NATURE AND THE NATURE RESEARCH JOURNALS PRESS RELEASE
For papers that will be published online on 14 September 2008
This press release is copyrighted to the Nature journals mentioned below.
This press release contains:
· Summaries of newsworthy papers:
Nature: New colon tumour gene gives fresh therapeutic lead
Neuroscience: Deaf people learn new speech patterns
Immunology: The tuberculosis bacterium’s stealthy ways
Genetics: Susceptibility to bladder cancer
Chemical Biology: Dual gating in one motion
Genetics: Risk factor for common kidney disease
And finally... Nature: A new take on tooth evolution
· 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.
PICTURES: To obtain artwork from any of the journals, you must first obtain permission from the copyright holder (if named) or author of the research paper in question (if not).
NOTE: Once a paper is published, the digital object identifier (DOI) number can be used to retrieve the abstract and full text from the journal web site (abstracts are available to everyone, full text is available only to subscribers). To do this, add the DOI to the following URL: http://dx.doi.org/ (For example, http://dx.doi.org/10.1038/ng730). For more information about DOIs and Advance Online Publication, see http://www.nature.com/ng/aop/.
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.
[1] Nature: New colon tumour gene gives fresh therapeutic lead
DOI: 10.1038/nature07179
Cancer researchers have identified a gene that promotes the growth of colon cancers, potentially creating a new avenue for treating many cases of the disease. The gene, called CDK8, drives the proliferation of colon cancer cells, and therefore the growth of tumours.
The gene appears to be overactivated in many colon cancer cells, report the US and Spanish research team led by William Hahn. That means that suppressing its activity could offer a new way to restrict the growth of tumours with this particular defect, they suggest online in this week’s Nature.
The research team made the discovery by screening tumour cells in the lab for genes that promote their proliferation. They then checked their findings against genetic data from tissue samples taken from human colon cancers and found that the CDK8 gene was amplified in many cases, leading to increased activity. CDK8, the activity of which influences a suite of other genes, is the latest newly discovered cancer gene among the many that influence the complex genetics of the disease.
Author contact:
William Hahn (Dana-Farber Cancer Institute, Boston, MA, USA)
Tel: +1 617 632 2641; E-mail: [email protected]
[2] Neuroscience: Deaf people learn new speech patterns
DOI: 10.1038/nn.2193
Scientists have discovered the reason why people who have lost their hearing retain the ability to speak intelligibly for many years. The study, online this week in Nature Neuroscience, shows that people who become deaf as adults can use information from sensations in the vocal tract to compensate for disturbances of speech movements.
David Ostry and Sazzad Nasir asked deaf adults to speak short syllables while their jaw motion was disturbed. Initially, this produced a curvature of the jaw movement and a distortion of their speech, but over the course of several hundred repetitions, they were able to adapt their speech movements to reduce these errors. The researchers found that deaf people and those with hearing show about the same amount of adaptation following training.
This work indicates that speech production relies on sensations from the muscles, skin and soft tissues of the vocal tract, and that people who become deaf in adulthood can use these non-auditory inputs to learn speech.
Author contacts:
David Ostry (McGill University, Montreal, Quebec, Canada)
Tel: +1 514 398 6111; Email: [email protected]
Sazzad Nasir (McGill University, Montreal, Quebec, Canada)
Tel: +1 514 398 6111; E-mail: [email protected]
[3] Immunology: The tuberculosis bacterium’s stealthy ways
DOI: 10.1038/ni.1654
Mycobacterium tuberculosis - the bacterium that causes most cases of tuberculosis - spreads infection by blocking a naturally triggered immune response that would cause the infected cells to die. The research, published online this week in Nature Immunology, provides possible new avenues for designing inhibiting drugs to prevent mycobacterial diseases.
Mycobacteria tuberculosis infects immune cells called macrophages, which function as temporary ‘incubators’ while the bacteria multiply. Eventually the macrophages burst releasing the bacteria to infect other cells. Normally macrophages infected with bacteria would undergo a form of cell death called apoptosis and trigger an immune response.
Heinz Remold and colleagues found that M. tuberculosis prevent macrophages from undergoing apoptosis. Instead, M. tuberculosis caused macrophages to die by necrosis, another form of cell death that allows the bacteria to escape from their host cells and infect new cells. By revealing how M. tuberculosis can evade the immune system this study provides significant insight into the development of tuberculosis disease.
