New methods to derive embryonic stem cells; Dark spins light up; Nanocrystals detect DNA; Malaria protection - two variants at odds; The moral of the story; Maintaining suppression

NATURE AND THE NATURE RESEARCH JOURNALS PRESS RELEASE - For papers that will be published online on 16 October 2005

NATURE AND THE NATURE RESEARCH JOURNALS PRESS RELEASE

This press release contains:
* New methods to derive embryonic stem cells - Nature
* Dark spins light up - Nature Physics
* Nanocrystals detect DNA - Nature Materials
* Malaria protection - two variants at odds - Nature Genetics
* The moral of the story - Nature Neuroscience
* Maintaining suppression - Nature Immunology
* 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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***************************NATURE************************************
(<http://www.nature.com/nature>)

[1] & [2] New methods to derive embryonic stem cells

[1] DOI: 10.1038/nature04257 &
[2] DOI: 10.1038/nature04277

The process of deriving human embryonic stem cells, which involves embryo
destruction, has caused controversy in science and politics. Two papers
published online by Nature now provide different means of deriving such
cells from mice without eliminating a cloned embryo that has the potential
to develop.
Rudolf Jaenisch and Alexander Meissner report that it is possible to
create cloned mouse embryos that inherently lack the ability to implant in
the uterus and develop further. The method involves preventing the formation
of a cell layer - called the trophectoderm - that later attaches the embryo
to the uterine wall. The scientists achieve this by blocking the action of
Cdx2, a gene that encodes the earliest known proteins involved in the
development of this layer. The cloned, Cdx2-deficient mouse embryos were
morphologically abnormal, but could efficiently generate embryonic stem
cells that could expand into different cell types when cultured. Because
Cdx2 might be needed for therapeutic strategies using these cells, the
scientists made the gene knockout reversible, so the Cdx2 gene could be
turned back on once the embryonic stem cell culture was established.
Robert Lanza and his colleagues show a new way to derive mouse
embryonic stem cell lines that, unlike current methods, does not disrupt the
embryo's ability to implant into the womb and develop. The procedure is
based on a technique used in fertility treatments, called pre-implantation
genetic diagnosis, where embryos are screened for genetic defects. If
healthy, they are then implanted into the uterus and develop normally. Lanza
and colleagues used a single-cell biopsy taken from mouse embryos to produce
five putative embryonic stem cell lines. These embryos were then implanted
into mouse uteri, where they developed to birth. The authors propose that if
the procedure works on human embryos it would allow the banking of such
cells for children born from transferred embryos.

Author contact:
Rudolf Jaenisch (Whitehead Institute for Biomedical Research, Massaschusetts
Institute of Technology, Cambridge, MA, USA) paper no: [1]
Tel: +1 617 258 5186, E-mail: [email protected]

Bob Lanza (Advanced Cell Technology, Worcester, MA, USA) paper no: [2]
Tel: +1 508 756 1212 ext.655, E-mail: [email protected]

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

[3] Evidence for de novo imprinted X-chromosome inactivation independent of
meiotic inactivation in mice
DOI: 10.1038/nature04155

[4] Gigaxonin-controlled degradation of MAP1B light chain is critical to
neuronal survival
DOI: 10.1038/nature04256

**********************NATURE PHYSICS*************************
(http://www.nature.com/naturephysics)

[5] Dark spins light up

DOI: 10.1038/nphys141

Want to see a diamond? Forget the jewellery store - try a physics
laboratory. In the November issue of Nature Physics, Ryan Epstein and
colleagues demonstrate the power of their microscope for imaging individual
nitrogen atoms that sit at vacant sites in the diamond structure. Such
'vacancy' centres have a long lifetime within the diamond host and could be
used as the basis for a room-temperature quantum computer.
Because of the potential application as a bit of quantum information, the
single magnetic spin (pointing up or down) associated with the extra
electron of a nitrogen atom has featured in many different experiments. The
latest involves a room-temperature microscope that detects light emitted by
a nitrogen vacancy centre. Through their precise control of the alignment of
the magnetic field, the researchers can also detect local non-luminescing
impurities that couple to the nitrogen vacancy centres. The vacancy centres
light the way to neighbouring 'dark' spins that normally would not be
detected. These dark spins have a longer life-time than that of the vacancy
atoms, and could be potentially more useful for applications involving
quantum information processing.

