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VOL.464 NO.7291 DATED 15 APRIL 2010
This press release contains:
· Summaries of newsworthy papers:
Reproduction: Reducing mitochondrial mutations
Astronomy: Homing in on extrasolar planets
Opinion: Preimplantation diagnosis at twenty
Genomics: Cancer genome network
Cancer: Genome remodelling in breast cancer
Genetics: Rare hair loss gene identified
Neuroscience: A spot for every scent
Physics: How interdependent networks fail
Immunology: Inflammatory remarks
Biology: Antibody design cranks up a notch
Neuroscience: Controlling neural circuits
And finally… Truly random? The answer is 42
· Mention of papers to be published at the same time with the same embargo
· Geographical listing of authors
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[1] Reproduction: Reducing mitochondrial mutations (AOP)
DOI: 10.1038/nature08958
***This paper will be published electronically on Nature's website on 14 April 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 15 April, but at a later date. ***
It may be possible to prevent the transmission of mitochondrial mutations in human embryos using nuclear transfer techniques. Although this has been demonstrated in non-human primates, research published online in Nature this week is proof of principal in humans.
Mitochondrial DNA (mtDNA) is transmitted maternally and mutations are a common cause of genetic disease. Douglass Turnbull and colleagues transferred pronuclei between human zygotes and showed onward development to the blastocyst stage in vitro. They also show that carry-over of donor zygote mtDNA is minimal, thus the technique could potentially be used to prevent the transmission of mtDNA disease in humans.
CONTACT
Douglass Turnbull (Newcastle University, UK)
Tel: +44 191 222 8565; E-mail: [email protected]
[2] Astronomy: Homing in on extrasolar planets (pp 1018-1022)
A device called a ‘vortex coronagraph’ has been used to image an extrasolar planet that is very close to its host star. This technical advance, reported this week in Nature, will improve the planet-finding capability of ground-based telescopes, and enable space-based telescopes searching for faint planets to be smaller and more affordable.
Attempts to find extrasolar planets by direct imaging are hampered by the bright scattered light from their host stars. The starlight can be masked by a coronagraph, but because of the wave properties of light, starlight spills beyond the edge of an opaque mask, obscuring faint planets if their angular distance from the star is less than about ten times the diffraction beamwidth.
Eugene Serabyn and colleagues now show that they can reduce the inaccessible zone for planet detection to less than two diffraction beamwidths, by using a coronagraph that shifts the phase of the incoming starlight, causing destructive interference. The ability to see planets at such small angles from their host stars will enable the search for Earth-like planets to be extended to a distance that encompasses several hundred stars, increasing the likelihood of discovering terrestrial analogues.
CONTACT
Eugene Serabyn (Jet Propulsion Laboratory, Pasadena, CA, USA)
Tel: +1 818 393 5243; E-mail: [email protected]
Opinion: Twenty years of preimplantation diagnosis (pp 978-979)
It is time to trust informed prospective parents, guided by clinical geneticists, to decide “whether a condition warrants preimplantation genetic diagnosis”, argues an Opinion piece in Nature this week.
Twenty years ago, a Nature paper reported the first pregnancies to have been brought about following preimplantation genetic diagnosis. Alan Handyside, first author of that paper, argues that today DNA technologies are set to revolutionize fertility science in ways that were unimaginable two decades ago and that these new possibilities will come with ethical and social challenges.
Handyside says that “future regulation should focus not on the seriousness of an inherited condition — currently the main determinant of whether selection is allowed — but on what information about their embryos parents should have access to and what they may do with it”. Although societies might take time to adjust, it is important that authorities don’t legislate against emerging possibilities, he writes: “Legislation is inflexible, whereas regulating within the current law allows authorities to reflect societal changes.”
CONTACT
Alan Handyside (The Bridge Centre, London, UK)
Tel: +44 7714 236623; E-mail: [email protected]
[3] Genomics: Cancer genome network (pp 993-998)
Hundreds of individual human cancer genome sequences are expected to be published in 2010, and thousands more each year after that. The generation of such a comprehensive catalogue of cancer genomic data is made possible by the coordinated efforts of the International Cancer Genome Consortium (ICGC).
In a Perspective article in this week’s Nature, members of the ICGC describe the framework and goals agreed upon by cancer genome scientists and funding agencies in October 2007. Attainment of these goals will be crucial for significantly advancing the field of cancer research.
