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This press release contains:
* Summaries of newsworthy papers:
* Astrophysics: One outburst after another
* Pathology: Cellular discovery could help fight against sleeping sickness
* Climate science: The soil carbon conundrum
* Atmospheric science: Photochemistry on organic materials
* Chemistry: Breaking the backbones of macromolecules
* Development: Kidney support
* Genetics: Protein teamwork underlies skeleton
* Genetics: It's all in the expression
* And finally...Frogs sidestep predation by looking nasty - but not too nasty
* Mention of papers to be published at the same time with the same embargo
* Geographical listing of authors
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, ,  Astrophysics: One outburst after another (pp 181-183; pp 184-186; p 164, N&V)
An immense cosmic explosion that happened when the Universe was just 900
million years or so old has just been detected. In this week's Nature, three
teams of astronomers describe their observations of this, the oldest
detected outburst, called GRB 050904, in September 2005.
The explosion, which happened around 12.8 billion years ago, released an
intense flash of gamma rays, hence the name gamma-ray burst, or GRB.
Outbursts like GRB 050904, which last for seconds to minutes, are thought to
be generated by the collapse of massive stars, perhaps to form black holes.
Events this bright can be detected very far away, which is equivalent to
saying very long ago, as the light from very distant objects can take
billions of years to reach us. But GRB 050904 is far more distant, and thus
much older, than any gamma-ray burst seen before. It is like a flash from
close to the beginning of time. It therefore has the potential to tell
researchers what the early Universe looked like.
The observations of GRB 050904 with the Swift satellite are reported by an
international team led by Giancarlo Cusumano. Daniel Reichart and co-workers
used measurements of the infrared afterglow to estimate the burst's
redshift, and a Japanese team headed by Nobuyuki Kawai determined the
redshift precisely using an optical/infrared spectrum.
Daniel Reichart (University of North Carolina, Chapel Hill, NC, USA) Paper 
Tel: +1 919 962 5310; E-mail: [email protected]
Nobuyuki Kawai (Tokyo Institute of Technology, Tokyo, Japan) Paper 
Tel: +81 3 5734 2390; E-mail: [email protected]
Giancarlo Cusumano (National Institute for Astrophysics, Palermo, Italy) Paper 
Tel: +39 091 680 9479; E-mail: [email protected]
Enrico Ramirez-Ruiz (Institute for Advanced Study, Princeton, NJ, USA) N&V
Tel: +1 609 734 8020; E-mail: [email protected]
 Pathology: Cellular discovery could help fight against sleeping sickness (pp 224-227; N&V)
The parasite that causes African sleeping sickness may have revealed an
Achilles' heel - it cannot survive in the human bloodstream without the use
of its flagellum, a protein 'tail' that allows it to swim, reveals a study
in this week's Nature. With little prospect of a vaccine against sleeping
sickness, this discovery could be a valuble lead in the search for new drugs
to control the disease.
Keith Gull and his colleagues made the discovery when surveying the
inventory of proteins that are involved in flagellar function. Many cells,
from both single- and multi-cellular organisms, produce flagellar
structures, but researchers had previously been unclear about exactly what
proteins are involved and what they do.
Gull and colleagues publish the results of their study, as well as
details of experiments in which they selectively disable certain proteins
and investigate the effects on the cell. In the case of the
sleeping-sickness parasite, Trypanosoma brucei, loss of flagellar function
means that the invaders are unable to survive in the human bloodstream - an
unexpected discovery that could go some way to alleviating the widespread
incidence of the disease in sub-Saharan Africa.
Keith Gull (University of Oxford, Oxford, UK)
Tel: +44 1865 285 455; E-mail: [email protected]
Scott Landfear (Oregon Health and Science University, Portland, OR, USA)
Tel: +1 503 494 2426; E-mail: [email protected]
 Climate science: The soil carbon conundrum (pp 165-173)
Despite much research, a consensus is yet to emerge on how temperature
effects the enormous amount of carbon stored in the world's soils -
including peatlands, wetlands and permafrost. Some argue that global soil
carbon stocks show little or no temperature sensitivity, thus limiting the
risk of major positive feedback contributing to climate change. Others
present evidence that soil carbon decomposition is temperature sensitive and
positive feedback is a serious concern.
In this week's Nature, Eric Davidson and Ivan Janssens review the studies so
far and propose avenues to carry the research forward. They conclude that
the overall response of global soil carbon stocks to climate change, and the
magnitude of the expected feedbacks to climate disruption, has not been
resolved. According to the researchers, unravelling the feedback effect is
particularly difficult because soil organic compounds are so diverse.
Different kinetic properties determine the temperature sensitivity of their
decomposition. Similarly, environmental constraints such as drought,
flooding or freezing also obscure temperature sensitivity.
Significantly more carbon is stored in the world's soils than is present in
the atmosphere. Inputs are primarily from leaf and root detritus, with
outputs dominated by the efflux of carbon dioxide from the soil surface.