Author contact:
Heinz Remold (Brigham and Women's Hospital Medicine, Boston, MA, USA)
Tel: +1 617 525 1061; E-mail: [email protected]
[4] Genetics: Susceptibility to bladder cancer
DOI: 10.1038/ng.229
Researchers have found a genetic variant associated with increased risk of urinary bladder cancer, according to a study published online this week in Nature Genetics.
One of the more tantalizing stories to emerge from recent genetic association studies of cancer has been that a series of variants in a small region on chromosome 8 predispose to a range of cancers, including those of the prostate, colon and breast.
Kari Stefansson and colleagues carried out a genome-wide association study of bladder cancer, and found a variant in the same region to confer extra risk of this disease, but not of any of the other cancers. The previously reported variants are near the gene MYC, which encodes a protein whose deregulation is known to be associated with malignant growth. The susceptibility variant for bladder cancer is even closer to MYC, strengthening the case that these risk variants might affect cancer risk by altering the expression of MYC.
The team were unable to find functional evidence for altered MYC expression in blood or fat tissue from individuals with bladder cancer, however, indicating that further work will be needed to explain the role of this region in cancer susceptibility.
Author contact:
Kari Stefansson (deCODE Genetics, Reykjavik, Iceland)
Tel: +354 570 1900; E-mail: [email protected]
Additional media contact:
Edward M Farmer (Director of Corporate Communication, deCODE Genetics)
Tel: +1 646 417 4555; E-mail: [email protected]
[5] Chemical Biology: Dual gating in one motion
DOI: 10.1038/nchembio.112
Scientists have discovered how sodium influences a group of potassium channels, according to a paper to be published online this week in Nature Chemical Biology. This discovery improves our understanding of ion channels and may offer new insights into the function of known drugs like cardiac glycosides.
Ion channels are proteins that sit in the cell membrane and allow ions such as sodium and chloride to pass from one side of the membrane to the other; this action can cause the buildup of electrical gradients that result in biological processes like the firing of neurons. The activity of inwardly rectifying potassium (Kir) channels is further controlled by a specific lipid in the membrane. Some of the Kir channels are also controlled by sodium, termed ‘dual gating’, but it was not clear how these two signals would both be needed for channel activity.
Diomedes Logothetis and colleagues used a combined computational-experimental approach to show that sodium prevents the interaction of an aspartate amino acid with an arginine amino acid by binding to the aspartate amino acid. This frees the arginine amino acid to interact with the lipid, which explains how the signals coordinate. This molecular-level insight expands our view of the function of these important channels, represents a potential new avenue for drug design.
Author contact:
Diomedes Logothetis (Virginia Commonwealth University, Richmond, VA, USA)
Tel: +1 804 828 5878, E-mail: [email protected]
[6] & [7] Genetics: Risk factor for common kidney disease
DOI: 10.1038/ng.226
DOI: 10.1038/ng.232
Scientists have identified the first common genetic variants that increase risk of end-stage kidney disease (ESKD), report two studies published online this week in Nature Genetics. ESKD is characterized by the near-total loss of kidney function, which requires dialysis or a transplant, and affects millions of people worldwide every year.
In the American population ESKD is more common in African Americans than in European Americans. This difference can be exploited by a method known as ‘admixture mapping’, in which the genome is scanned for variants that occur both more frequently in individuals with the disease and in regions that are inherited from African populations.
Two groups led by Wen Hong Linda Kao and Cheryl Winkler used this approach to show that variants in the gene MYH9 are associated with susceptibility to ESKD and a specific form of ESKD, known as focal segmental glomerulosclerosis (FSGS), respectively. MYH9, which is expressed in the kidney, encodes one of a family of proteins that make up nonmuscle myosin, and has diverse roles in cells. The authors suggest that variation at MYH9 accounts for a substantial fraction of the increased risk of ESKD in African Americans.
Author contacts:
Cheryl Winkler (National Cancer Institute, Frederick, MD, USA) Author paper [6]
Tel: +1 301 846 5747; E-mail: [email protected]
Wen Hong Linda Kao (Johns Hopkins University, Baltimore, MD, USA) Author paper [7]
Tel: +1 410 614 0945; E-mail: [email protected]
[8] And finally... Nature: A new take on tooth evolution
DOI: 10.1038/nature07304
The textbook view of tooth evolution may be due a rethink with the discovery that axolotl teeth are formed from two cell layers, not one, in the developing embryo.
