Spintronics take the next logical step - Nature Physics; How a genetic mutation influences schizophrenia - Nature Neuroscience; Discovery of a context-dependent oncogene - Nature Cell Biology

Nature and the Nature Research Journals Press Release-For papers published online on 23 October 2005

NATURE AND THE NATURE RESEARCH JOURNALS PRESS RELEASE

For papers published online on 23 October 2005

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

This press release contains:
* Summaries of newsworthy papers:
* Spintronics take the next logical step - Nature Physics
* How a genetic mutation influences schizophrenia - Nature Neuroscience
* Discovery of a context-dependent oncogene - Nature Cell Biology
* 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 http://press.nature.com. Press contacts for
the Nature journals are listed at the end of this release.

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FOLLOWING ITEMS. IF PUBLISHING ONLINE, PLEASE CARRY A HYPERLINK TO THE
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***************************NATURE PHYSICS****************************
(http://www.nature.com/naturephysics)

[1] Spintronics take the next logical step

DOI: 10.1038/nphys149

MP3 players and iPods wouldn't exist if not for the application of 'spin
valve' read-heads - in which an electron's spin rather than its charge is
manipulated - a technique that has revolutionized the performance of
computer hard disk drives. In the November issue of Nature Physics,
Christian Schoenenberger and colleagues describe a carbon nanotube
transistor that operates on a similar principle, opening up a promising
avenue towards the introduction of spin-based devices into computer chips.
Conventional electronic circuits in computer chips process
information by encoding it in the form of electronic charge. But this is not
the only way. The spin of an electron can in principle be used to perform
all the same operations as charge, which is one of the key aims of the
emerging field of spin-electronics, or spintronics. The putative advantages
of spin-based circuits over charge-based circuits include lower power
consumption and heat generation, higher speed, smaller devices, and most
importantly, the potential to do things, such as quantum computation, that
conventional electronics can't.
The authors have developed a device that consists of a single carbon
nanotube connected to two magnetic electrodes - which control the
orientation of the spins of the electrons injected into the device. Below
this, they placed a third isolated magnetic electrode - which controls the
passage of injected spins through the device. Theoretical proposals for
constructing so-called 'spin transistors' have been around for many years,
but this is the first time that such a device has been convincingly
realized.

Author contact:
Christian Schoenenberger (University of Basel, Switzerland)
Tel: +41 61 267 36 90, E-mail: [email protected]

Other papers from Nature Physics to be published online at the same time and
with the same embargo:

[2] Membrane disruption by optically controlled microbubble cavitation
DOI: 10.1038/nphys148

*************************NATURE NEUROSCIENCE************************
(<http://www.nature.com/natureneuroscience>)

[3] & [4] How a genetic mutation influences schizophrenia

[3] DOI: 10.1038/nn1562 &
[4] DOI: 10.1038/nn1572

A major risk factor for schizophrenia is a genetic mutation called 22q11.2
microdeletion, which occurs in 1 of 4000 people. One third of people with
this mutation develop schizophrenia or another psychotic disorder. Two
groups shed light on the linkage between the mutated genes and the cognitive
and physiological changes that may be involved in schizophrenia, in the
November issue of Nature Neuroscience.
In one study, Doron Gothelf and colleagues administered
psychological tests to children with and without 22q11.2 syndrome and
examined them again several years later, in late adolescence or early
adulthood. They found a strong effect of a particular mutation in the gene
COMT, which produces a protein that breaks down the neurotransmitter
dopamine. Subjects with this mutation had an abnormal decrease in the size
of the prefrontal cortex (a brain region involved in reasoning and control),
as well as lower IQs and more frequent psychotic symptoms than subjects
without the mutation.
In the other study, Maria Karayiorgou and colleagues examined a
mouse model of schizophrenia that contains a mutation in the gene for the
enzyme proline dehydrogenase (PRODH), which breaks down the proposed
neuromodulator proline. They report that this deficiency in PRODH alters the
expression of the COMT gene. Interaction between these two genes modulated
several schizophrenia-related phenotypes in these mice, such that COMT
inhibition exaggerated or induced behavioral deficits in the PRODH-deficient
mice. This synergistic interaction between these genes could explain the
high disease risk associated with deletions in the 22q11.2 locus.