Author contact:
David Awschalom (University of California, Santa Barbara, CA, USA)
Tel: +1 805 893 2121, E-mail: [email protected]

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

[6] A critical assessment of the superconducting pairing symmetry in
NaxCoO2·yH2O
DOI: 10.1038/nphys126

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

[7] Nanocrystals detect DNA

DOI: 10.1038/nmat1508

Fluorescent nanocrystals - also known as quantum dots - come in handy as DNA
sensors, as reported in the November issue of Nature Materials. Sensing DNA
directly in a solution and without having to go through tedious separation
and amplification procedures is a great challenge in molecular biology. The
results of these analyses are critical for diagnosing genetic diseases.
Tza-Huei Wang and colleagues present a straightforward and sensitive method
that, being based on the fluorescence emission from quantum dots rather than
from molecular probes, circumvents the infamous problem of background
fluorescence which makes it difficult to detect the real signal.
As a practical demonstration of its utility, this sensor system could
successfully spot the genetic signature of an ovarian tumour in clinical
samples.

Author contact:
Tza-Huei Wang (Johns Hopkins University, Baltimore, MD, USA)
Tel: +1 410 516 7086, E-mail: [email protected]

Additional contact for comment on paper:
Benoit Dubertret (Ecole Supérieure de Physique et de Chimie Industrielles,
Paris, France)
Tel: +33 1 40 79 45 95; E-mail: [email protected]

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

[8] Formation of asymmetric one-sided metal-tipped semiconductor nanocrystal
dots and rods
DOI: 10.1038/nmat1505

[9] The evolution of vesicles from bulk lamellar gels
DOI: 10.1038/nmat1501

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

[10] Malaria protection - two variants at odds

DOI: 10.1038/ng1660

Malaria has exerted large selective force on human populations, including
the selection for genes that protect against malaria infection. A study in
the November issue of Nature Genetics now shows that co-inheritance of two
of the most common genetic variants, which individually confer protection,
may cancel the protective effects.
Tom Williams and colleagues found that children with both variants show no
increased protection from malaria infection, while children with only a
single variant showed increased protection. The study compared the rates of
developing severe malaria in two cohorts of children in Kenya, categorized
by these two genetic traits. The genetic traits considered were sickle cell
trait and alpha+ thalassemia, two prevalent genetic variants in sub-Saharan
Africa, that individually confer protection from malaria. Hemoglobin, a
protein required for the transport of oxygen by red blood cells, is altered
in both conditions. Sickle-cell disease causes red blood cells to change
shape, leading the cells to become stuck in capillaries and deprive the
downstream tissues of oxygen. This causes painful attacks that eventually
damage internal organs and can cause strokes and anemia. Alpha thalassemia
can result in reduced ability of the blood cells to carry oxygen and lead to
mild to severe anemia.

Author Contacts:
Thomas Williams (The Kenya Medical Research Institute, Kilifi, Kenya)
Tel: + 254 41 522 063, E-mail: [email protected]

Additional contact:
Thomas E. Wellems (National Institute of Allergy and Infectious Diseases,
Bethesda, MD, USA)
Tel: +1 301 496 4021, E-mail: [email protected]

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

[11] Mutations in dynamin 2 cause dominant centronuclear myopathy
DOI: 10.1038/ng1657

[12] Identification of a ferrireductase required for efficient
transferrin-dependent iron uptake in erythroid cells
DOI: 10.1038/ng1658

