NATURE AND THE NATURE RESEARCH JOURNALS PRESS RELEASE
For papers that will be published online on 4 September 2005
* Largest ever deer gets rightful place on family tree - Nature
* Reproductive biology: enhancing sperm vitality - Nature Chemical Biology
* Stem cell instability further down the line - Nature Genetics
* Modeling metastasis - Nature Genetics
* A key initiator of allergy and asthma - Nature Immunology
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] Largest ever deer gets rightful place on family tree
DOI: 10.1038/nature04134
Researchers have sampled the DNA of the now-extinct Irish elk, the largest
deer ever to have lived, in a bid to end a 100-year debate over how it is
related to today's smaller deer. The creature, which died out around 8,000
years ago, has been the subject of fascination, not least because of its
huge stature and unwieldy antlers, which could grow to 3.5 metres across.
The analysis, led by Adrian Lister, paints the most comprehensive picture
yet of the deer family tree, and shows that the Irish elk (Megaloceros
giganteus) was closely related to the present-day fallow deer species Dama
dama and Dama mesopotamica. The Irish elk DNA samples came from skeletons
found as far afield as Ireland and western Siberia.
The researchers took a two-pronged approach to compiling the family tree. As
they explain in this week's Nature, they combined analysis of DNA sequences
with a comparison of some 74 body characteristics of the various deer
species, giving two different, but closely matching, versions of the family
tree. Using two styles of analysis allows for firmer conclusions about the
Irish elk's true evolutionary status, they add.
Author contact:
Adrian Lister (University College London, UK)
Tel: +44 20 7679 3719, Cell: +44 7966 222 953, E-mail: [email protected]
Ian Barnes, co-author (University College London, UK)
Tel: +44 207 679 2654, Cell: +44 7753 447 426, E-mail: [email protected]
Ceiridwen Edwards, co-author (Trinity College, Dublin, Ireland)
Tel: +353 1 608 1265, E-mail: [email protected]
*********************NATURE CHEMICAL BIOLOGY*********************
(http://www.nature.com/nchembio)
[2] Reproductive biology: enhancing sperm vitality
DOI: 10.1038/nchembio730
During artificial insemination procedures mammalian sperm cells are
particularly vulnerable to oxidative damage, which reduces the functional
lifespan of sperm and consequently affects fertility. In an article in the
October issue of Nature Chemical Biology, researchers report the application
of a new hybrid polymer that boosts antioxidant levels in porcine sperm,
enhancing both vitality and lifespan. This approach could be applied to
increase fertility rates in humans or other mammals, such as rare or
endangered species, in which sperm may have to be transported over long
distances.
Hybrid polymers containing both antioxidant and targeting elements were
designed by Benjamin Davis and colleagues to seek out the surface of
mammalian sperm cells. This cell-surface interaction is mediated by a
carbohydrate-binding protein that specifically recognizes galactose, a
monosaccharide sugar. When the galactose-containing polymer binds to the
surface of the sperm-cell, it is transported across the cell membrane,
whereupon the antioxidant vitamin E is released. Treated cells had lower
oxidative damage, resulting in enhanced lifespan and physiological
properties. Using a fluorescence-labeled polymer, the authors were able to
visualize sperm cell internalization of galactose-containing polymers. On
the other hand, a galactose-free polymer was not internalized, demonstrating
that polymer internalization depends on the galactose interaction with the
sperm cell surface.
This work provides a viable approach for enhancing the vitality of porcine
sperm. Its further application could potentially enhance fertilization rates
in other mammals and provide a useful means to discover new
carbohydrate-protein interactions.
Author contact:
Benjamin G. Davis (University of Oxford, UK)
Tel: +44 1865 275652, E-mail: [email protected]
Additional contact for comment on paper:
Eilish Donnelly (Queen's University Belfast, Northern Ireland, UK)
Tel: +44 28 9063 5020, E-mail: [email protected]
********************NATURE GENETICS*************************
(http://www.nature.com/naturegenetics)
[3] Stem cell instability further down the line
DOI: 10.1038/ng1631
A study in the October issue of Nature Genetics reports that human embryonic
stem cell lines cultured for a long period of time develop changes in their
genomes that may make them unusable for therapeutic purposes.
While all cultured cells develop small mutations over time, some previous
work had suggested that large-scale genetic alterations in embryonic stem
cells were rare. Using a more sensitive technique, Aravinda Chakravarti and
colleagues now show that stem cell lines that are cultured at length tend to
accumulate more significant changes in certain regions of the genome,
including large deletions and amplifications. Some of these regions are
known to be involved in human cancers.