The main aim of the ICGC is to catalogue 50 different types and subtypes of cancer in adults and children. However, as the participants note, the huge scope of this project coupled with the need for high-quality and standardized data can make this a daunting task. By coordinating research efforts and standardizing data collection and presentation across studies, ICGC members hope to optimize the opportunity to merge and compare data sets. As stated in the article, there is a need for a “delicate balance between protecting participants’ personal data and sharing these data to accelerate cancer research.”
CONTACT
Thomas Hudson (Ontario Institute for Cancer Research, Toronto, Canada)
Tel: +1 416 673 6650; E-mail: [email protected]
[4] Cancer: Genome remodelling in breast cancer (pp 999-1005; N&V)
A new sequencing study of basal-like breast cancer reveals how the tumour genome changes as cells spread. The findings, reported in this week’s Nature, suggest that metastases arise from a minority of cells found in the primary tumour, shedding light on the molecular process of metastasis.
Richard K. Wilson and colleagues compared the genomes of a primary tumour and brain metastasis taken from an African-American patient with basal-like breast cancer. The samples shared 20 identical mutations, whereas the metastasis also contained a handful of unique genetic features. Taken together, the results suggest that cells harbouring a distinct subset of the primary tumour mutation repertoire may be selected for during metastasis.
The team also sequenced the genome from a xenograft sample — a portion of the primary tumour that had been grafted under the skin of immunocompromised mice; a commonly used way to study tumorigenesis. The comparison of the metastatic and xenograft genomes with that of the primary tumour led to the conclusion that metastases arise from a small subset of primary tumour cells.
Basal-like breast cancer, which often responds poorly to standard chemotherapy, can be fatal and clinical progress has been limited by a meagre understanding of the underlying genetic events. The tumour has a highly unstable genome, so a key question is whether metastasis is driven by mutations that occur after the tumour cells arrive at the distant site, or whether the primary tumour generates cells with metastatic-promoting mutations. In this case at least, the results indicate that the latter is true.
CONTACT
Richard Wilson (Washington University in St Louis, MO, USA)
Tel: +1 314 286 1924; E-mail: [email protected]
Joe Gray (Berkeley, CA, USA) N&V Author
Tel: +1 510 495 2438; E-mail: [email protected]
[5] Genetics: Rare hair loss gene identified (pp 1043-1047)
The gene involved in a rare hair loss disorder is identified in Nature this week. Hereditary hypotrichosis simplex (HHS) affects fewer than 200,000 people in the US population. Using genetic linkage analysis, Angela Christiano and colleagues are able to show how the mutated gene affects the hair follicle.
The hair follicle miniaturization that occurs in HHS is a degenerative process that reduces the dimensions of the epithelial and mesenchymal cell compartments, converting thick hair to fine, downy hair. The team shows that the gene involved in HHS, APCDD1, encodes a membrane-bound glycoprotein abundantly expressed in human hair follicles. Functional studies show that APCDD1 inhibits Wnt signalling, and is thus a novel component of this signal transduction pathway with a potentially important role in human hair growth.
CONTACT
Angela Christiano (Columbia University, New York, NY, USA)
Tel: +1 212 305 9565; E-mail: [email protected]
[6] Neuroscience: A spot for every scent (AOP)
DOI: 10.1038/nature08961
***This paper will be published electronically on Nature's website on 14 April 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 15 April, but at a later date. ***
The olfactory bulb of zebrafish has small discrete groups of neurons that process different odors and drive the perception of abrupt changes in scents. These findings, presented this week in Nature, are consistent with models stating that there are discrete states of neuronal circuits, and could be relevant in other sensory and cognitive processes.
Sensory stimuli are sorted into specific perceptual categories in the brain, which correspond to distinct patterns of neuronal activity. In theory, the neuronal pattern for these categories can be recorded if there is abrupt switching between the distinct patterns of neuronal circuits.
Rainer Friedrich and colleagues accomplished this task by presenting zebrafish with a gradually morphing — either in concentration or molecular composition — set of odors while recording neuronal activity patterns in the olfactory bulb. The scientists found that neuronal circuits were largely insensitive to changes in odor concentration. However, morphing one odor into another resulted in an abrupt transition in odor representation in the neuronal circuits. This abrupt change in odor representation was mediated by a small group of neurons in the higher processing centers of the olfactory bulb, rather than a global network of neurons. Friedrich and colleagues concluded that the olfactory bulb classifies odors into many discrete and specific neuronal patterns.
