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This press release is copyright Nature.
VOL.461 NO.7267 DATED 22 OCTOBER 2009
This press release contains:
· Summaries of newsworthy papers:
Neuroscience: Repairing memory after a sleepless night
Imaging: High-sensitivity stimulated emission microscopy
News Features: The Road to Copenhagen
Opinion: Views from around the world
Hearing: Cells process painful sounds
Oncology: Signalling pathway link to cancer
Plant biology: Understanding melon sex determination
Oncology: Cancer link to microenvironment
And finally… Why have sex with someone else
· Mention of papers to be published at the same time with the same embargo
· Geographical listing of authors
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[1] Neuroscience: Repairing memory after a sleepless night (pp 1122-1125)
The cognitive deficits caused by sleep deprivation may be reversible by reducing the concentration of a specific enzyme in the hippocampus of the brain. The findings, reported in this week’s Nature, could present a new approach to treating the memory and learning deficits of insomnia.
Sleep deprivation afflicts millions of people and can lead to short- and long-term memory and learning problems. Ted Abel and colleagues found that sleep deprivation in mice affects an important molecular pathway in the hippocampus — a region of the brain known to be important for memory and learning. Mice deprived of sleep had increased levels of the enzyme PDE4 and reduced levels of the molecule cAMP, the latter of which is crucial in forming new synaptic connections in the hippocampus as a result of learning.
By administrating an inhibitor of PDE4 to the sleep-deprived mice, the researchers were able to reverse the decrease in cAMP concentration. This reversal also helped to rescue deficits in synaptic connections in the hippocampus and therefore counteract some of the memory consequences of sleep deprivation.
CONTACT
Ted Abel (University of Pennsylvania, Philadelphia, PA, USA)
Tel: +1 215 898 3100; E-mail: [email protected]
[2] Imaging: High-sensitivity stimulated emission microscopy (pp 1105-1109; N&V)
Colourful, non-fluorescent tiny molecules, such as haemoglobin, can now be imaged with high resolution and sensitivity thanks to a new microscopy technique revealed in this week’s Nature. The technique promises to find broad applications in medical imaging and biological research.
The method exploits a property called stimulated emission, in which a photon hitting an atom causes an electron to drop an energy level and results in the creation of another photon. Stimulated emission can be applied to all molecules, giving the technique a big advantage over other microscopy methods that either use fluorescent tags to mark key molecules, or exploit non-fluorescent techniques but with lower sensitivity. Stimulated emission microscopy thus offers the opportunity to study a plethora of non-fluorescent, colourful molecules, which have until now not been seen in super-resolution microscopy.
Xiaoliang Sunney Xie and colleagues demonstrate proof-of-principle in a handful of biological systems. In particular, they show that the technique can be used to monitor the delivery of a particular non-fluorescent drug across the skin, highlighting distribution of the blue dye at both cellular and tissue levels . They also demonstrate detailed imaging of the blood vessels in a nude mouse ear, tracking the position of single red blood cells within individual capillaries and raising the prospect of three-dimensional mapping of blood oxygenation levels.
CONTACT
Xiaoliang Sunney Xie (Harvard University, Cambridge, MA, USA)
Tel: +1 617 496 9925; E-mail: [email protected]
Stefan Hell (Max-Planck-Institute for Biophysical Chemistry, Gottingen, Germany) N&V author
Tel: +49 551 201 2501; E-mail: [email protected]
News Features: The Road to Copenhagen (pp 1042-1052)
In this week’s issue, Nature's News and Opinion sections look at some of the key negotiation issues in the lead up to the United Nations climate summit in Copenhagen in December. The package of articles focuses on the developing world and the part that it will play in negotiations and in battling climate change.
In one News Feature, Anjali Nayar reports from the Himalayas in Bhutan, a country at the forefront of adaptation efforts among the world's poorest nations. Bhutan was the first nation to obtain support for its adaptation work from the Least Developed Countries Fund, established by the United Nations to help developing countries prepare for the effects of global warming. She reports on flood-prevention efforts to lower the water level of a lake that is swollen by water from a melting glacier.
In a second News Feature, Jeff Tollefson is in Peru investigating a relatively simple and inexpensive method that tropical countries can use to assess how much carbon is in their forests. These nations will need to conduct such inventories if they are to receive carbon-credit money for their efforts to stop deforestation and forest degradation.