Eric Davidson (Woods Hole Research Center, Falmouth, MA, USA)
Tel: +1 508 540 9900; E-mail: [email protected]
 Atmospheric science: Photochemistry on organic materials (pp 195-198)
Humic acid, a complex organic material and a product of plant decomposition,
is involved in the production of atmospheric nitrous acid, shows a study in
this week's Nature. Atmospheric nitrous acid is a precursor for the
so-called hydroxyl radical, which is responsible for the breakdown of many
air pollutants in the lower atmosphere (the troposphere).
Konrad Stemmler and colleagues set out to unravel the mechanism responsible
for the formation of enhanced concentrations of atmospheric nitrous acid
during the day. By exposing thin films of humic acid as well as natural soil
samples to nitrogen dioxide in light and dark conditions, they show that
nitrogen dioxide is converted to nitrous acid with the help of a photochemical reaction taking place on the organic material. The authors suggest that nitrous acid produced in this way could explain the recently observed high concentrations of nitrous acid during daytime.
Given that humic acid and other organic materials are widely distributed on
surfaces in the natural environment, this newly discovered production
mechanism could have a potentially significant impact on the chemistry of
Konrad Stemmler (Paul Scherrer Institute, Villigen, Switzerland)
Tel: + 41 563 104301; E-mail: [email protected]
 Chemistry: Breaking the backbones of macromolecules (pp 191-194, N&V)
We don't normally expect carbon-carbon covalent bonds to break easily; just
think of the strength of diamond. Yet in new research reported in this
week's Nature, it seems that the scission of such bonds is more easily
achieved than chemists had previously appreciated.
Sergi Sheiko and colleagues used atomic force microscopy (AFM) to study the
effects of adsorption on a series of brush-like macromolecules with long
side chains. The observations show that this simple and common process not
only induces deformations in these molecules, but also spontaneously induces
the rupture of the carbon-carbon bonds in the molecules' backbones.
The phenomenon occurs as the macromolecules reorganize themselves in order
to maximize the number of contacts with the surface; which in turn induces
tension along the polymer backbone. It is the first indication that relatively weak interactions can conspire to break covalent bonds as strong as the carbon-carbon bond.
The findings call into question the generally accepted view that macromolecules synthesized in solution remain intact after deposition onto a substrate. The work has implications for the design of molecules with highly branched architectures - either to avoid undesired degradation or to ensure they break at pre-determined sites.
Sergei Sheiko (University of North Carolina at Chapel Hill, Chapel Hill, NC, USA)
Tel: +1 919 843 5270; E-mail: [email protected]
Steve Granick (Univsity of Illinois, Urbana, IL, USA)
Tel: +1 217 333 5720; E-mail: [email protected]
Sung Chul Bae (Univsity of Illinois, Urbana, IL, USA)
Tel: +1 217 244 7386; E-mail: [email protected]
 Development: Kidney support (DOI:10.1038/nature04662)
***Paper  will be published electronically on Nature's website on 8 March
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 9 March, but at a later date.***
Results of a study published online this week by Nature reveal how a protein
that acts as a linker between cell adhesion molecules and the cellular
skeleton is important for kidney function.
In the kidney, podocyte cells put out foot-like processes that knit together
and form a specialized junction (called the slit diaphragm) that helps to
determine which molecules are filtered from the blood into the urine. Tony
Pawson and his team show that a protein called Nck is vital for the correct
working of these junctions, as mice lacking Nck from their podocytes are
born with severe kidney problems.
The team show that this is because the cell adhesion molecule nephrin, which
is a building block of the slit diaphragm, binds to Nck. Nck in turn
controls the cellular skeleton essential for creation of the foot processes.
Anthony Pawson (Mount Sinai Hospital, Toronto, Canada)
Tel: +1 416 586 8262; E-mail: [email protected]
 Genetics: Protein teamwork underlies skeleton (pp 220 - 223)
Researchers in this week's Nature show how mutations in two different
proteins can cause osteopetrosis, a rare congenital human disorder in which
the bones become too dense.
Researchers knew that mutations in Ostm1 and ClC-7 can both cause the
condition. Thomas Jentsch and his colleagues now show that in mice, Ostm1
forms a molecular complex with ClC-7, a membrane ion channel. This protein
complex is trafficked to lysosomes, cellular compartments that degrade other
molecules, and to the border of bone-degrading osteoclast cells.
Each component of this complex is unstable without the other, so mutations
in either protein can disrupt bone resorption in osteopetrosis. The team
found that mice lacking Ostm1, like those without ClC-7, also have a wider
spectrum of problems characteristic of lysosomal storage disease, a group of
lysosome disorders also seen in humans.