The authors also found mutations in the mitochondrial DNA, which could
affect the metabolic functions of the cells, as well as changes in the
patterns of DNA methylation-a chemical mark that typically regulates the
expression of genes-in most of the extensively cultured cell lines. This
latter finding stands in contrast to a recent study reporting stable
methylation patterns at select genes.
The authors note that embryonic stem cell lines cultured for only a short
time do not exhibit these structural changes in their genomes, making them
suitable for therapeutic applications. For those cell lines that have been
cultured for longer periods, such as those currently approved for research
funding by the US government, the authors recommend monitoring them for
various types of mutations using standardized and sensitive techniques.
Additional embryonic stem cell lines that have not been extensively cultured
will likely be needed, they conclude.
Author contact:
Aravinda Chakravarti (Johns Hopkins University School of Medicine,
Baltimore, MD, USA)
Tel: +1 410 502 7525, E-mail: [email protected]
[4] & [5] Modeling metastasis
[4] DOI: 10.1038/ng1635 &
[5] DOI: 10.1038/ng1634
Two studies in the October issue of Nature Genetics report findings that
improve our understanding of metastasis, the process by which cancer cells
break free of a localized tumor and migrate to other parts of the body where
they give rise to more widespread disease.
Kent Hunter and colleagues show that mice that have been engineered
to develop mammary cancer have an increased incidence of metastatic disease
when they harbor a particular variant of the gene Sipa1. This gene encodes a
protein that is induced by signals promoting cell proliferation. Its
expression alters the adhesive properties of cells and increases their
ability to metastasize. This finding lends support to the idea that normal
variants may predispose certain individuals to metastatic cancer once a
tumor has developed.
In the accompanying study, Robert Weinberg and colleagues describe a
new mouse model of melanoma. Melanomas typically have a very high likelihood
of metastasizing, and the authors show that this may in part be due to the
program of gene expression that is found in normal melanocytes before they
become cancerous. Melanocytes are derived from migratory cells called neural
crest cells, and Weinberg and co-workers show that a protein called Slug,
which is required for cell migration in normal melanocytes, also promotes
metastasis in melanomas. Like the results of Hunter and colleagues, this
work is consistent with the idea that normal variation in genetic background
may explain why some individuals are more likely than others to develop
metastatic cancer.
Author contact:
Kent Hunter (National Cancer Institute, NIH, Bethesda, MD, USA)
Tel: +1 301 435 8957, E-mail: [email protected] paper no: [4]
Robert Weinberg (Whitehead Institute for Biomedical Research, MIT,
Cambridge, MA, USA)
Tel: +1 617 258 5159, E-mail: [email protected] paper no: [5]
Other papers from Nature Genetics to be published online at the same time
and with the same embargo:
[6] Induction of tumor growth by altered stem-cell asymmetric division in
Drosophila melanogaster
DOI: 10.1038/ng1632
[7] XPF nuclease-dependent telomere loss and increased DNA damage in mice
overexpressing TRF2 result in premature aging and cancer
DOI: 10.1038/ng1633
[8] Identification of mutations in CUL7 in 3-M syndrome
DOI: 10.1038/ng1628
************************NATURE IMMUNOLOGY************************
(http://www.nature.com/natureimmunology)
[9] A key initiator of allergy and asthma
DOI: 10.1038/ni1247
Mice that express a particular protein in their lungs develop an asthma-like
disease very similar to human asthma and other allergic inflammatory
diseases. This new finding reported in the September issue of Nature
Immunology opens up new ways of studying how disabling lung inflammation may
be prevented.
Asthma is the most common serious chronic disease of childhood, affecting
nearly five million children in the United States alone. The hallmarks of
human asthma and allergy include increased numbers of immune cells in lung
tissue. These cells are the key players responsible for secreting
inflammatory factors that lead to the clinical symptoms associated with
asthma. Many of the processes that subsequently lead to severe lung
inflammation are known and most current treatments for allergy and asthma
are aimed at blocking them. Unfortunately, most of these treatments only
alleviate symptoms rather than prevent their underlying causes.
Steven Ziegler and colleagues provide clues that may allow treatments to
prevent lung inflammation from occurring in the first place. The team
studied a protein already known to be associated with inflammation, thymic
stromal lymphopoetin (TSLP), to see if it was also responsible for symptoms
of severe lung inflammation in mice. Mice that produced TSLP specifically
in lung cells showed greatly increased disease that had most of the
hallmarks of human asthma and other allergic inflammatory diseases. Zeigler
and colleagues also evaluated mice that were deficient in TSLP, and these
mice showed few signs of lung inflammation and failed to develop asthma-like
disease.
Importantly, this work shows that a single protein is a key factor in the
appearance of lung inflammatory disease, which may open up new avenues of
research into treatments that prevent lung inflammation before the onset of
debilitating symptoms.
