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This press release is copyright Nature.
VOL.468 NO.7321 DATED 11 NOVEMBER 2010
This press release contains:
· Summaries of newsworthy papers:
Neuroscience: Taking the stress out of Parkinson’s disease?
Neuroscience: Rethinking schizophrenia
Neuroscience: The circuitry of fear
Biology: The regeneration game
Neuroscience: New model of Rett syndrome
News and Comment: Matters of the mind
Earth science: An early terrestrial date for oxygenation
Neuroscience: Light it up
Nanoelectronics: High-performance transistors by transfer printing
And finally… Maggot bodies sense bright light
· Mention of papers to be published at the same time with the same embargo
· Geographical listing of authors
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[1] Neuroscience: Taking the stress out of Parkinson’s disease? (AOP)
DOI: 10.1038/nature09536
Anti-hypertensive dihydropyridine drugs could help lessen cell death in Parkinson’s disease, suggests a Nature study that helps pinpoint why the dopamine-secreting neurons of the substantia nigra (SN) are selectively culled during the disease process.
Dopamine-secreting SN neurons are unusual in that they generate rhythmic spontaneous electrical activity without input from other cells. But this innate pacemaking activity creates oxidative stress in the cells’ mitochondria, D. James Surmeier and colleagues show. Knocking out DJ-1, a gene associated with early onset Parkinson’s disease, selectively increases oxidative stress in these already-stressed cells, helping explain why these particular neurons die in Parkinson’s disease.
The pacemaking activity occurs as calcium ions enter the neuron via tiny membranous pores called ion channels. And treating cells with a calcium channel blocker selectively decreases mitochondrial oxidative stress in dopamine-secreting SN neurons, the team demonstrate. So with dihydropyridines already approved for use in humans, it’s hoped these calcium channel blockers might represent a novel neuroprotective strategy for both idiopathic and familial forms of Parkinson’s disease.
CONTACT
D. James Surmeier (Northwestern University, Chicago, IL, USA)
Tel: +1 312 503 4904; E-mail: [email protected]
[2], [3] & [4] Neuroscience: Rethinking schizophrenia (pp 187-212)
In a review of 100 years of schizophrenia history and science in Nature this week, Thomas Insel maintains that the future of the disease lies with ‘rethinking’ of schizophrenia as a neurodevelopmental disorder, and that this refocus is likely to yield new opportunities for treatment development and understanding of disease mechanism. Treatments have been in use for half of this century but there is still little evidence that they have improved outcomes.
Schizophrenia is a debilitating mental disorder affecting about 1 percent of the world’s population. Treatment options have advanced little in the past half century, and the outcome for most sufferers is unsatisfactory. Three Perspectives in a schizophrenia special issue in Nature discuss how better understanding of the emergence of schizophrenia in patients’ brains before its behavioural manifestation could lead scientists towards new types of personalised and pre-emptive treatment.
In another piece, Andreas Meyer-Lindenberg discusses how modern imaging techniques are branching out from the usual functional and structural realm, and focusing on mechanisms of disease risk. These new strategies, such as imaging genetics, give a much needed view into the neural system mediated by heritable risk linked to common variants associated with schizophrenia. Meyer-Lindenberg suggests that characterising mechanisms of illness through such improved imaging techniques can interface with present translation and drug development processes.
In the third Perspective, Jim van Os and colleagues review current understanding of the environmental influences on schizophrenia and the major challenges that lie ahead in teasing them out. The authors argue that longitudinal research is needed to uncover the interaction between genetics and the environment, which determines how the expression of vulnerability in the general population may give rise to more severe psychopathology.
CONTACT
Thomas Insel (National Institute of Mental Health, Bethesda, MD, USA) Author paper [2]
Tel: +1 301 443 3673; E-mail: [email protected]
Andreas Meyer-Lindenberg (University of Heidelberg/Medical Faculty Mannheim, Heidelberg, Germany) Author paper [3]
Tel: +49 612 1703 2001; E-mail: [email protected]
Jim van Os (Maastricht University, Netherlands) Author paper [4]
Tel: +31 4338 75443; E-mail: [email protected]
[5] & [6] Neuroscience: The circuitry of fear (pp 270-282)
The functional architecture of central amygdala microcircuits in the brain and their role in the acquisition and regulation of conditioned fear behaviour is reported in two papers published in Nature this week. The work could potentially open the door for further investigation into animal models of phobia or anxiety and the mechanism of action of drugs used to treat such disorders.