CONTACT
Rainer Friedrich (Friedrich Miescher Institute for Biomedical Research, Basel, Switzerland)
Tel: +41 61 697 8614; E-mail: [email protected]
[7] Physics: How interdependent networks fail (pp 1025-1028; N&V)
Systems of interdependent networks are more susceptible to catastrophic breakdown than each of their component networks would be in isolation; and properties that make isolated networks more robust can make coupled networks more vulnerable. These findings, published this week in Nature, highlight the need to consider interdependent network properties when designing critical coupled infrastructures, such as power and communications systems.
Real-world networks are often coupled together, so that failure of nodes in one network may lead to failure of dependent nodes in other networks. The result may be a catastrophic cascade of failures, as happened in the electrical blackout that affected much of Italy in September 2003.
Sergey Buldyrev and colleagues provide a framework for understanding such cascading failures in interacting networks. They discover that, as with isolated networks, there is a critical fraction of disrupted nodes above which the entire system breaks down, but this fraction is smaller for the coupled networks. Moreover, whereas isolated networks are stabilized by having a broad ‘degree distribution’ (a wide range in the number of connections each node has to other nodes), in interdependent networks this makes failure more likely. This surprising behaviour must be taken into account if robustness is to be preserved in interconnected networks.
CONTACT
Sergey Buldyrev (Yeshiva University, New York, NY, USA) – co-author
Tel: +7 812 428 7116; E-mail: [email protected]
Roni Parshani (Bar-Ilan University, Ramat-Gan, Israel) – co-author
Tel: +972 544448629; E-mail: [email protected]
Gerald Paul (Boston University, MA, USA) – co-author
Tel: +1 781 861 6279; E-mail: [email protected]
Eugene Stanley (Boston University, MA, USA) – co-author
Tel: +1 857 891 1941; E-mail: [email protected]
Shlomo Havlin (Bar-Ilan University, Ramat-Gan, Israel) – co-author
Tel: +972 3 531 8436; E-mail: [email protected]
Alessandro Vespignani (Bloomington, IN, USA) N&V author
Tel: +1 812 856 1829; [email protected]
[8] Immunology: Inflammatory remarks (AOP)
DOI: 10.1038/nature08949
***This paper will be published electronically on Nature's website on 14 April 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 15 April, but at a later date. ***
The discovery of a white blood cell population that mediates intestinal immune pathology could represent a new target for therapies against inflammatory bowel disease.
Fiona Powrie and colleagues focussed on a bacterially driven form of colitis. The leukocytes, which respond to the inflammatory molecule interleukin (IL)-23, accumulate in the colon where they promote inflammation via the production of two proteins: IL-17 and interferon-gamma.
IL-23-driven inflammation is more usually linked to the action of T-helper 17 cells, a particular type of immune cell. But this study, reported in this week’s Nature, highlights the ability of IL-23 to influence other cell types and drive T-cell-independent colitis. This newly discovered IL-23-driven pathway may contribute to inflammatory bowel disease, the authors speculate.
CONTACT
Fiona Powrie (University of Oxford, UK)
Tel: +44 1865 2285494; E-mail: [email protected]
[9] Biology: Antibody design cranks up a notch (pp 1052-1057)
Two new antibodies designed to block specific Notch receptors may prove to be useful anticancer drugs and basic research tools, a Nature study suggests.
The Notch signalling pathway has a key role in cell communication, fate and growth, and aberrant Notch signalling has been implicated in many diseases, including cancer. Christian W. Siebel and colleagues have generated highly specific antibodies to two of the four Notch receptors, Notch1 and Notch2. The anti-Notch1 antibody blocks tumour growth in various mouse cancer models, by inhibiting cancer cell growth and preventing the formation of new tumour-nourishing blood vessels.
Less specific drugs that block multiple Notch receptors already exist, but they can cause intestinal toxicity and block other signalling pathways. The new antibodies have an improved safety profile and are highly specific. This makes them clinically attractive, and a useful research tool for teasing apart the roles of specific Notch receptors.
CONTACT
Christian Siebel (Genentech, South San Francisco, CA, USA)
Tel: +1 650 225 2751; E-mail: [email protected]
[10] Neuroscience: Controlling neural circuits (AOP)
DOI: 10.1038/nature08928
***This paper will be published electronically on Nature's website on 14 April 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 15 April, but at a later date. ***
A study in this week’s Nature suggests that the protein neuregulin 1 (Nrg1) and its receptor ErbB4 control the development of so-called inhibitory neural circuits in the mammalian cerebral cortex, which are needed to fine-tune the level of activity of other neurons. The work provides a new perspective to the involvement of these genes in the origins of schizophrenia.