Author contact:
Maria Karayiorgou (The Rockefeller University, New York, NY, USA) paper no:
[3]
Tel: +1 212 327 7328, E-mail: [email protected]

Author contact:
Doron Gothelf (Stanford University, CA, USA) paper no: [4]
Tel: +1 650 725 3980, E-mail: [email protected]

Other papers from Nature Neuroscience to be published online at the same
time and with the same embargo:

[5] Activity-dependent decrease of excitability in rat hippocampal neurons
through increases in Ih
DOI: 10.1038/nn1568

[6] Neural correlates of binocular rivalry in the human lateral geniculate
nucleus
DOI: 10.1038/nn1554

[7] Cbln1 is essential for synaptic integrity and plasticity in the
cerebellum
DOI: 10.1038/nn1576

[8] Lbx1 and Tlx3 are opposing switches in determining GABAergic versus
glutamatergic transmitter phenotypes
DOI: 10.1038/nn1569

*********************NATURE CELL BIOLOGY*********************
(<http://www.nature.com/naturecellbiology>)

[9] Discovery of a context-dependent oncogene

DOI: 10.1038/ncb1314

The paradoxical behaviour of Krüppel-like Factor 4 (KLF4) - both a
tumour-supressor or oncogenic, depending on the context - is given an
explanation in the November issue of Nature Cell Biology. KLF4 regulates
genes involved in cell division and embryonic development, and has been
implicated in gastro-intestinal cancer as a tumour suppressor. In other
settings, such as breast cancer, KLF4 is overexpressed and positively
contributes to tumorigenesis.
The team found that KLF4 allows cells to avoid senescence - a process of
cellular ageing resulting in loss of cell division. However, KLF4 was also
found to be a potent inhibitor of proliferation in normal non-senescing
cells. This switch in behaviour is linked to several genes known to have
key roles in cell growth and cancer. KLF4 represses the tumour suppressor
p53, while at the same time activating the p21CIP1 cell-cycle inhibitor.
p21CIP1 function is lost in most cancers. In this context the repression of
p53 frees cells from the shackles of this important growth regulator to
expose KLF4's hidden growth-promoting potential. This allows for cell
transformation, as well as suppression of cell suicide, or apoptosis.
Depletion of KLF4 from breast cancer cells restored expression of the cancer
surveillance gene p53 and allowed apoptosis to occur. These data show that
overexpression of KLF4 and loss of p21CIP1 co-operate in cancer formation.
The study suggests that, depending on the setting, KLF4 is an enticing
target for cancer therapy. However, in cases where p21CIP1 is active,
inhibition of KLF4 may actually promote cancer formation. This study is a
striking example of the importance of thoroughly understanding the molecular
role of cancer genes before designing therapeutic approaches.

Author contact:
Daniel S. Peeper (The Netherlands Cancer Institute, Amsterdam, The
Netherlands)
Tel: +31 20 5122 0022, E-mail: [email protected]

Other papers from Nature Cell Biology to be published online at the same
time and with the same embargo:

[10] Root gravitropism requires lateral root cap and epidermal cells for
transport and response to a mobile auxin signal
DOI: 10.1038/ncb1316

[11] The Polo kinase Plk4 functions in centriole duplication
DOI: 10.1038/ncb1320

[12] Phosphatidylinositol transfer protein-alpha in netrin-1-induced PLC
signalling and neurite outgrowth
DOI: 10.1038/ncb1321

[13] Tankyrase-1 polymerization of poly(ADP-ribose) is required for spindle
structure and function
DOI: 10.1038/ncb1322

*****************************************************************

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

Nature (<http://www.nature.com/nature>)

[14] Eye-specific effects of binocular rivalry in the human lateral
geniculate nucleus
DOI: 10.1038/nature04169

[15] Glyoxalase 1 and glutathione reductase 1 regulate anxiety in mice
DOI: 10.1038/nature04250

NATURE MATERIALS (<http://www.nature.com/naturematerials>)

[16] Electronic structure and exchange coupling of Mn impurities in III-V
semiconductors
DOI: 10.1038/nmat1509

[17] The quantum spin-valve in cobalt atomic point contacts
DOI: 10.1038/nmat1510

[18] Probing of bonding changes in B2O3 glasses at high pressure with
inelastic X-ray scattering
DOI: 10.1038/nmat1511

[19] Integrated fibres for self-monitored optical transport
DOI: 10.1038/nmat1512

[20] Nanoparticle networks reduce the flammability of polymer nanocomposites
DOI: 10.1038/nmat1502

Nature MEDICINE (<http://www.nature.com/naturemedicine>)

[21] Sonic hedgehog myocardial gene therapy: tissue repair through transient
reconstitution of embryonic signaling
DOI: 10.1038/nm1313

[22] Regulation of lung injury and repair by Toll-like receptors and
hyaluronan
DOI: 10.1038/nm1315

Nature BIOTECHNOLOGY (http://www.nature.com/naturebiotechnolgy)

[23] Computational design and experimental validation of
oligonucleotide-sensing allosteric ribozymes
DOI: 10.1038/nbt1155

[24] Cell-specific targeting of nanoparticles by multivalent attachment of
small molecules
DOI: 10.1038/nbt1159

NATURE GENETICS (<http://www.nature.com/naturegenetics>)

[25] Mutation of Vps54 causes motor neuron disease and defective
spermiogenesis in the wobbler mouse
DOI: 10.1038/ng1661