Although the central amygdala (CEA) is known to have a role in the expression of conditioned fear, there is currently a big gap in our knowledge concerning how this behaviour is controlled at a neuronal level. By using classical fear conditioning in mice, Andreas Lüthi and colleagues find that there is neuronal activity in the lateral subdivision of the CEA during fear acquisition. Conditioned fear responses, however, appear to be driven by output neurons in the medial subdivision of the CEA. They show that by inactivating the lateral subdivision of the CEA the acquisition of fear is interfered with.
David Anderson and colleagues use molecular genetic approaches to map the functional connectivity of a subpopulation of neurons located in the lateral subdivision of the CEA. From this, they identify an inhibitory microcircuit within the lateral subdivision that helps to control the level of conditioned freezing that occurs in response to fear.
These papers suggest that there are many highly organized microcircuits at play within the CEA during fear conditioning and the work could help to enhance our understanding of how defined neuronal circuits in the mammalian brain control behaviour.
CONTACT
Andreas Lüthi (Friedrich Miescher Institute for Biomedical Research, Basel, Switzerland) Author paper [5]
Tel: +41 616 978271; E-mail: [email protected]
David Anderson (California Institute of Technology, Pasadena, CA, USA) Author paper [6]
Tel: +1 626 395 6821; E-mail: [email protected]
Wulf Haubensak (California Institute of Technology, Pasadena, CA, USA) Co-author paper [6]
E-mail: [email protected]
[7] Biology: The regeneration game (pp 310-315)
A molecular pathway that helps endothelial cells sustain liver regeneration after partial surgical removal of the liver is revealed in this week’s Nature. The study has therapeutic implications.
Liver sinusoidal endothelial cells promote regeneration of the mouse liver via activation of the VEGFR2-Id1 pathway, Shahin Rafii and colleagues demonstrate. Upregulation of the pathway induces the cells to secrete molecules such as Wnt2 and HGF, which trigger the proliferation of hepatocytes and liver regrowth.
The study confirms that endothelial cells are not simply passive conduits that deliver nutrients and oxygen, but active entities that can instruct the formation of new organs. And transplanting these endothelial cells alongside hepatocytes may prove an effective strategy for achieving durable liver regeneration.
CONTACT
Shahin Rafii (Weill Medical College of Cornell University, New York, NY, USA)
Tel: +1 917 287 3801; E-mail: [email protected]
[8] Neuroscience: New model of Rett syndrome (pp 263-269)
A new mouse model of Rett syndrome offers insights into the cellular and biochemical changes underlying this neurodevelopmental disorder. The findings are reported in Nature this week.
A study of the new model, by Huda Zoghbi and colleagues, suggests that neurons that communicate via the inhibitory signalling molecule GABA may be faulty, leading to the autism-like repetitive behaviours characteristic of this disorder. So strategies targeting GABA neurons may prove useful in the treatment of certain neuropsychiatric disorders.
Rett syndrome can be caused by mutations in the MECP2 gene, and whilst several rodent models of Rett syndrome have been generated carrying complete or cell-type specific deletions and mutations of the gene, these display only a subset of Rett-related symptoms. The new model, described in this week’s Nature, sees MECP2 deleted in just GABA neurons, and the result is a mouse that displays multiple key features of the disorder.
CONTACT
Huda Zoghbi (Baylor College of Medicine, Houston, TX, USA)
Tel: +1 713 798 6558; E-mail: [email protected]
News and Comment: Matters of the mind (pp 154-159 and 163-166)
The challenges of trying to understand the early development of schizophrenia are explored in a News Feature in Nature this week. Paranoia, confusion, hypersensitivity and hallucination can emerge at the same time as developmental changes to thinking, emotion and behaviour that take place during normal adolescence, an overlap that has made this period a particular focus of research. The idea that early symptoms could be used to identify those who might be at high risk of developing schizophrenia years later remains controversial.
