Common contributor to chromosome instability in cancer cells

Summaries of newsworthy papers include Can Alzheimer’s disease be infectious?, New drug target for leukaemia, Quick, look sharp, Regulating an ancient arm of our immunity, Activating genes in live animals and Sex cells harbour longevity secrets


For papers that will be published online on 07 June 2009

This press release is copyrighted to the Nature journals mentioned below.

This press release contains:

· Summaries of newsworthy papers:

Nature: Common contributor to chromosome instability in cancer cells

Cell Biology: Can Alzheimer’s disease be infectious?

Genetics: New drug target for leukaemia

Nature: Quick, look sharp

Immunology: Regulating an ancient arm of our immunity

Methods: Activating genes in live animals

And finally … Nature: Sex cells harbour longevity secrets

· 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 Press contacts for the Nature journals are listed at the end of this release.

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[1] Nature: Common contributor to chromosome instability in cancer cells
DOI: 10.1038/nature08136

A newly discovered mechanism may underlie the chromosomal instabilities so commonly seen in cancer cells. The finding not only sheds light on cancer disease progression, but also helps in understanding the basic mechanisms of how cells divide.

Cancer cells with abnormal sets of chromosomes often carry extra centrosomes — cellular structures that help chromosomes separate along a spindle structure during cell division. In this week’s Nature, David Pellman and colleagues use live cell imaging to show that extra centrosomes can promote abnormal chromosome separation. This leads to the chromosome instabilities and may drive the evolution of malignant cell types.

The abnormal segregation occurs because chromosomes fail to attach properly to the spindle that would normally help to separate them. This feature, known as merotely, is known to occur in some cancer cells and has also been linked with chromosome instability.

Author contact:
David Pellman (Dana-Farber Cancer Institute, Boston, MA, USA)
Tel: +1 617 632 4918; E-mail: [email protected]

[2] Cell Biology: Can Alzheimer’s disease be infectious?
DOI: 10.1038/ncb1901

Tangles observed in the brains of Alzheimer’s patients induce the formation of similar inclusions when injected into the brains of healthy mice, reports a study online this week in Nature Cell Biology. This indicates that the tangles have contagious properties and may be similar to prions, which are associated with infectious brain diseases such as 'mad cow disease' and human Creutzfeldt-Jakob disease (CJD).

Markus Tolnay and colleagues extracted sections of brain from mice expressing a mutant form of human tau protein, a component of the Alzheimer’s neurofibrillary tangles. These brain extracts were injected into specific regions in the brains of wild-type mice. They observed that the brain extracts induced normal human tau proteins in the wild-type mice to assemble into neurofibrillary tangles. In addition, these newly formed tangles were able to spread to nearby regions in the brain.

Previously, the formation of tau inclusions observed in the neurodegenerative disease of the tauopathy family had not been thought to be contagious. Prion proteins are thought to infect and propagate by abnormally folding into a structure that is able to convert their normal counterparts into a similar abnormal structure.

This study opens new avenues in tauopathies research that will aim to understand how an abnormal form of tau can spread and how similar tauopathies and prion disease are.

Author contact:
Markus Tolnay (University Hospital, Basel, Switzerland)
Tel: +41 612 652 873; E-mail: [email protected]

[3] Genetics: New drug target for leukaemia
DOI: 10.1038/ng.389

A genetic change in leukaemia cells that is essential to their proliferation, but also makes the cells vulnerable to an existing drug, has been identified in a paper online this week in Nature Genetics. The research highlights specific cells that could be used as drug targets in the treatment of certain types of leukaemia.

Shaoguang Li and colleagues used one particular mouse model of chronic myeloid leukaemia (CML) caused by a mutation called BCR-ABL that fuses together two normally separate genes just as it does in human leukaemia. They found that the mice with this mutation, but lacking a third gene, called Alox5, did not get the leukaemia.

Since drugs targeting Alox5 function have already been developed, the researchers tested one of these and found it prolonged the life of the mice with leukaemia, without impairing the production of normal blood cells. This research demonstrates that a strategy to target specifically the progenitor cells that initiate this leukemia, rather than the bulk of the cancer cells, is feasible.

Author contact:
Shaoguang Li (University of Massachusetts Medical School, Worcester, MA, USA)
Tel: +1 508 865 1691; E-mail: [email protected]

[4] Nature: Quick, look sharp
DOI: 10.1038/nature08103

The way in which our visual system allows us to quickly detect items of interest in a scene is reported in Nature this week. The work advances our current knowledge about brain mechanisms that underlie behaviour, in particular, attention.