Online in this week’s Nature, Robert Cerny and colleagues demonstrate that axolotl teeth are derived from both ectoderm and endoderm - two of the three cell layers found early on in the developing vertebrate embryo. This goes against the theory that vertebrate teeth arise from ectoderm alone.
Their studies also suggest that the developmental machinery producing teeth evolved just once, and that tooth formation is driven by signals released from neural crest cells.
Author contact:
Robert Cerny (Charles University in Prague, Czech Republic)
Tel: +420 22 195 1851; E-mail: [email protected]
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Items from other Nature journals to be published online at the same time and with the same embargo:
Nature (http://www.nature.com/nature)
[9] E2F1 represses beta-catenin transcription and is antagonized by both pRB and CDK8
DOI: 10.1038/nature07310
[10] The mode of Hedgehog binding to Ihog homologues is not conserved across different phyla
DOI: 10.1038/nature07358
[11] The type IV mucolipidosis-associated protein TRPML1 is an endolysosomal iron release channel
DOI: 10.1038/nature07311
NATURE CELL BIOLOGY (http://www.nature.com/naturecellbiology)
[12] GPHR is a novel anion channel critical for acidification and functions of the Golgi apparatus
DOI: 10.1038/ncb1773
[13] A functional RNAi screen links O-GlcNAc modification of ribosomal proteins to stress granule and processing body assembly
DOI: 10.1038/ncb1783
NATURE GENETICS (http://www.nature.com/naturegenetics)
[14] Functional SNPs in CD244 increase the risk of rheumatoid arthritis in a Japanese population
DOI: 10.1038/ng.205
[15] Rheumatoid arthritis susceptibility loci at chromosomes 10p15, 12q13 and 22q13
DOI: 10.1038/ng.218
[16] Common variants at CD40 and other loci confer risk of rheumatoid arthritis
DOI: 10.1038/ng.233
NATURE GEOSCIENCE (http://www.nature.com/ngeo)
[17] Coseismic fluid-rock interactions at high temperatures in the Chelungpu fault
DOI: 10.1038/ngeo308
[18] Changes in ocean denitrification during Late Carboniferous glacial-interglacial cycles
DOI: 10.1038/ngeo307
[19] Stable intermediate-spin ferrous iron in lower-mantle perovskite
DOI: 10.1038/ngeo309
[20] Intermediate-spin ferrous iron in lowermost mantle post-perovskite and perovskite
DOI: 10.1038/ngeo310
NATURE MATERIALS (http://www.nature.com/naturematerials)
[21] Asymmetric caging in soft colloidal mixtures
DOI: 10.1038/nmat2286
Nature MEDICINE (http://www.nature.com/naturemedicine)
[22] Divergent TLR7 and TLR9 signaling and type I interferon production distinguish pathogenic and nonpathogenic AIDS virus infections
DOI: 10.1038/nm.1871
NATURE METHODS (http://www.nature.com/nmeth)
[23] Identification of genetic variants using bar-coded multiplexed sequencing
DOI: 10.1038/nmeth.1251
[24] Optogenetic analysis of synaptic function
DOI: 10.1038/nmeth.1252
NATURE NANOTECHNOLOGY (http://www.nature.com/nnano)
[25] Direct observation of chemical reactions on single gold nanocrystals using surface plasmon spectroscopy
DOI: 10.1038/nnano.2007.246
[26] Imaging the passage of a single hydrocarbon chain through a nanopore
DOI: 10.1038/nnano.2007.263
[27] CMOS-compatible fabrication of room-temperature single-electron devices
DOI: 10.1038/nnano.2007.267
[28] Spatial periodicity in molecular switching
DOI: 10.1038/nnano.2007.269
Nature NEUROSCIENCE (http://www.nature.com/natureneuroscience)
[29] Sparse odor representation and olfactory learning
DOI: 10.1038/nn2192
Nature PHYSICS (http://www.nature.com/naturephysics)
[30] High-sensitivity diamond magnetometer with nanoscale resolution
DOI: 10.1038/nphys1075
[31] Time-resolved dynamics of the spin Hall effect
DOI: 10.1038/nphys1076
[32] Crystallization of strongly interacting photons in a nonlinear optical fibre
DOI: 10.1038/nphys1074
Nature STRUCTURAL & MOLECULAR BIOLOGY (http://www.nature.com/natstructmolbiol)
[33] Mal3, the Schizosaccharomyces pombe homolog of EB1, changes the microtubule lattice
DOI: 10.1038/nsmb.1482
[34] Phosphorylation switches the general splicing repressor SRp38 to a sequence-specific activator
DOI:10.1038/nsmb.1485
[35] Activation of tyrosine kinases by mutation of the gatekeeper threonine
DOI:10.1038/nsmb.1486
[36] The effect of H3K79 dimethylation and H4K20 trimethylation on nucleosome and chromatin structure
DOI:10.1038/nsmb.1489
[37] Cell-cycle coordination between DNA replication and recombination revealed by a vertebrate N-end rule degron-Rad51
DOI: 10.1038/nsmb.1490
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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.