The article is part of a collection of pieces in this week’s issue focusing on schizophrenia — the challenges it presents and how some of them might be overcome. A second News Feature examines acute difficulties of drug discovery for schizophrenia and the academic and industry groups now tackling the problem afresh.
In a Comment piece, Norman Sartorius argues that short-lived campaigns are not enough to change the prevailing negative attitudes towards the mentally ill. The stigma that people with mental illnesses are incapable of holding down jobs or maintaining relationships, and are dangerous, irrational and incurable is one of the biggest barriers to improving the lives of those with mental illness. This, he says, will be curbed only if anti-stigma efforts become a permanent fixture of health and social services.
And Til Wykes, in a second Comment article, calls for more rigorous studies of a little known but promising treatment for schizophrenia called cognitive remediation therapy. Relatively cheap, and with few side effects, it could be as valuable in treatment as medication.
Contact for background information:
Helen Pearson (Chief Features Editor, Nature)
Tel: +1 212 726 9340; E-mail: [email protected]
Comment author contacts:
Norman Sartorius (Association for the Improvement of Mental Health Programmes, Geneva, Switzerland)
E-mail: [email protected]
Til Wykes (King’s College London, UK)
Tel: +44 20 7848 5040 or tel: +44 20 7848 0596; E-mail: [email protected]
[9] Earth science: An early terrestrial date for oxygenation (pp 290-293)
The Earth’s atmosphere seems to have been sufficiently oxygen-rich to support complex life forms as early as about 1.2 billion years ago. This conclusion, reported in this week’s Nature, comes from a study of sulphur isotopes in terrestrial sediments preserved in northwest Scotland.
Ancient sediments have provided evidence for increases in atmospheric oxygen concentration about 2.3 billion years ago (the Palaeoproterozoic era) and 0.8 billion years ago (the Proterozoic era), with the most recent increase thought to be connected to the subsequent evolutionary expansion of animal life. One indicator of environmental oxygenation is the fractionation of the sulphur isotope 34S between coexisting sulphate and sulphide minerals, which is greater when sulphide-oxidizing bacteria participate in the sulphur cycle. A distinct increase in this fractionation, from less than 25 per thousand before a billion years ago to over 50 per thousand after 0.64 billion years ago, has been interpreted as marking the later rise in atmospheric oxygen, and the evolution of sulphide-oxidizing bacteria. Other lines of evidence have suggested that atmospheric oxygenation occurred much earlier, but without leaving its mark on the delta34S signature in marine sediments.
John Parnell and colleagues now report delta34S fractionations exceeding 50 per thousand in terrestrial sediments deposited in the Mesoproterozoic 1.18 billion years ago. This suggests that, at this time, near-surface environments such as lake and river sediments were already sufficiently oxygenated to support a complex biota.
CONTACT
John Parnell (University of Aberdeen, UK)
This author is travelling and will be available from 08 November on:
Tel: +44 1224 273 464; E-mail: [email protected]
[10] Neuroscience: Light it up (pp 300-304; N&V)
Fruit flies possess distinct neurons that are activated by lights going on or off, a Nature paper suggests.
Vertebrate retinas also possess such ON and OFF neurons participating in motion detection, so the study by Alexander Borst and colleagues highlights a mechanism that seems conserved across evolution. It at last brings functional significance to long-known anatomical similarities between vertebrate retina and insect eye.
CONTACT
Alexander Borst (Max Planck Institute for Neurobiology, Martinsried, Germany)
Tel: +49 89 8578 3250; E-mail: [email protected]
Chi-Hon Lee (National Institute of Child Health and Human Development, Bethesda, MD, USA) N&V author
Tel: +1 301 435 1940; E-mail: [email protected]
[11] Nanoelectronics: High-performance transistors by transfer printing (pp 286-289; N&V)
A fabrication technique borrowed from large-area electronics has now been used to create nanoscale transistors that incorporate ultrathin layers of the compound semiconductor indium arsenide on a conventional silicon substrate. The new approach, described in this week’s Nature, provides a way to combine the excellent performance of compound semiconductors with the ease of processing of silicon electronics.
