This press release contains:
---Summaries of newsworthy papers:
Ageing: Sirtuin increases lifespan in male mice
Biology: How the biological clock influences the heart
Oncology: Translating the role of mTOR signalling in prostate cancer
News and Comment: Legacy of a beautiful mind
Materials science: Like water off a duck’s back
Cancer: Receptor loss promotes metastases in mammary tumours
Physics: Superconductors get a second wind under pressure
Perspective: The open road for computer programs
Neuroscience: Looking into visual responses
Quantum physics: Fault-tolerant topological quantum computing
And finally... Men might not 'become extinct' after all
---Mention of papers to be published at the same time with the same embargo
---Geographical listing of authors
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[1] Ageing: Sirtuin increases lifespan in male mice (AOP; N&V)
DOI: 10.1038/nature10815
One of the mammalian sirtuin proteins, SIRT6, may have a role in regulating lifespan, according to a study published in Nature this week. Researchers demonstrate in mice that enhanced levels of SIRT6 are associated with an increased lifespan in males.
The role of sirtuins in regulating the lifespan of lower organisms is currently a hotly debated issue. Mammals have seven sirtuin proteins, and so far none of those studied has been shown to affect the longevity of mice. Haim Cohen and colleagues now show that overexpression of SIRT6 increases lifespan in male mice, but not in females. The study does not reveal how SIRT6 affects lifespan; why this effect is male-specific also remains to be seen.
CONTACT
Haim Cohen (Bar-Ilan University, Ramat-Gan, Israel)
Tel: +1 972 3531 8383; E-mail: [email protected]
Richard Miller (University of Michigan, Ann Arbor, MI, USA) N&V author
Tel: +1 734 936 2122; E-mail: [email protected]
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[2] Biology: How the biological clock influences the heart (AOP)
Evidence that links circadian rhythms with the development of arrhythmia in mice is presented in Nature this week. The findings raise the possibility that circadian factors may contribute to the diurnal variation seen in the occurrence of sudden cardiac death.
Many aspects of the cardiovascular system exhibit variation that follows circadian rhythms (also known as the biological clock). For example, the occurrence of sudden cardiac death caused by ventricular arrhythmias increases within a few hours of waking in the morning, and peaks again in the evening. Mukesh Jain and colleagues show that a transcription factor that alters susceptibility to arrhythmia in mice is regulated by components of the circadian clock. The transcription factor Klf15 is involved in controlling cardiac electrical stability.
This proof-of-principle study in mice provides a mechanistic link between circadian rhythms and cardiac arrhythmia. Whether similar circadian mechanisms explain sudden cardiac death in humans remains to be seen. These observations offer novel insights into previously unrecognized triggers of electrical instability in the heart, the authors note.
CONTACT
Mukesh Jain (Case Western Reserve University, Cleveland, OH, USA)
Tel: +1 216 368 3607; E-mail: [email protected]
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[3] Oncology: Translating the role of mTOR signalling in prostate cancer (AOP)
DOI: 10.1038/nature10912
The mechanisms through which a key signalling pathway regulates the progression of prostate cancer are explored in a paper published in Nature.
The mammalian target of rapamycin (mTOR) signalling pathway is important in the regulation of protein translation and is activated in many human cancers, making mTOR inhibitors a key therapeutic target. Davide Ruggero and colleagues use a sequencing technique known as ribosome profiling to show how mTOR controls protein translation at a genome-wide level. In prostate cancer cells and in mouse prostate tumours, they find that mTOR regulates the translation of several genes involved in metastasis and cancer invasion (when cancer cells break away from the primary tumour and ‘invade’ the surrounding tissue). The authors also report that inhibition of mTOR signalling with the inhibitor INK128 — currently in clinical trials but described fully for the first time here — reduces the progression of prostate cancers to invasive carcinomas in a mouse model.
Together, the findings further our understanding of how the ‘cancerous’ translation machinery steers specific cancer cell behaviours, including metastasis, and may be therapeutically targeted.
