NATURE AND THE NATURE RESEARCH JOURNALS PRESS RELEASE
For papers that will be published online on 27 May 2007
This press release is copyrighted to the Nature journals mentioned below.
This press release contains:
· Summaries of newsworthy papers:
Breast cancer susceptibility genes identified – Nature and Nature Genetics
DNA breakage in living colour – Nature Genetics
Forever blowing bubbles – Nature Nanotechnology
Checking immune activation – 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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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 & NATURE GENETICS***********************
(http://www.nature.com/nature)
(http://www.nature.com/ng)
[1], [2] & [3] Oncology: Breast cancer susceptibility genes identified
DOI: 10.1038/nature05887
DOI: 10.1038/ng2075
DOI: 10.1038/ng2064
Four novel breast cancer susceptibility genes are identified in a study published online this week in Nature. The large, genome-wide association study also points to many more genetic markers that should be pursued for their link to the disease. Together with two related papers online in Nature Genetics, these findings increase our knowledge of the genetic component of breast cancer risk, much of which has remained uncharacterised.
Known susceptibility genes — such as BRCA1 and BRCA2 — account for less than 25% of the familial risk of breast cancer. It is believed that a combination of many additional genetic factors, each playing a smaller role, also contribute to the disease. To look for further susceptibility alleles Douglas F. Easton and colleagues conducted an analysis, as part of which 30 single nucleotide polymorphisms (SNPs) were tested in 21,860 patients and 22,578 controls. The authors identify four genes positively associated with genetic susceptibility to breast cancer (FGFR2, TNRC9, MAP3K1 and LSP1). Further investigation indicates that many additional susceptibility alleles of more modest effect may also be identifiable by this approach.
Most previously identified breast cancer susceptibility genes are involved in DNA repair, but the associations reported here appear to relate more to the control of cell growth or to cell signalling. Only one of the genes — FGFR2 — had a clear prior relevance to breast cancer.
In Nature Genetics this week, two studies provide further evidence of the risk for breast cancer. One paper, from David J. Hunter and colleagues, identifies alleles for the gene FGFR2 as being particularly associated with the risk of sporadic postmenopausal breast cancer. Another paper, from Simon Stacey, Kari Stefansson and colleagues, reports genetic variants on each of chromosomes 2 and 16, which both increase the risk of oestrogen-receptor-positive breast cancer. One of these variants is located in close proximity to the gene TNRC9, which was also identified in the study from Easton and colleagues.
Author contacts:
Douglas F. Easton (University of Cambridge, UK) Author paper [1]
Please contact the author of paper [1] through:
Emma Gilgunn-Jones (Press Officer, Cancer Research UK, London, UK)
Tel: +44 207 061 8311; E-mail: [email protected]
David J. Hunter (Harvard School of Public Health, Boston, MA, USA) Author paper [2]
Tel: +1 617 525 2755; E-mail: [email protected]
Kari Stefansson (deCODE Genetics, Reykjavik, Iceland) Author paper [3]
E-mail: [email protected]
Simon Stacey (deCODE Genetics, Reykjavik, Iceland) Author paper [3]
E-mail: [email protected]
You may also contact the authors of paper [3] through:
Edward Farmer (Director of Corporate Communication, deCODE Genetics, Reykjavik, Iceland)
Tel: +1 646 417 4555; E-mail: [email protected]
[4] DNA breakage in living colour
DOI: 10.1038/ng2051
Spontaneous breaks of replicating DNA in bacteria occur at a rate much lower than suspected, according to a study to be published online this week in Nature Genetics. This is the first direct measurement of DNA breakage in normal living cells, and suggests that the potential for such damage to cause larger chromosomal rearrangements is much greater than previously realized.
The cellular machinery that replicates DNA sometimes stalls. While these stalled ‘replication forks’ can be resolved by cleaving the DNA, which allows replication to start again, the frequency of these spontaneous breaks has been unknown. Jeanine Pennington and Susan Rosenberg devised a way to visualize individual bacteria (E. coli) with such a break by inserting a gene encoding a green fluorescent protein that would be triggered by the cell’s response to DNA damage.
The authors observed that approximately one per cent of the cells in their experiment had at least one spontaneous break per generation. Previous reports based on indirect measurements had suggested a rate 20- to 100-fold higher. This low rate of spontaneous breakage suggests that each break must be a much more potent cause of the dangerous genetic instability that can result from the attempt to repair them. The authors suggest that cells, including those of higher organisms, have likely developed robust ways to avoid the creation of such DNA breaks.