CONTACT
Richard Monastersky (News Editor, Nature News, Washington, DC, USA)
Tel: +1 202 737 4855; E-mail: [email protected]
Opinion: Views from around the world (pp 1054-1057)
In an Opinion article in Nature this week, Rajendra Pachauri, chairman of the Intergovernmental Panel on Climate Change, contends that India wants to be a constructive partner in the Copenhagen negotiations. He says that the country hopes to get credit for taking domestic actions even though it cannot accept any mandatory limits on emissions.
In another article, Jiahua Pan examines the stated goal by G8 leaders to seek a global emissions reduction of 50% by 2050, with 80% cuts by the developed world. Pan argues that wealthier nations will need to make greater emissions cuts than they realize to reach equity with developing nations.
Finally, Raúl Estrada-Oyuela, who guided the negotiations that produced the Kyoto Protocol in 1997, argues that success in Copenhagen will depend on the skills of the lead negotiator.
CONTACT
Rajendra Pachauri (The Energy and Resources Institute, New Delhi, India)
E-mail: [email protected]
Jiahua Pan (Institute for Urban & Environmental Studies, Chinese Academy of Social Sciences, Beijing, China)
E-mail: [email protected]
Raúl Estrada-Oyuela (Buenos Aires, Argentina)
E-mail: [email protected]
[3] Hearing: Cells process painful sounds (pp 1126-1129)
A particular type of neuron found in the ear may help to process painfully loud sounds, a Nature study suggests. The findings could explain why partial hearing loss is sometimes associated with a heightened sensitivity to loud, or even moderate, sound.
Type II cochlear afferent neurons are thin nerve cells thought to relay information from the inner ear to the brain. But the cells are relatively scarce and their exact function has been a mystery. Paul Fuchs and colleagues demonstrate that these cells can convey electrical information. The cells receive inputs from cochlear outer hair cells which vibrate in response to sounds and they are activated by ATP — a chemical known to be released during tissue damage. Together, the findings suggest that this cell type could be important for processing traumatic sound that can damage the cochlea.
CONTACT
Paul Fuchs (Johns Hopkins University School of Medicine, Baltimore, MD, USA)
Tel: +1 410 955 6311; E-mail: [email protected]
[4] & [5] Oncology: Signalling pathway link to cancer (AOP)
DOI: 10.1038/nature08460
DOI: 10.1038/nature08462
***This paper will be published electronically on Nature's website on 21 October at 1800 London time / 1300 US Eastern time (which is also when the embargo lifts) as part of our AOP (ahead of print) programme. Although we have included it on this release to avoid multiple mailings it will not appear in print on 22 October, but at a later date. ***
The NF-kappaB signalling pathway has a vital role in certain cancers, according to two Nature studies published this week. The results highlight potential targets for therapeutic design.
Mutated versions of the KRAS gene are found in many human tumours, most of which are aggressive and respond poorly to standard therapies. Cancerous cells containing mutated KRAS depend on a key component of the NF-kappaB signalling pathway, the enzyme TBK1, William Hahn and colleagues show. Suppressing TBK1 causes these cells to die in a tissue culture model.
Tyler Jacks and colleagues demonstrate that NF-kappaB signalling is actively involved in the development and maintenance of lung tumours in mice carrying mutated Kras and lacking the tumour suppressor protein p53. Together, the studies suggest that drugs that inhibit NF-kappaB or TBK1 could prove useful targeted therapies for the treatment of cancer patients with defined Kras mutations.
CONTACT
William Hahn (Dana-Farber Cancer Institute, Boston, MA, USA) Author paper [4]
Tel: +1 617 632 2641; E-mail: [email protected]
Tyler Jacks (Massachusetts Institute of Technology, Cambridge, MA, USA) Author paper [4]
Tel: +1 617 253 0262; E-mail: [email protected]
[6] Plant biology: Understanding melon sex determination (pp 1135-1138)
A model for the mechanism that determines the sex of melon flowers is proposed in this week’s Nature.
Male flowers express the gene CmWIP1, Abdelhafid Bendahmane and colleagues report. But the same gene is silenced in female flowers. This silencing is caused by an epigenetic change, meaning that the DNA sequence of CmWIP1 remains unchanged. In this case, a mobile genetic element called a transposon has become inserted into the plant genome near the CmWIP1 gene, where it triggers chemical changes that switch the gene off.
CONTACT
Abdelhafid Bendahmane (French National Institute for Agricultural Research, Evry, France)
Tel: +33 1 60 87 45 02; E-mail: [email protected]
[7] Oncology: Cancer link to microenvironment (pp 1084-1091)
A key signalling pathway that operates in mammary gland connective tissue cells helps to suppress the development of mammary tumours, a Nature paper suggests. The study is important because it helps tease apart the complex links between tumour microenvironment and cancer development.