[26] Global hypomethylation of the genome in XX embryonic stem cells
DOI: 10.1038/ng1663

[27] Efficiency and power in genetic association studies
DOI: 10.1038/ng1669

Nature IMMUNOLOGY (<http://www.nature.com/natureimmunology>)

[28] Inducing and expanding regulatory T cell populations by foreign antigen
DOI: 10.1038/ni1265

Nature STRUCTURAL & MOLECULAR BIOLOGY
(<http://www.nature.com/natstructmolbiol>)

[29] ERj1p uses a universal ribosomal adaptor site to coordinate the 80S
ribosome at the membrane
DOI: 10.1038/nsmb998

[30] ERj1p has a basic role in protein biogenesis at the endoplastic
reticulum
DOI: 10.1038/nsmb1007

[31] Induced structure of a helical switch as a mechanism to regulate
enzymatic activity
DOI: 10.1038/nsmb1006

[32] Sequential phosphorylation and multisite interactions characterize
specific target recognition by the FHA domain of Ki67
DOI: 10.1038/nsmb1008

[33] A single spacer nucleotide determines the specificities of two mRNA
regulatory proteins
DOI: 10.1038/nsmb1010

[34] HIV-2 genomic RNA contains a novel type of IRES located downstream of
its initiation codon
DOI: 10.1038/nsmb1011

****************************************************************************
***********************************

GEOGRAPHICAL LISTING OF AUTHORS

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.

BELGIUM
Ghent: 10

CHINA
Shanghai: 8, 12
Taipei, Taiwan: 32

DENMARK
Aarhus: 25

FRANCE
Gif sur Yvette: 34
Lyon: 34
Montpellier: 26
Paris: 5

GERMANY
Berlin: 29
Bielefeld: 25
Braunschweig: 25
Homburg: 29
Martinsried near Munich: 11
Tuebingen: 11

ISRAEL
Ramat Aviv: 4

ITALY
Rome: 21

JAPAN
Kanazawa: 7
Sapporo: 7
Tokyo: 7, 8

REPUBLIC OF KOREA
Seoul: 18

THE NETHERLANDS
Amsterdam: 9
Utrecht: 3

SWEDEN
Umea: 10

SWITZERLAND
Basel: 1
Geneva: 4

TURKEY
Istanbul: 19

UNITED KINGDOM
Cambridge: 10, 11
Cardiff: 26
Dundee: 2
Edinburgh: 26
Fife: 2
Hinxton: 26
London: 14, 26
Nottingham: 10
Warrington: 16
York: 10

UNITED STATES OF AMERICA
Alabama
Birmingham: 12
Tuscaloosa: 16
California
La Jolla: 8, 15
Palo Alto: 7
San Diego: 15
San Francisco: 31
Stanford: 4
Connecticut
New Haven: 22, 28
District of Columbia
Washington: 18
Georgia
Atlanta: 2
Augusta: 12
Illinois
Argonne: 18
Chicago: 18
Maine
Bar Harbor: 12
Maryland
Bethesda: 32
Gaithersburg: 20
Massachusetts
Great Barrington: 10
Charlestown: 24
Cambridge: 19, 21, 27
Boston: 8, 13, 21, 22, 27, 28
Michigan
Ann Arbor: 25
New Jersey
Princeton: 6
New York
Buffalo: 17
New York: 3, 28
Ohio
Columbus: 32
Pennsylvania
Philadelphia: 20
Pittsburgh: 32
Tennessee
Memphis: 3, 7, 30
Oak Ridge: 16
Texas
Austin: 5
Houston: 29
Utah
Salt Lake City: 22, 23
Washington
Seattle: 4, 15
Wisconsin
Madison: 33

PRESS CONTACTS...

For media inquiries relating to embargo policy for all the Nature Research
Journals:

Katharine Mansell (Nature London)
Tel: +44 20 7843 4658; E-mail: [email protected]

For media inquiries relating to editorial content/policy for the Nature
Research Journals, please contact the journals individually:

Nature Biotechnology (New York)
Kathy Aschheim
Tel: +1 212 726 9346; E-mail: [email protected]

Nature Cell Biology (London)
Bernd Pulverer
Tel: +44 20 7843 4892; E-mail: [email protected]

Nature Chemical Biology (Boston)
Beatrice Chrystall
Tel: +1 617 475 9241, E-mail: [email protected]

Nature Genetics (New York)
Orli Bahcall
Tel: +1 212 726 9311; E-mail: [email protected]

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

Nature Materials (London)
Maria Bellantone
Tel: +44 20 7843 4556; E-mail: [email protected]

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

Nature Neuroscience (New York)
Sandra Aamodt (based in California)
Tel: +1 530 795 3256; E-mail: [email protected]

Nature Structural & Molecular Biology (New York)
Ed Feng
Tel: +1 212 726 9351; E-mail: [email protected]

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Published: 23 Oct 2005

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