CONTACT
Davide Ruggero (University of California, San Francisco, CA, USA)
Tel: +1 415 514 9755; E-mail: [email protected]
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News and Comment: Legacy of a beautiful mind (pp 455-465)
If Alan Turing were alive today, he would surely be working at the interface of artificial and natural intelligence. As part of a special issue of Nature celebrating the centenary of Turing’s birth, four experts debate whether the brain is a good model for machine intelligence.
Roboticist Rodney Brooks argues that by modelling the brain and computers on each other, we are in an intellectual blind alley. We need a conceptual leap to realize truly intelligent machines, he says. Neuroscientist and chess master Demis Hassabis suggests that we might derive new technologies based on the brain’s algorithms, and physiologist Dennis Bray sees inspiration in the complex workings of the cell. Computer scientist and entrepreneur Amnon Shashua contends that brains and machines are inherently different and that we should harness the abilities of both. A related News Feature assesses the prospects of the Human Brain Project — an ambitious scheme to build a supercomputer simulation that integrates everything we know about the brain.
In other contributions to the special, Nobel-winning biologist Sydney Brenner reflects on parallels between Turing’s logic machines and genetic code, biophysicist and embryologist John Reinitz argues that Turing’s work on pattern formation is still cutting edge, and mathematician Barry Cooper considers the incomputable aspects of the Universe. He argues that if computing can successfully factor in the way that high-level phenomena, such as river flow and zebra stripes, can emerge from the interactions between many biological, physical and chemical processes, great scientific leaps could be made. “If we look at the world with new eyes,” he says, “allowing computation full expression, we may come to startling conclusions.”
For background information, please contact the press office.
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[4] Materials science: Like water off a duck’s back (pp 510-513)
Research that helps predict how liquid droplets interact with flexible fibres is published in Nature this week. The elasticity of fibres is important in a variety of applications, such as the strengthening of paper on drying or the role of feathers in keeping birds warm and dry. Interactions with liquids can affect fibre function; for example, feather barbs can become matted, thereby reducing insulation.
Studying droplet behaviour on flexible fibres, Howard Stone and colleagues identify six parameters, including droplet size and mechanical properties of the fibres, that control how a droplet wets the fibres. Depending on the parameters, the droplet can remain tightly spherical (bridging the fibres), partially wet the fibres, or fully wet the fibres causing them to cling together. The authors demonstrate in a natural system — a goose feather — that by adjusting drop volume they can control the matting of fibre arrays. The study suggests that in living systems different parameters could have evolved to aid survival; for example, to cope with environmental conditions or to collect water.
From a technological perspective, careful control of these parameters offers new opportunities in the adsorption of droplets for functional microstructured materials. Furthermore, the paper emphasizes that drop volume can be used to control wetting in sprays such as hairsprays and in the de-oiling of birds suffering contamination from oil spillages.
CONTACT
Howard Stone (Princeton University, NJ, USA)
Tel: +1 609 258 9493; E-mail: [email protected]
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[5] Cancer: Receptor loss promotes metastases in mammary tumours (pp 538-541)
A study using a mouse model of mammary cancer shows that loss of a specific ‘dependence’ receptor, which controls cell survival and death (apoptosis), promotes metastasis formation. These findings are published in Nature this week and support the tumour-suppressing role of this receptor.
The deleted in colorectal cancer (DCC) gene encodes a dependence receptor and, as its name suggests, is frequently deleted in colorectal cancers and many other cancers. Anton Berns and colleagues constrain its function as a tumour suppressor gene in a mouse model of mammary carcinoma with mutant DCC. They demonstrate that loss of DCC leads to a loss of pro-apoptotic activity and enhanced tumour cell survival. These data indicate that loss of DCC function is not selected for in primary tumour development but that its loss facilitates metastasis.
DCC-deficient metastases have been associated with a worse prognosis and a higher risk of recurrent disease in some cancers.
CONTACT
Anton Berns (The Netherlands Cancer Institute, Amsterdam, The Netherlands)
Tel: +31 2 0512 1991; E-mail: [email protected]
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[6] Physics: Superconductors get a second wind under pressure (AOP)
DOI: 10.1038/nature10813
A record-breaking superconducting transition temperature for iron-based superconductors is reported in this week’s Nature. The work describes how superconductivity vanishes as pressure in a system is increased, then reappears in a second phase with a higher transition temperature.