In everyday life we quickly focus on objects in our surroundings that are relevant and useful for our ongoing behaviour. These objects fit into specific categories and looking at them may lead to us not noticing other features in our environment that don’t fit into the category. For example, looking for cars when crossing a road may result in not noticing people in our same visual scene.

Using functional magnetic resonance imaging, Marius Peelen and colleagues looked at the neural mechanisms for extracting object category information from complex natural scenes. They report that the pattern of neural activity in the object-selective area of the brain contained information regarding the target category and this even occurred when viewing scenes that were task irrelevant and presented outside the area that attention was focused on. The team also reported that, overall, subjects were able to select relevant pictures in each test successfully and did not respond to irrelevant images.

The findings suggest that an object-category-based biasing mechanism in the brain could be at work during object attention which operates parallel with the visual system. This particular mechanism is very different from others that have been previously identified which relate to spatial and feature-based attention.

Author contact:
Marius Peelen (Princeton University, NJ, USA)
Tel: +1 609 258 8179; E-mail: [email protected]

[5] & [6] Immunology: Regulating an ancient arm of our immunity
DOI: 10.1038/ni.1755
DOI: 10.1038/ni.1756

Two new studies published in Nature Immunology reveal how the ancient arm of our immune system is regulated to avoid collateral tissue damage and how staphylococcal bacteria likewise evade this response. The new findings provide insights for designing therapies for such immune-mediated diseases.

A collection of circulating blood proteins, known as complement, detects and eliminates targeted cells but can also indiscriminately attack host cells if not properly regulated. The complement system can be activated by several pathways, all centering on the generation of an enzyme called C3 convertase, the structure of which was previously unknown.

Piet Gros, John Lambris, and their colleagues teamed up to generate co-crystals of C3 convertase with SCIN, a staphylococcal protein that inhibits the complement system and may contribute to the virulence of these bacteria. The authors found that the central component of the C3 convertase is C3b, which may form a complex with its parent molecule C3. This complex formation may clarify the mechanisms behind activation and ‘self-amplifcation’ of the complement response. SCIN appears to ‘freeze’ the C3 convertase in an inactive state, preventing this enzyme from further activating the complement system and thus protecting the bacteria from the host’s immune response.

This team generated another co-crystal of C3b with the human complement system inhibitor called factor H, which is known to prevent spontaneous C3b activation. They found that C3b self-amplification is prevented because factor H binds to C3b and helps to strip off C3 from the active complex, likewise preventing further activation.

Author contacts:
Piet Gros (Utrecht University, Netherlands) Author paper [5]
Tel: +31 30 2533127; E-mail: [email protected]

John Lambris (University of Pennsylvania, Philadelphia, PA, USA) Author paper [6]
Tel: +1 215 746 5765; E-mail: [email protected]

[7] Methods: Activating genes in live animals
DOI 10.1038/nmeth.1340

Tools to precisely regulate gene expression in single cells or whole organisms are reported online this week in Nature Methods. The research could prove useful in the field of developmental biology where specific patterns of expression are central to many unanswered questions.

To understand the function of genes, it is advantageous to induce their expression in a live organism while controlling the spatial and temporal aspects of expression. With this in mind, Sidney Cambridge and colleagues modified a system known to work in cell culture so that it also worked within organisms.

The authors took small molecules known to activate genes adjacent to a particular promoter and inactivated these molecules by linking them to UV light–sensitive chemical compounds — a process known as caging. Exposing cells containing caged molecules to innocuous levels of UV light removes the cage and allows activation of the gene regulated by the molecule-sensitive promoter. By precisely timing and localizing the activating light, the authors induced gene expression in single cells as well as whole organisms of mouse embryos and tadpoles.

Author contact
Sidney Cambridge (University of Heidelberg, Germany)
Tel: +49 6221 54 8687; E-mail: [email protected]

[8] Nature: Sex cells harbour longevity secrets
DOI: 10.1038/nature08106

The secret of long life may reside within the gene expression profile of sex cells, a Nature paper suggests.

Gary Ruvkun and colleagues show that the gene expression profile of long-lived nematode worm mutants resembles that of ‘germline’ cells rather than non-germline cells. The finding makes sense because it's known that the sex cells of multicellular organisms are essentially immortal, whereas non-germline cells pick up genetic mutations and ‘age’ across the lifespan. Switching to germline characteristics may therefore confer health benefits and longevity to these mutant worms.