Author contact:
Susan Rosenberg (Baylor College of Medicine, Houston, TX, USA)
Tel: +1 713 798 6924; E-mail: [email protected]
Other papers from Nature Genetics to be published online at the same time and with the same embargo:
[5] A conserved molecular pathway mediates myoblast fusion in insects and vertebrates
DOI: 10.1038/ng2055
***************************NATURE NANOTECHNOLOGY***********************************
(http://www.nature.com/nnano)
[6] Forever blowing bubbles
DOI: 10.1038/nnano.2007.150
A surprising new approach to tackling the problem of controlling semiconductor nanowires and carbon nanotubes is presented in online this week in Nature Nanotechnology.
Bubble blowing – or blown film extrusion as it is known in the trade – is already widely used to make plastic bags and other products. Now Charles Lieber and co-workers have shown that it can be used in nanotechnology to control the spacing and alignment of tiny components. The authors suspended either nanowires or nanotubes in a polymer and blew bubbles from the suspension. The bubbles grew to 25 centimetres in diameter and 50 centimetres in height. Moreover, the nanowires or nanotubes were all regularly spaced and pointed in the same direction.
The reasons for this regular spacing and alignment are not fully understood, but the process could prove useful for applications. In an accompanying News & Views article, Alan Dalton writes “there is no doubt, however, that once these issues are addressed and the process is further optimized, the production of nanowire and nanotube films using blown-film extrusion will be an important advance for many application areas.”
Author contact:
Charles Lieber (Harvard University, Cambridge, MA, USA)
Tel: +1 617 496 3169; E-mail: [email protected]
Alan Dalton (University of Surrey, UK) N&V author
Tel: +44 1483 686 787; E-mail: [email protected]
Other papers from Nature Nanotechnology to be published online at the same time and with the same embargo:
[7] Growth and alignment of polyaniline nanofibres with superhydrophobic, superhydrophilic and other properties
DOI: 10.1038/nnano.2007.147
[8] Tunable non-equilibrium gating of flexible DNA nanochannels in response to transport flux
DOI: 10.1038/nnano.2007.148
*****************************NATURE IMMUNOLOGY ************************************
(http://www.nature.com/natureimmunology)
[9] Checking immune activation
DOI: 10.1038/ni1469
Armed 'killer' cells can re-enter lymph nodes to destroy dendritic cells – a specialized type of immune cell – according to a report published this week online in Nature Immunology. Such killing by antigen-specific T cells reduces further priming of naive immune cells of similar specificity, thereby preventing excessive immune cell activation. The results overturn prevailing notions that lymph nodes provide restrictive environments that prevent entry of activated T cells.
Sallusto and colleagues show 'resting' lymph nodes continue to bar entry to previously activated immune ‘killer’ cells called effector memory CD8+ T cells. Upon inflammatory signals that occur during infection, however, lymph nodes are activated and transiently express a chemical signal called CXCL9 and recruits memory T cells directly from the bloodstream. These memory cells express a receptor called CXCR3 that recognizes CXCL9.
In addition to checking further immune activation, the CXCL9 entry pathway provides a means to combat pathogens, including viruses such as HIV that replicate in lymph node tissues. The study should also be instructive to those working toward more effective vaccine development and improving efficacy.