Iron chalcogenides are a part of a family of super-high temperature superconductors that demonstrate superconductivity at temperatures around 32 kelvin and have a range of technical applications. Pressure has an important role in the production and control of superconductivity in iron-based superconductors. Liling Sun and colleagues show that when subjected to increasing pressure, superconducting iron chalcogenides have a second superconducting region with considerably higher transition temperature (48 kelvin) than the first maximum. This second phase suddenly re-emerges at pressures above 11.5 gigapascals.
The authors explain that pressure can be used to tweak electronic and structural properties of materials without altering the chemistry. They add that high-pressure studies are a useful method of investigating the mechanisms of superconductivity.
CONTACT
Liling Sun (Chinese Academy of Sciences, Beijing, China)
Tel: +86 10 8264 9148; E-mail: [email protected]
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[7] Perspective: The open road for computer programs (pp 485-488)
Most scientific papers rely on computer software for data collection and manipulation, but should the computer code be released alongside the paper or is a ‘natural language’ description of the code sufficient? In a Perspective article in this week’s Nature, Darrel Ince and colleagues argue that anything less than release of the full source code hinders the reproducibility of published results.
It is generally accepted that the data accompanying published scientific papers should be made available on request but journal policies differ in terms of their requirements for the release of computer program source code. Some require the full source code to be made available; others, including Nature, require a description of the computational algorithms used, which is intended to be detailed enough to allow others to write their own code to do similar analysis.
Even releasing the full computer code associated with a given paper does not guarantee reproducibility of results, but the inherent ambiguities in natural language descriptions mean that withholding the code increases the chances that efforts to reproduce results will fail, the authors argue. They propose several potential solutions: journals should require authors to declare the degree of source code accessibility associated with a scientific paper, for example, and funders should provide metadata repositories that describe both programs and data produced by researchers.
CONTACT
Darrel Ince (Open University, Milton Keynes, UK)
E-mail: [email protected]
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[8] Neuroscience: Looking into visual responses (AOP)
DOI: 10.1038/nature10835
The function of a group of neurons in the earliest steps of visual processing is uncovered in this week’s Nature. The study establishes a specific role in visual information processing played by a particular layer within the stack of neurons that make up the mouse cerebral cortex. This layer seems to control the size of responses in other layers to visual stimuli.
The cerebral cortex in sensory areas of the brain is composed of six distinct but interconnected neuronal layers. However, the exact role of individual layers is not well understood, largely due to a lack of tools for manipulating only neurons in particular layers. Massimo Scanziani and colleagues use a technique called optogenetics to specifically manipulate neuron activity in layer 6 of the primary visual cortex in the mouse. They find that layer 6 modulates the size of the response of superficial layer neurons to visual stimuli without altering which stimuli they respond to, a computation called gain change.
The authors suggest that these findings represent an important step towards examining specific functions of distinct circuits in cortical processing.
CONTACT
Massimo Scanziani (University of California, San Diego, La Jolla, CA, USA)
Tel: +1 858 822 3839; E-mail: [email protected]
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[9] Quantum physics: Fault-tolerant topological quantum computing (pp 489-494; N&V)
A method that could facilitate scalable quantum computing is demonstrated in Nature this week.
Scalable quantum computing can be realised only if qubits (which store quantum information) are manipulated fault-tolerantly. This means that the error rate caused by qubit decoherence (a process that corrupts quantum information) is kept below a certain threshold. A prime candidate for achieving this effect is a method called topological error correction, which combines topological quantum computation with error correction.
Jian-Wei Pan and colleagues now report an experimental demonstration of this technique. Their experiment uses state-of-the-art quantum optics technology involving eight-photon cluster states with the required topological properties. This important proof-of-principle experiment illustrates the viability of topological error correction for fault-tolerant quantum information processing.