Thomas Jentsch (Centre for Molecular Biology, Hamburg, Germany)
Tel: +49 40 42803 4741; E-mail: [email protected]
 Genetics: It's all in the expression (pp 242-245; N&V)
Changes in the expression level of certain genes may underlie some of the
fundamental differences between humans and chimpanzees, suggests a study in
this week's Nature. Previous studies have concentrated on comparing the
genomic sequences themselves, but by looking at the levels of gene
expression we may gain new insights into the selective pressures driving
Gilad and colleagues compared gene expression in humans,
chimpanzees, orangutans and rhesus macaques. Using a multi-species gene
array, they were able to identify a series of genes that have been expressed
at a stable level throughout the 70-million-year evolution of these species.
The authors found that several of these genes are associated with human
disease, suggesting that this property (constant levels of expression over
evolution) may be used to identify other disease gene candidates.
A small number of human genes show a rapid divergence in the level
of expression when compared with the other primates. Most of these genes are
upregulated, and they encode transcription factors, which are often linked
with divergence at the organismal level. The authors propose that
differences in the expression of these genes could account for the large
number of phenotypic changes in the human lineage.
Yoav Gilad (University of Chicago, Chicago, IL, USA)
Tel: +1 773 702 8507; E-mail: [email protected]
Rasmus Nielsen (University of Copenhagen, Copenhagen, Denmark)
Tel: +45 353 21279; E-mail: [email protected]
 And finally...Frogs sidestep predation by looking nasty - but not too nasty (pp 208-211)
Many edible animals avoid ending up as something's dinner by copying the
appearance of poisonous animals - an effect called batesian mimicry. A new
study in this week's Nature describes a species of frog that maximizes its
chances of survival by mimicking the less toxic of two local poisonous
species - a seemingly counterintuitive tactic, but one that helps the frog
to avoid the attentions of as many predators as possible.
Catherine Darst and Molly Cummings made their discovery in a group of frogs
in the Ecuadorian Amazon. The non-poisonous frog, Allobates zaparo, shares
territory with a very poisonous frog, Epipedobates parvulus, and another
related but less noxious one, E. bilinguis, both of which have similar but
distinct patterns of red warning spots. The authors found that where the
three species overlap, A. zaparo tends to mimic E. bilinguis - the less
poisonous of the two.
This seems confusing - instead, one might expect the mimic to display a
pattern somewhere between the two, or for some mimics to copy one poison
frog, while some mimic the other. But by studying the process by which
chickens learn to avoid the poisonous frogs, Darst and Cummings show how the
mimics get away with it. The more-poisonous frogs educate predators to avoid
anything that looks remotely like the noxious animal. But with less-toxic
frogs, the learning is much more specific. So by copying the less-poisonous
species, A. zaparo remains unmolested by predators, regardless of which
poison frogs they had previously encountered.
Catherine Darst (University of Texas, Austin, TX, USA)
Tel: +1 512 471 5162; E-mail: [email protected]
ALSO IN THIS ISSUE...
 Stochastic spineless expression creates the retinal mosaic for colour vision (pp 174-180)
 Quasiparticle breakdown in a quantum spin liquid (pp 187-190)
 Cryptic striations in the upper mantle revealed by hafnium isotopes in southeast Indian ridge basalts (pp 199-202)
 Stratified prokaryote network in the oxic-anoxic transition of a deep-sea halocline (pp 203-207)
 V1 spinal neurons regulate the speed of vertebrate locomotor outputs (pp 215-219)
 Nanomotor rotates microscale objects (p 164)
ADVANCE ONLINE PUBLICATION
***This paper will be published electronically on Nature's website on 8
March 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 9 March, but at a later date.***
 CD69 acts downstream of interferon-a/b to inhibit S1P1 and
lymphocyte egress from lymphoid organs (DOI:10.1038/nature04606)
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.
Sao Paulo: 1
La Serena: 1
Hamburg: 9, 16
Leicester: 1, 3
Berkley: 1, 2, 3, 10
La Jolla: 16
Rohnert Park: 3
San Francisco: 18
New Haven: 10
District of Columbia
Washington DC: 3
Honolulu: 1, 14
Chicago: 1, 10
Baltimore: 1, 13
Greenbelt: 1, 3
Woods Hole: 5
St Louis: 12
Los Vegas: 3
Los Alamos: 3
New York: 12, 16
Chapel Hill: 1, 7
University Park: 1
Oak Ridge: 13
For North America and Canada
Katie McGoldrick, Nature Washington
Tel: +1 202 737 2355; E-mail: [email protected]
For Japan, Korea, China, Singapore and Taiwan
Rinoko Asami, Nature Tokyo
Tel: +81 3 3267 8751; E-mail: [email protected]
For the UK/Europe/other countries not listed above
Ruth Francis, Nature London
Tel: +44 20 7843 4562; E-mail [email protected]
Zoe Corbyn, Nature London
Tel: +44 20 7843 4658; E-mail: [email protected]
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