AUSTRALIA
Parkville: 25
AUSTRIA
Vienna: 21
BELGIUM
Leuven: 4
CANADA:
Montreal: 2
Toronto: 24
Waterloo: 21
CHINA
Hong Kong: 29
Shanghai: 11
CZECH REPUBLIC
Prague: 8
FRANCE
Grenoble: 19
Montpellier: 19
GERMANY
Bayreuth: 19, 20
Berlin: 28
Cologne: 18
Dortmund: 4
Dresden: 8
Düsseldorf: 21
Frankfurt: 24
Julich: 21
GREECE
Athens: 21
Heraklion: 21
HUNGARY
Budapest: 4, 20
ICELAND
Reykjavik: 4
ITALY
Brescia: 4
Rome: 21
Trieste: 28
Turin: 4
JAPAN
Hyogo: 17
Kanagawa: 14
Kochi: 17
Miyagi: 14
Osaka: 12, 17
Saitama: 12
Sendai: 26
Tokyo: 12, 14, 26
Wako: 12
NETHERLANDS
Amsterdam: 16
Hengelo: 4
Leiden: 16
Maastricht: 4
Nijmegen: 4
SINGAPORE
Singapore: 16
SLOVAKIA:
Banská Bystrica: 4
SPAIN
Barcelona: 1
Bellaterra: 32
Zaragoza: 4
SWEDEN
Gothenburg: 4
Linköping: 11
Stockholm: 4, 16
TAIWAN
Taipei: 17
UNITED KINGDOM
Aberdeen: 15
Birmingham: 4
Cambridge: 37
Leeds: 4, 15
London: 4, 15, 16
Manchester: 15, 16
Oxford: 15
Sheffield: 15
Surrey: 33
UNITED STATES OF AMERICA
Alabama
Birmingham: 7
Arizona
Phoenix: 7, 23
Tempe: 18
California
Alameda: 16
Berkeley: 22, 30, 35
Davis: 16
Irvine: 7
Livermore: 20
Los Angeles: 7
San Diego: 23
San Francisco: 36
Santa Barbara: 31
Stanford: 10
Colorado
Fort Collins: 36
Connecticut
New Haven: 2
District of Columbia
Washington: 6, 20
Georgia
Atlanta: 22
Illinois
Argonne: 19, 20
Chicago: 5, 6, 7, 19, 20
Iowa
Iowa City: 18
Kentucky
Lexington: 18
Louisiana
New Orleans: 6
Maine
Lewiston: 30
Maryland
Baltimore: 7, 10
Bethesda: 6, 7, 10, 29
Chevy Chase: 36
Frederick: 6, 7
Gaithersburg: 29
Massachusetts
Boston: 1, 3, 7, 9, 11, 13, 16, 35
Cambridge: 1, 5, 7, 16, 30, 32, 35
Charlestown: 9
Worcester: 3
Michigan
Ann Arbor: 11
New Jersey
Princeton: 24
New York
Manhasset: 16
New Hyde Park: 6
New York: 5, 6, 34
North Carolina
Winston-Salem: 6, 7
Ohio
Cincinnati: 18
Cleveland: 6, 7
Pennsylvania
Lancaster: 6
West Point: 22
Texas
Arlington: 18, 27
Austin: 20
College Station: 30
Galveston: 6
Houston: 16
San Antonio: 7
Virginia
Richmond: 5
Wisconsin
Marshfield: 6
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]
Katherine Anderson (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 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 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)
Alison Stoddart
Tel: +44 20 7843 4593; 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 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 (NPG)
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