CONTACT
Jian-Wei Pan (University of Science and Technology of China, Hefei, China)
Tel: +86 55 1360 6493; E-mail: [email protected]
James Franson (University of Maryland, Baltimore County, MD, USA) N&V author
Tel: +1 410 455 8115; E-mail: [email protected]
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[10] And finally... Men might not 'become extinct' after all (AOP)
DOI: 10.1038/nature10843
An analysis of Y chromosome gene loss provides data that are contradictory to the prevalent hypothesis that the human Y chromosome might disappear in the future. The study, which is reported in this week’s Nature, reconstructs evolution of the male-specific region of the Y chromosome over the past 25 million years. This constructive comparative analysis is enabled by sequencing of the male-specific region of the Y chromosome of the rhesus monkey, only the third sex chromosome sequenced to date.
The male-specific region of the Y chromosome retains only three percent of the genes from its ancestral autosome (a non-sex chromosome) owing to genetic decay. To explore historical gene loss and conservation patterns, Jennifer Hughes and colleagues compare the structure of rhesus monkey, which they sequence for the purpose of this study, human and chimpanzee Y chromosomes. They show that during Y chromosome evolution, involving rearrangements in different regions, ancestral gene decay is rapid at first but then tails off quickly. Older regions (or strata) are stable and have not lost any genes in the past 25 million years.
Chimpanzees and humans are separated by only six million years of evolution, whereas the rhesus monkey (an Old World monkey) is a more distant relative. Human and Old World monkey lineages diverged around 25 million years ago, thus the rhesus monkey provides a means for investigating gene loss since this time. The authors conclude that sequencing Y chromosomes from a wider range of divergent lines may enable refinement the reconstruction of Y chromosome evolution presented here.
CONTACT
Jennifer Hughes (Whitehead Institute for Biomedical Research, Cambridge, MA, USA)
Tel: +1 617 258 5174; E-mail: [email protected]
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ALSO IN THIS ISSUE…
[11] Ubiquitin-dependent regulation of COPII-coat size and function (pp 495-500; N&V)
[12] Structural basis of highly conserved ribosome recycling in eukaryotes and archaea (pp 501-506)
[13] Maintenance of muscle stem cell quiescence by microRNA-489 (pp 524-528)
[14] Structure and dynamics of the M3 muscarinic acetylcholine receptor (pp 552-556)
ADVANCE ONLINE PUBLICATION
[15] Sequencing of neuroblastoma identifies chromothripsis and defects in neuritogenesis genes
DOI: 10.1038/nature10910
[16] The mechanism of E2 ubiquitin-conjugating enzyme inhibition by OTUB1
DOI: 10.1038/nature10911
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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. 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.
AUSTRALIA
Melbourne: 9
CANADA
Vancouver: 9
CHINA
Beijing: 6
Guangzhou: 6
Hangzhou: 6
Hefei: 9
Shanghai: 6
FRANCE
Paris: 4
Valbonne: 2
GERMANY
Gauting: 12
Icking: 12
Munich: 12
Regensburg: 12
ISRAEL
Jerusalem: 1
Ramat-Gan: 1
SOUTH KOREA
Ansan: 14
SWEDEN
Lund: 15
SWITZERLAND
Fribourg: 2
THE NETHERLANDS
Amsterdam: 5, 15
Rotterdam: 15
UNITED KINGDOM
Kingston: 7
London: 7
Milton Keynes: 7
UNITED STATES OF AMERICA
California
Berkeley: 11
La Jolla: 3, 8
Palo Alto: 13
San Francisco: 3
Stanford: 13, 14
District of Columbia
Washington: 6
Illinois
Argonne: 6
Maryland
Baltimore: 3, 12, 16
Bethesda: 14, 16
Gaithersburg: 6
Massachusetts
Boston: 2
Cambridge: 10
Missouri
St. Louis: 10
New Jersey
Princeton: 4
New York
New York: 14
Ohio
Cincinnati: 2
Cleveland: 2
Texas
Dallas: 14
Houston: 2, 10
Pittsburgh: 1
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PRESS CONTACTS…
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Tel: +1 212 726 9231; 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
Rebecca Walton, Nature, London
Tel: +44 20 7843 4502; E-mail: [email protected]
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