As electronic devices continue to shrink, some inherent limitations in the properties of silicon are prompting an investigation of compound semiconductors as high-performance alternatives. Although many schemes have been proposed for growing compound semiconductors on, or joining them to, silicon wafers, these approaches are often too complex to be practical, or produce devices that suffer from high defect density or poor interface quality.
Ali Javey and colleagues avoid these problems by using a flexible polymer stamp to lift single-crystal indium arsenide nanoribbons from their growth substrate, and transfer them to an oxidized silicon substrate. The clean, adhesive-free interfaces that result from this process, combined with the high quality of the crystalline thin films, result in nanoscale transistors with excellent device performance. The technique should be applicable beyond indium arsenide, to integrate other compound semiconductors with silicon technology.
CONTACT
Ali Javey (University of California, Berkeley, CA, USA)
Tel: +1 510 643 7263; E-mail: [email protected]
John Rogers (University of Illinois, Urbana, IL, USA) N&V author
Tel: +1 217 244 4979; E-mail: [email protected]
[12] And finally… Maggot bodies sense bright light (AOP)
DOI: 10.1038/nature09576
Fruitfly larvae have light-sensitive cells in their body wall that help them to sense and squirm away from bright light, a study in this week’s Nature suggests.
The cells are found in every body segment, and projections from them cover the body wall almost entirely, Yuh Nung Jan and colleagues report. The photoreceptors respond to ultraviolet, violet and blue light.
The ability to sense light independently of the eyes is present in many animals but is usually confined to specialized organs. Here, the photoreceptors are widespread, and the phototransduction machinery used by them appears to be distinct from other Drosophila photoreceptor molecules, but similar to a system recently identified in nematode neurons.
CONTACT
Yuh Nung Jan (University of California, San Francisco, CA, USA)
Tel: +1 415 476 8747; E-mail: [email protected]
ALSO IN THIS ISSUE…
[13] Hidden magnetic excitation in the pseudogap phase of a high-Tc superconductor (pp 283-285; N&V)
[14] The mechanism of retroviral integration from X-ray structures of its key intermediates (pp 326-329)
[15] Iron-catalysed oxidation intermediates captured in a DNA repair dioxygenase (pp 330-333)
ADVANCE ONLINE PUBLICATION
[16] Growth of graphene from solid carbon sources
DOI: 10.1038/nature09579
[17] Suppression of inflammation by a synthetic histone mimic
DOI: 10.1038/nature09589
[18] Planar polarized actomyosin contractile flows control epithelial junction remodelling
DOI: 10.1038/nature09566
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
Ottawa: 8
CHINA
Changchun: 13
Shanghai: 15
CROATIA
Zagreb: 13
FRANCE
Bordeaux: 6
Gif sur Yvette: 13
Grenoble: 13
Marseille: 18
Villebon sur Yvette: 17
GERMANY
Berlin: 8
Freiburg: 6
Garching: 13
Göttingen: 13
Heidelberg: 6, 18
Mannheim: 3
Martinsreid: 10
Stuttgart: 13
Tübingen: 6
JAPAN
Nara: 7
NETHERLANDS
Maastrict: 4
SOUTH KOREA
Ulsan: 11
SWITZERLAND
Basel: 5, 6
TAIWAN
Hsinchu: 11
UNITED KINGDOM
Aberdeen: 9
Glasgow: 9
London: 4, 14
Stevenage: 17
UNITED STATES OF AMERICA
California
Berkeley: 11
La Jolla: 8
Los Angeles: 5
Pasadena: 5
San Francisco: 8, 12
Stanford: 5, 6, 13
Illinois
Chicago: 1, 15
Maryland
Bethesda: 2
Minnesota
Minneapolis: 13
New Mexico
Albuquerque: 11
New York
Hempstead: 7
New York: 7, 8, 12, 17
Texas
Houston: 8, 16
Virginia
Ashburn: 12
Wisconsin
Madison: 15
PRESS CONTACTS…
From North America and Canada
Neda Afsarmanesh, Nature New York
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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