papers from Nature Immunology to be published online at the same time and with the same embargo:
[9] Visualization of the earliest steps of gamma delta T cell development in the adult thymus
DOI: 10.1038/ni1371
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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 <http://www.nature.com/naturematerials>)
[10] Dynamic particle tracking reveals the ageing temperature of a colloidal glass
DOI: 10.1038/nphys366
Nature MEDICINE (<http://www.nature.com/naturemedicine>)
[11] Embryonic and tumorigenic pathways converge via Nodal signaling: role in melanoma aggressiveness
DOI: 10.1038/nm1448
[12] A previously unidentified alternatively spliced isoform of t(8;21) transcript promotes leukemogenesis
DOI: 10.1038/nm1443
[13] ErbB2 receptor tyrosine kinase signaling mediates early demyelination induced by leprosy bacilli
DOI: 10.1038/nm1433
[14] Memory TH2 cells induce alternatively activated macrophages to mediate protection against nematode parasites
DOI: 10.1038/nm1451
Nature NEUROSCIENCE (<http://www.nature.com/natureneuroscience>)
[15] Presynaptic fluctuations and release-independent depression
DOI: 10.1038/nn1746
Nature STRUCTURAL & MOLECULAR BIOLOGY (<http://www.nature.com/natstructmolbiol>)
[16] The finger subdomain of yeast telomerase cooperates with Pif1p to limit telomere elongation
DOI: 10.1038/nsmb1126
[17] Regulation of MLL1 H3K4 methyltransferase activity by its core components
DOI: 10.1038/nsmb1128
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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.
CHINA
Suzhou: 12
FRANCE
Lyon: 16
Marseille: 9, 16
Paris: 14
GERMANY
Bielefeld: 3
Braunschweig: 3
Dresden: 3
ITALY
Messina: 3
Naples: 16
JAPAN
Fukuoka: 2
Tokyo: 8
NETHERLANDS
Amsterdam: 6, 14
SPAIN
Madrid: 3
SWITZERLAND
Epalinges: 16
UNITED KINGDOM
Belfast: 9
London: 15
UNITED STATES OF AMERICA
California
Duarte: 2
La Jolla: 12
Pasadena: 2
Illinois
Chicago: 11, 12
Maywood: 11
Maryland
Baltimore: 7
Beltsville: 14
Bethesda: 14
Massachusetts
Cambridge: 6, 17
Missouri
St Louis: 4
New Jersey
Newark: 14
New Mexico
Albuquerque: 12
New York
New York: 10, 13, 17
Yorktown Heights: 3
Pennsylvania
Philadelphia: 7
Texas
Houston: 17
Virginia
Charlottesville: 5
Washington
Seattle: 1, 4
Wisconsin
Madison: 5
PRESS CONTACTS…
For media inquiries relating to embargo policy for all the Nature Research Journals:
Helen Jamison (Nature London)
Tel: +44 20 7843 4658; 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 Medicine (New York)
Juan Carlos Lopez
Tel: +1 212 726 9325; 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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