Author contact:
Gary Ruvkun (Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA)
Tel: +1 617 726 5959; E-mail: [email protected]

Items from other Nature journals to be published online at the same time and with the same embargo:

Nature (

[9] Subcellular homeostasis of phytohormone auxin is mediated by the ER-localized PIN5 transporter
DOI: 10.1038/nature08066


[10] CPAP is a cell-cycle regulated protein that controls centriole length
DOI: 10.1038/ncb1889

[11] Cell shape changes indicate a role for extrinsic tensile forces in Drosophila germ-band extension
DOI: 10.1038/ncb1894

[12] Epidermal growth factor-like domain 7 (EGFL7) modulates Notch signalling and affects neural stem cell renewal
DOI: 10.1038/ncb1896


[13] A glycopeptide regulating stem cell fate in Arabidopsis thaliana
DOI: 10.1038/nchembio.182


[14] Bimetallic Pd(III) complexes in palladium-catalysed carbon–heteroatom bond formation
DOI: 10.1038/nchem.246


[15] REL, encoding a member of the NF-kB family of transcription factors, is a newly defined risk locus for rheumatoid arthritis
DOI: 10.1038/ng.395

[16] Kif1b is essential for mRNA localization in oligodendrocytes and development of myelinated axons
DOI: 10.1038/ng.376

[17] Mutation in TACO1, a translational activator of COX I, results in cytochrome c oxidase deficiency and late-onset Leigh Syndrome
DOI: 10.1038/ng.390


[18] Macrophage colony-stimulating factor induces the proliferation and survival of macrophages via a pathway involving DAP12 and beta-catenin
DOI: 10.1038/ni.1744

[19] Immune complex relay by subcapsular sinus macrophages and noncognate B cells drives antibody affinity maturation

[20] Immunological synapse formation inhibits, via NF-kappaB and FOXO1, the apoptosis of dendritic cells
DOI: 10.1038/ni.1750


[21] Composite domain walls in a multiferroic perovskite ferrite
DOI: 10.1038/nmat2469

[22] Nonlinear transport in semiconducting polymers at high carrier densities
DOI: 10.1038/nmat2470


[23] Effective, low-titer antibody protection against low-dose repeated mucosal SHIV challenge in macaques
DOI: 10.1038/nm.1974

[24] Hematopoietic colony stimulating factors mediate tumor-nerve interactions and bone cancer pain
DOI: 10.1038/nm.1976


[25] ‘Injecting’ yeast
DOI: 10.1038/ nmeth.1335


[26] Droplet networks with incorporated protein diodes show collective properties
DOI: 10.1038/nnano.2009.121

[27] Observation of the triplet exciton in EuS-coated single-walled nanotubes
DOI: 10.1038/nnano.2009.122

[28] Nanoscale shape-memory alloys for ultrahigh mechanical damping
DOI: 10.1038/nnano.2009.142


[29] Motivation and cognitive control in the human prefrontal cortex
DOI: 10.1038/nn.2321

[30] bCaMKII controls the direction of plasticity at parallel fiber–Purkinje cell synapses
DOI: 10.1038/nn.2329

[31] HDAC1 and HDAC2 regulate oligodendrocyte differentiation by disrupting the beta-catenin–TCF interaction
DOI: 10.1038/nn.2333

[32] NADPH oxidase is the primary source of superoxide induced by NMDA receptor activation
DOI: 10.1038/nn.2334

[33] Mutant LRRK2R1441G BAC transgenic mice recapitulate cardinal features of Parkinson’s disease
DOI: 10.1038/nn.2349

[34] Regulation of AMPA receptor extrasynaptic insertion by 4.1N, phosphorylation and palmitoylation
DOI: 10.1038/nn.2351

Nature PHYSICS (

[35] Demonstration of an ultracold microoptomechanical oscillator in a cryogenic cavity
DOI: 10.1038/nphys1301

[36] Realization of collective strong coupling with ion Coulomb crystals in an optical cavity
DOI: 10.1038/nphys1302

[37] Resolved-sideband and cryogenic cooling of an optomechanical resonator
DOI: 10.1038/nphys1303

[38] Resolved-sideband cooling and position measurement of a micromechanical oscillator close to the Heisenberg uncertainty limit
DOI: 10.1038/nphys1304