Oscar Marin and colleagues have analysed the pattern of gene expression for Nrg1 and ErbB4, and knocked out or ramped up gene expression, in transgenic mice. Their results show that ErbB4, probably mediated by Nrg1, regulates the connectivity of certain classes of interneurons whose activity depends on the neurotransmitter GABA.
Several studies have associated Nrg1 and ErbB4 with schizophrenia, but exactly how these proteins are involved in the progression of the disease has been unclear. Although preliminary, this work opens new avenues for research.
CONTACT
Oscar Marin (CSIC & Universidad Miguel Hernández, Sant Joan d'Alacant, Spain)
Tel: +34 9659 19384; E-mail: [email protected]
[11] And finally… Truly random? The answer is 42 (pp 1021-1024; N&V)
An experiment that generates 42 genuinely random numbers is published in Nature this week. As well as having conceptual implications, this work has practical implications for cryptography and for numerical simulations of physical and biological systems.
True randomness does not exist in classical physics, where randomness is necessarily a result of forces that may be unknown but do exist. Quantum systems, however, are intrinsically random. But randomness is difficult to prove because it is not readily distinguishable from noise and other uncontrollable factors. Antonio Acín and colleagues show that the non-local correlations of entangled quantum particles can be used to certify the presence of genuine randomness. It is thereby possible to design a cryptographically secure random number generator that does not require any assumption about the internal working of the device. They then perform a proof-of-concept experiment in a system of two entangled atoms in which 42 new random numbers are generated.
CONTACT
Antonio Acín (Institut de Ciencies Fotoniques, Castelldefels, Spain)
Tel: +34 935 534062; E-mail: [email protected]
Valerio Scarani (National University of Singapore, Singapore) N&V Author
Tel: +65 65162813; E-mail: [email protected]
ALSO IN THIS ISSUE…
[12] Real-time tRNA transit on single translating ribosomes at codon resolution (pp 1012-1017; N&V)
[13] Dissection of genetically complex traits with extremely large pools of yeast segregants (pp 1039-1042; N&V)
[14] Phosphate oxygen isotopic evidence for a temperate and biologically active Archaean ocean (pp 1029-1032)
[15] Functional genomic screen for modulators of ciliogenesis and cilium length (pp 1048-1051)
[16] Migrastatin analogues target fascin to block tumour metastasis (pp 1062-1066)
[17] Long non-coding RNA HOTAIR reprograms chromatin state to promote cancer metastasis (pp 1071-1076)
[18] CpG islands influence chromatin structure via the CpG-binding protein Cfp1 (pp 1082-1086)
ADVANCE ONLINE PUBLICATION
***This paper will be published electronically on Nature's website on 14 April 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 15 April, but at a later date. ***
[19] Widespread transcription at neuronal activity-regulated enhancers
DOI: 10.1038/nature09033
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.
BELGIUM
Brussels: 11
ESTONIA
Tallinn: 14
GERMANY
Hamburg: 19
Leipzig: 8
ISRAEL
Ramat-Gan: 7
ITALY
Trento: 5
JAPAN
Saitama: 12
KOREA
Suwon: 15
NETHERLANDS
Amsterdam: 17
NORWAY
Trondheim: 14
SPAIN
Albacete: 10
Barcelona: 11
Castelldefels: 11
Saint Joan d’Alacant: 10
SWITZERLAND
Basel: 6
Geneva: 11
Oxford: 8
Schwerzenbach: 5
UNITED KINGDOM
Cambridge: 11, 18
Edinburgh: 18
Newcastle: 1
UNITED STATES OF AMERICA
California
Davis: 10
Foster City: 17
La Jolla: 15
Menlo Park: 12
Pasadena: 2
San Francisco: 19
South San Francisco: 9
Stanford: 5, 9, 12, 17
Connecticut
New Haven: 14
Maryland
Baltimore: 12, 17, 19
College Park: 11
Massachusetts
Boston: 7, 19
Cambridge: 17
Missouri
St Louis: 4
New Jersey
Princeton: 13
New York
New York: 5, 7, 13, 16
Upton: 16
North Carolina
Chapel Hill: 4
Texas
Dallas: 19
Wisconsin
Madison: 19
Paper [3] is authored by The International Cancer Genome Consortium (ICGC). There are 177 institutions in The ICGC and we have not included them within the geographical listing. We will post a PDF with the full list of authors and their affiliations on the Nature press site.
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From Japan, Korea, China, Singapore and Taiwan
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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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