[13] A mutation in Sec15l1 causes anemia in hemoglobin deficit (hbd) mice
DOI: 10.1038/ng1659

[14] Mutations in SECISBP2 result in abnormal thyroid hormone metabolism
DOI: 10.1038/ng1654

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

[15] The moral of the story

DOI: 10.1038/nn1575

The perceived moral character of a player's opponent in a trust game
influences activity in reward-related brain areas, reports a study in the
November issue of Nature Neuroscience. The results also suggest that people
rely less on feedback about the outcome of their choices when they have
prior information about an opponent's character.
Elizabeth Phelps and colleagues used functional magnetic resonance
imaging (fMRI) to track people's brain activity as they played a game. On
each round, participants chose whether to keep a monetary reward or to share
it with an opponent. If their opponent also chose to share the reward,
participants would get more money than if they had chosen to keep the reward
initially. But if their opponent kept the reward when they chose to share,
participants would receive no money. Sharing a reward was therefore a risky
choice, which could result in a greater reward or a complete loss.
Before the game, participants read descriptions of their opponents'
life events that portrayed the opponent in a positive, negative or neutral
context. The opponents' responses during the game were the same for all
three types of opponent. However, subjects made the risky choice to share
their reward with the 'good' opponent significantly more often. Activity in
the caudate nucleus - part of the brain that normally differentiates between
good and bad feedback - signaled feedback information only for the 'neutral'
partner in this study. These findings suggest that 'trial and error'
learning can be modified by social context.

Author contact:
Elizabeth Phelps (New York University, NY, USA)
Tel: +1 212 998 8337; E-mail: [email protected]

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

[16] Drosophila melanogaster homolog of Down syndrome critical region 1 is
critical for mitochondrial function
DOI: 10.1038/nn1564

[17] Induction of sharp wave-ripple complexes in vitro and reorganization of
hippocampal networks
DOI: 10.1038/nn1571

[18] Encoding a temporally structured stimulus with a temporally structured
neural representation
DOI: 10.1038/nn1559

[19] MPS-1 is a K+ channel beta-subunit and a serine/threonine kinase
DOI: 10.1038/nn1557

[20] The essential role of stimulus temporal patterning in enabling
perceptual learning
DOI: 10.1038/nn1546

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

[21] & [22] Maintaining suppression

[23] DOI: 10.1038/ni1263 &
[24] DOI: 10.1038/ni1264

Autoimmune pathology often occurs because some immune cells are not
regulated properly. This important function is usually the responsibility of
a special class of cells called regulatory T cells (Treg cells). A pair of
new reports in the November issue of Nature Immunology show that Treg cells
require the immune modulator interleukin 2 (IL-2) for their maintenance and
long-term function rather than for development, as previously thought.
How Treg cells develop has been worked out in some detail and the prevailing
model included a fundamental function for IL-2. In fact, for many years,
Treg cells were identified exclusively on the basis of expression of the
IL-2 receptor. But the new studies by Alexander Rudensky and Ludger Klein
rely instead on identifying Treg cells by a different molecule, Foxp3.
Using this identifier, both Rudensky and Klein unexpectedly demonstrate that
IL-2 signals are not required for Treg cell development. Instead, IL-2 is
required for the maintenance of Treg cells after they leave the thymus and
move into the circulation. This new model for the function of IL-2 will help
scientists understand how this critically important class of suppressor
cells keeps immunopathology at bay.