It has been thought for some time that the connective tissue surrounding tumours — also known as the tumour microenvironment — is important for helping the tumour to grow and survive, but it was not clear how. Gustavo Leone and colleagues show that deletion of the tumour suppressor gene Pten in fibroblasts — connective tissue cells — of mammary glands leads to the accelerated development of mammary tumours in mice. Furthermore, tumour development goes hand in hand with other changes in the local cellular environment, such as increased blood vessel formation and immune cell infiltration.
Pten loss and related changes in gene expression can also be observed in the connective tissue of human breast tumours, suggesting that the signalling system operates in man as well as mouse. The team also highlights Pten’s influence on a transcription factor called Ets2 as being critical for Pten’s tumour suppressive functions in the connective tissue.
CONTACT
Gustavo Leone (The Ohio State University, Columbus, OH, USA)
Tel: +1 614 688 4567; E-mail: [email protected]
[8] And finally… Why have sex with someone else? (AOP)
DOI: 10.1038/nature08496
***This paper will be published electronically on Nature's website on 21 October at 1800 London time / 1300 US Eastern time (which is also when the embargo lifts) as part of our AOP (ahead of print) programme. Although we have included it on this release to avoid multiple mailings it will not appear in print on 22 October, but at a later date. ***
Why have sex with someone else when you can have sex with yourself? Because cross-fertilization aids rapid evolution and avoids inbreeding, a study of nematode worms reported in this week’s Nature suggests.
These particular advantages of cross- versus self-fertilization have been mooted many times, but have proved hard to test experimentally. In this study, Patrick Phillips and colleagues subject Caenorhabditis elegans to selective pressures in the lab to show that both benefits play a role in promoting outcrossing. The results help explain why cross-fertilization is so prevalent, despite the associated high costs of having to produce males
CONTACT
Patrick Phillips (University of Oregon, Eugene, OR, USA)
Tel: +1 541 346 0916; E-mail: [email protected]
ALSO IN THIS ISSUE…
[9] The DNA-damage response in human biology and disease (pp 1071-1078)
[10] Information Causality as a Physical Principle (pp 1101-1104)
[11] Trench-parallel anisotropy produced by serpentine deformation in the hydrated mantle wedge (pp 1114-1117)
[12] Unexpected Consequences of a Sudden and Massive Transposon Amplification on Rice Gene Expression (pp 1130-1134)
[13] Structural basis for biosynthetic programming of fungal aromatic polyketide cyclization (pp 1139-1143; N&V)
[14] Structural basis for translational fidelity ensured by tRNA lysidine synthetase (pp 1144-1148)
GEOGRAPHICAL LISTING OF AUTHORS…
The following list of places refers to the whereabouts of authors on the papers numbered in this release. For example, London: 4 - this means that on paper number four, there will be at least one author affiliated to an institute or company in London. 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.
CANADA:
Quebec: 7
Toronto: 1
CZECH REPUBLIC
Prague: 9
FRANCE
Montfavet: 6
Versailles: 6
GERMANY
Cologne: 4
Dortmund: 4
JAPAN
Higashi-Hiroshima: 11
Kyoto: 12
Shizuoka: 11
Tokyo: 14
Yokohama: 14
POLAND
Gdansk: 10
SINGAPORE
Singapore: 10
UNITED KINGDOM
Bristol: 10
Cambridge: 9
Glasgow: 1
UNITED STATES OF AMERICA
California
Irvine: 13
Georgia
Athens: 12
Maryland
Baltimore: 3, 13
Chevy Chase: 4
Massachusetts
Boston: 4
Cambridge: 2, 4, 5
Minnesota
Minneapolis: 12
New York
New York: 14
Ohio
Columbus: 7
Oxford: 7
Oregon
Eugene: 8
Pennsylvania
Philadelphia: 1
PRESS CONTACTS…
From North America and Canada
Neda Afsarmanesh, Nature New York
Tel: +1 212 726 9231; E-mail: [email protected]
Katie McGoldrick, Nature Washington
Tel: +1 202 737 2355; E-mail: [email protected]
From Japan, Korea, China, Singapore and Taiwan
Mika Nakano, Nature Tokyo
Tel: +81 3 3267 8751; E-mail: [email protected]
From the UK/Europe/other countries not listed above
Jen Middleton, Nature London
Tel: +44 20 7843 4502; E-mail [email protected]
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