Author contact:
Steven Ziegler (Benaroya Research Institute, Seattle, WA, USA)
Tel: +1 206 344 7950, E-mail: [email protected]
Other papers from Nature Immunology to be published online at the same time
and with the same embargo:
[10] Interaction between conventional dendritic cells and natural killer
cells is integral to the activation of effective antiviral immunity
DOI: 10.1038/ni1244
[11] BCL6 interacts with the transcription factor Miz-1 to suppress the
cyclin-dependent kinase inhibitor p21 and cell cycle arrest in
germinal-center B cells
DOI: 10.1038/ni1245
************************************************************
Items from other Nature journals to be published online at the same time and
with the same embargo:
NATURE MATERIALS (http://www.nature.com/naturematerials)
[12] Rotor-stator molecular crystals of fullerenes with cubane
DOI: 10.1038/nmat1468
[13] An interfacial instability in a transient wetting layer leads to
lateral phase separation in thin spin-cast polymer-blend films
DOI: 10.1038/nmat1476
[14] Electron transport in very clean, as-grown suspended carbon nanotubes
DOI: 10.1038/nmat1478
Nature MEDICINE (http://www.nature.com/naturemedicine)
[15] A crucial role for GRK2 in regulation of endothelial cell nitric oxide
synthase function in portal hypertension
DOI: 10.1038/nm1289
Nature NEUROSCIENCE (http://www.nature.com/natureneuroscience)
[16] fMRI evidence for the neural representation of faces
DOI: 10.1038/nn1538
[17] Patterned expression of Purkinje cell glutamate transporters controls
synaptic plasticity
DOI: 10.1038/nn1539
[18] Cortical responses to invisible objects in the human dorsal and ventral
pathways
DOI: 10.1038/nn1537
[19] Tuning for spectro-temporal modulations as a mechanism for auditory
discrimination of natural sounds
DOI: 10.1038/nn1536
NATURE CELL BIOLOGY (http://www.nature.com/naturecellbiology)
[20] Membrane-bound Ubx2 recruits Cdc48 to ubiquitin ligases and their
substrates to ensure efficient ER-associated protein degradation
DOI: 10.1038/ncb1299
[21] Multiple roles for separase auto-cleavage during the G2/M transition
DOI: 10.1038/ncb1303
[22] Microtubule-dependent microtubule nucleation based on recruitment of
gamma-tubulin in higher plants
DOI: 10.1038/ncb1306
Nature STRUCTURAL & MOLECULAR BIOLOGY
(http://www.nature.com/natstructmolbiol)
[23] E2 conjugating enzymes must disengage from their E1 enzymes before
E3-dependent ubiquitin and ubiquitin-like transfer
DOI: 10.1038/nsmb984
[24] Telomere end-binding proteins control the formation of G-quadruplex DNA
structures in vivo
DOI: 10.1038/nsmb982
**************************************************
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.
AUSTRALIA
Brisbane: 10
Crowley: 10
East Melbourne: 10
Nedlands: 10
CANADA
Hamilton: 1
London: 3
Toronto: 16
FRANCE
Amiens: 8
Dardilly: 10
Evry: 4
Le Kremlin Bicetre: 8
Paris: 8
GERMANY
Essen: 8
Heidelberg: 6
Martinsried near Munich: 20
Witten: 24
HUNGARY
Budapest: 12
IRELAND
Dublin: 1
ITALY
Florence: 8
Milan: 2
JAPAN
Hyogo: 22
Okazaki: 22
Tokushima: 22
Tokyo: 22
REPUBLIC OF KOREA
Daejeon: 4
LEBANON
Beirut: 8
THE NETHERLANDS
Nijmegen: 8
PORTUGAL
Lisbon: 8
SINGAPORE
Singapore City: 3
SPAIN
Barcelona: 6
Madrid: 7
SWEDEN
Goteborg: 3
SWITZERLAND
Lausanne: 8
UNITED KINGDOM
Birmingham: 2
Cambridge: 4, 24
Coventry: 2
Driffield: 2
Durham: 2
Glasgow: 16
Leicester: 1
London: 1, 8
Manchester: 8
Oxford: 1, 2
Sheffield: 13
UNITED STATES OF AMERICA
California
Berkeley: 19
San Francisco: 5
Stanford: 9, 14
Georgia
Athens: 3
Maryland
Baltimore: 3
Bethesda: 4, 10
Massachusetts
Amherst: 22
Boston: 5, 11
Cambridge: 5
Charlestown: 5
Minnesota
Minneapolis: 18
New Jersey
Nutley: 11
New York
Buffalo: 3
New York: 8, 11, 21
North Carolina
Chapel Hill: 23
Durham: 15
Oregon
Portland: 17
Tennessee
Memphis: 23
Texas
Dallas: 3, 15
Washington
Seattle: 9
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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