Author contact:
Alexander Rudensky (University of Washington, Seattle, WA, USA) paper no:
[21]
Tel: +1 206 685 7644, E-mail: [email protected]

Ludger Klein (Research Institute Of Molecular Pathology, Vienna, Austria)
paper no: [22]
Tel: +43 1 7973 0471, E-mail: [email protected]

Additional contact for comments on paper:
Fiona Powrie (Oxford University, UK)
Tel: +44 1865 285 489, E-mail: [email protected]

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

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

[23] T cells targeted against a single minor histocompatibility antigen can
cure solid tumors
DOI: 10.1038/nm1311

[24] Lymphopenia and interleukin-2 therapy alter homeostasis of CD4+CD25+
regulatory T cells
DOI: 10.1038/nm1312

[25] A crucial role for antigen-presenting cells and alloantigen expression
in graft-versus-leukemia responses
DOI: 10.1038/nm1309

[26] Akt1 regulates pathological angiogenesis, vascular maturation and
permeability in vivo
DOI: 10.1038/nm1307

[27] Restoration of immunity in lymphopenic individuals with cancer by
vaccination and adoptive T-cell transfer
DOI: 10.1038/nm1310

[28] Dopamine covalently modifies and functionally inactivates parkin
DOI: 10.1038/nm1314

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

[29] Distinct enzyme combinations in AKAP signalling complexes permit
functional diversity
DOI: 10.1038/ncb1315

[30] Nrarp functions to modulate neural-crest-cell differentiation by
regulating LEF1 protein stability
DOI: 10.1038/ncb1311

[31] Drosophila Ric-8 regulates Gai cortical localization to promote
Gai-dependent planar orientation of the mitotic spindle during asymmetric
cell division
DOI: 10.1038/ncb1319

[32] Drosophila Ric-8 is essential for plasma-membrane localization of
heterotrimeric G proteins
DOI: 10.1038/ncb1318

[33] Ric-8 controls Drosophila neural progenitor asymmetric division by
regulating heterotrimeric G proteins
DOI: 10.1038/ncb1317

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

[34] Insights into SARS-CoV transcription and replication from the structure
of the nsp7-nsp8 hexadecamer
DOI: 10.1038/nsmb999

[35] ATPase-dependent cooperative binding of ORC and Cdc6 to origin DNA
DOI: 10.1038/nsmb1002

[36] Structural perspective on the activation of RNase P RNA by protein
DOI: 10.1038/nsmb1004

***************************************************************
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.

AUSTRIA
Vienna: 23, 33

BELGIUM
Antwerp: 12

CANADA
Montreal: 24

CHINA
Beijing: 35
Shanghai: 21

FRANCE
Bordeaux: 12
Illkirch: 12
Paris: 3, 12, 32

GERMANY
Berlin: 18
Munich: 12

IRELAND
Dublin: 15

ISRAEL
Beer-Sheva: 18
Jerusalem: 8
Tel Aviv: 8

JAPAN
Kamakura: 10
Nagoya: 31
Tokyo: 10

KENYA
Kilifi: 11

THE NETHERLANDS
Amsterdam: 3

KINGDOM OF SAUDI ARABIA
Bisha: 15
Riyadh: 15

SINGAPORE
Singapore City: 34

SPAIN
Santiago de Compostela: 15

SWITZERLAND
Lausanne: 12

UNITED KINGDOM
Oxford: 11
Sheffield: 9

UNITED STATES OF AMERICA
California
Berkeley: 21
Santa Barbara: 5
Stanford: 4
Colorado
Boulder: 37
District of Columbia
Washington: 6
Florida
Gainesville: 26
Georgia
Atlanta: 13
Illinois
Chicago: 15, 27
Maine
Bar Harbor: 13
Maryland
Baltimore: 7, 28
Bethesda: 17, 19, 25, 31
Rockville: 28
Massachusetts
Boston: 12, 13, 14, 29
Cambridge: 1, 13
Michigan
Ann Arbor: 26
New Jersey
Hackensack: 26
Piscataway: 20
New York
Cold Spring Harbor: 36
Ithaca: 16
New York: 16, 22
Upton: 36
North Carolina
Chapel Hill: 34
Winston-Salem: 2
Ohio
Cleveland: 27
Oregon
Portland: 30
Pennsylvania
Philadelphia: 28
Texas
Houston: 13
Washington
Seattle: 3, 22, 27
Wisconsin
Madison: 2

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: 16 Oct 2005

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