Author contact:
Federica Sallusto (Institute for Research in Biomedicine, Bellinzona, Switzerland)
Tel: +41 91 820 0315; E-mail: [email protected]
Other papers from Nature Immunology to be published online at the same time and with the same embargo:
[10] Lymphoid reservoirs of antigen-specific memory T helper cells
DOI: 10.1038/ni1472
***************************************************************************************************************
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)
[11] Structure of phase III of solid hydrogen
DOI: 10.1038/nphys625
[12] Colossal magnetocapacitance and scale-invariant dielectric response in phase-separated manganites
DOI: 10.1038/nphys626
NATURE MATERIALS (http://www.nature.com/naturematerials)
[13] Dynamic in situ observation of rapid size and shape change of supported Pd nanoparticles during CO/NO cycling
DOI: 10.1038/nmat1924
[14] Zeolite A imidazolate frameworks
DOI: 10.1038/nmat1927
[15] Efficiency enhancement in low-bandgap polymer solar cells by processing with alkane dithiols
DOI: 10.1038/nmat1928
Nature MEDICINE (http://www.nature.com/naturemedicine)
[16] Retinaldehyde represses adipogenesis and diet-induced obesity
DOI: 10.1038/nm1587
Nature BIOTECHNOLOGY (http://www.nature.com/naturebiotechnology)
[17] Improved antimicrobial peptides based on acyl-lysine oligomers
DOI: 10.1038/nbt1309
[18] A ROCK inhibitor permits survival of dissociated human embryonic stem cells
DOI: 10.1038/nbt1310
Nature NEUROSCIENCE (http://www.nature.com/natureneuroscience)
[19] Cytoplasmic and mitochondrial protein translation in axonal and dendritic terminal arborization
DOI: 10.1038/nn1910
[20] The mirror neuron system is more active during complementary compared with imitative action
DOI: 10.1038/nn1911
[21] Cortical reorganization consistent with spike timing– but not correlation-dependent plasticity
DOI: 10.1038/nn1913
[22] Cyclin-dependent kinase 5 governs learning and synaptic plasticity via control of NMDAR degradation
DOI: 10.1038/nn1914
NATURE METHODS (http://www.nature.com/nmeth)
[23] Strategy for the fine characterization of glycosyltransferase specificity using isotopomer assembly
DOI: 10.1038/nmeth1050
Nature STRUCTURAL & MOLECULAR BIOLOGY (http://www.nature.com/natstructmolbiol)
[24] The DIX domain of Dishevelled confers Wnt signaling by dynamic polymerization
DOI: 10.1038/nsmb1247
[25] SET and PARP1 remove DEK from chromatin to permit access by the transcription machinery
DOI: 10.1038/nsmb1248
[26] Structural and biochemical insights into the regulation of protein phosphatase 2A by small t antigen of SV40
DOI: 10.1038/nsmb1254
[27] Structural basis of histone demethylation by LSD1 revealed by suicide inactivation
DOI: 10.1038/nsmb1255
***************************************************************************************************************
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
Carlton: 1
Brisbane: 1
Melbourne: 1
Newcastle: 21
Parkville: 1
Sydney: 21
CHINA
Beijing: 8
DENMARK
Copenhagen: 1
FINLAND
Helsinki: 1
Kuopio : 1
Vaasa : 1
FRANCE
Grenoble: 13
Lyon: 1
Strasbourg: 22
GERMANY
Berlin: 21
Bonn: 1
Hannover: 1
Heidelberg: 1, 24
Stuttgart: 1
Tubingen: 1
ICELAND
Reykjavik: 3
ISRAEL
Haifa: 17
Tel Aviv: 17
JAPAN
Hiroshima: 24
Hyogo: 24
Ibaraki: 23
Kobe: 18
Kyoto: 18
Obe: 18
Tokyo: 19, 23
KOREA
Goyang: 1
Seoul: 1
Ulsan: 1
NETHERLANDS
Amsterdam: 1
Leiden: 1
Nijmegen: 3, 20
Rotterdam: 1
NEW ZEALAND
Dunedin: 1
POLAND
Lodz: 1
Warsaw: 1, 21
SINGAPORE
Singapore: 1, 5
SPAIN
Calatayud: 3
Huesca: 3
Madrid: 1, 13
Zaragoza: 3
SWEDEN
Stockholm: 1, 3
SWITZERLAND
Bellinzona: 9
Bern: 9
TAIWAN
Taipei: 1
THAILAND
Bangkok: 1
UNITED KINGDOM
Cambridge: 1, 11, 24
London: 1
Manchester: 1
Sheffield: 1
Southampton: 1
St Andrews: 11
Sutton: 1
UNITED STATES OF AMERICA
Arizona
Tempe: 14
California
La Jolla: 10, 16
Los Angeles: 1, 3, 14
Mountain View: 1, 10
Pasadena: 18
Santa Barbara: 15
Stanford: 19
Florida
Gainesville: 12
Georgia
Atlanta: 2
Hawaii
Honolulu: 1, 3, 6
Maryland
Baltimore: 27
Bethesda: 1, 9, 2
Gaithersburg: 1
Rockville: 1
Massachusetts
Boston: 1, 16, 2
Cambridge: 6, 2
Minnesota
Minneapolis: 1
Rochester: 1
Missouri
St Louis: 2
New Jersey
Princeton: 26
Rahway: 16
New York
Ithaca: 25
New York: 16, 22, 25
North Carolina
Durham: 10
Raleigh: 10
Ohio
Cleveland: 9
Columbus: 7
Texas
Dallas: 22, 27
Houston: 4
Utah
Salt Lake City: 2
Wisconsin
Marshfield: 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 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 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 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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