[39] ATXR5 and ATXr6 are H3K27 monomethyltransferases required for chromatin structure and gene silencing
DOI: 10.1038/nsmb.1611

[40] A UPF3-mediated regulatory switch that maintains RNA surveillance
DOI: 10.1038/nsmb.1612

[41] Three-dimensional structure and flexibility of a membrane-coating module of the nuclear pore complex
DOI: 10.1038/nsmb.1618

***The following paper will be published electronically on Nature Medicine's website on 02 June at 2000 London time / 1500 US Eastern time. This paper is under embargo until this time, though the rest of the above articles on this release remain under embargo until 07 June at 1800 London time / 1300 US Eastern time ***

[42] Validated germline-competent embryonic stem cell lines from nonobese diabetic mice
DOI: 10.1038/nm.1996


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.

Adelaide: 40
Sydney: 20

Vienna: 9, 35

Ghent: 9

Montreal: 17
Toronto: 15

Beijing: 33
Sichuan: 31

Brno: 9
Olomouc: 9
Praha: 9

Aarhus: 36

Jyvaskyla: 15

Gif-sur-Yvette: 40
Paris: 29, 35
Saint-Martin-d’Heres: 15

Berlin: 7
Dresden: 7
Frankfurt: 12
Garching: 38
Heidelberg: 7, 24
Mannheim: 24
Munich: 7, 17, 24
Tuebingen: 2, 9
Wiesbaden: 17

Bangalore: 22

Brescia: 18

Bunkyo-ku: 21
Kanagawa: 21
Kyoto: 31
Miyazaki: 34
Nagoya: 13
Osaka: 18
Saitama: 21
Sendai-shi: 18, 21
Wako: 21

Amsterdam: 30
Rotterdam: 30
Utrecht: 5, 6, 23, 31

Bilbao: 28
Madrid: 3

Basel: 2, 24
Lausanne: 11, 38
Zurich: 9, 23

Taichung: 10
Taipei: 10

Cambridge: 2, 11, 42
Edinburgh: 16
London: 24
Newcastle: 17
Oxford: 26


Birmingham: 15

Alameda: 15
Davis: 15
La Jolla: 23
Los Angeles: 39
Pasadena: 35
San Diego: 40
San Francisco: 15, 20, 31
Santa Barbara: 22
Stanford: 16

Denver: 15

Tallahassee: 22

Argonne: 27
Chicago: 30

Bloomington: 39

Louisville: 27

Covington: 23

Baltimore: 34
Bethesda: 15
College Park: 35

Amhert: 26
Bedford: 33
Boston: 1, 3, 8, 11, 15, 26
Cambridge: 14, 27, 28, 34
Worcester: 3

Minneapolis: 24

St Louis: 18

Omaha: 15

New Jersey
Princeton: 4

New York
Manhasset: 15
New York: 15, 33, 35, 40, 41

Eugene: 36

Philadelphia: 5, 6
Pittsburgh: 15

Dallas: 31
Houston: 15, 40


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Tel: +44 20 7843 4658; E-mail: [email protected]

Neda Afsarmanesh (Nature New York)
Tel: +1 212 726 9231; E-mail: [email protected]

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Nature Cell Biology (London)
Bernd Pulverer
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Nature Chemical Biology (Boston)
Andrea Garvey
Tel: +1 617 475 9241, E-mail: [email protected]

Nature Chemistry (London)
Stuart Cantrill
Tel: +44 20 7014 4018; E-mail: [email protected]

Nature Genetics (New York)
Myles Axton
Tel: +1 212 726 9324; E-mail: [email protected]

Nature Immunology (New York)
Laurie Dempsey
Tel: +1 212 726 9372; E-mail: [email protected]

Nature Materials (London)
Vincent Dusastre
Tel: +44 20 7843 4531; E-mail: [email protected]

Nature Medicine (New York)
Juan Carlos Lopez
Tel: +1 212 726 9325; E-mail: [email protected]

Nature Methods (New York)
Hugh Ash
Tel: +1 212 726 9627; E-mail: [email protected]

Nature Nanotechnology (London)
Peter Rodgers
Tel: +44 20 7014 4019; Email: [email protected]

Nature Neuroscience (New York)
Kalyani Narasimhan
Tel: +1 212 726 9319; 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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Published: 07 Jun 2009

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