ScienceWeek July 14, 2007
Dan Agin
July 14, 2007
Vol. 11 - Number 27
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The tendency has always been strong to believe that whatever
received a name must be an entity or being, having an independent
existence of its own. And if no real entity answering to the name
could be found, men did not for that reason suppose that none
existed, but imagined that it was something peculiarly abstruse
and mysterious.
-- Stephen Jay Gould (1941-2002)
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Contents (full text below):
1. Climate Change: A Changing Climate for Prediction
2. Molecular Biology: How and When the Genome Sticks Together
3. Computer Science: Happy Birthday, Dear Viruses
4. Neuroscience: Autism's Cause May Be Abnormal Synapses
5. Extrasolar Planets: Water on Distant Worlds
6. Neurophysiology: Channelling Cold Reception
7. Mass Extinctions: Reading the Book of Death
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1.
Science 13 July 2007: Vol. 317. no. 5835, pp. 207 - 208 DOI:
10.1126/science.1145956
Climate Change: A Changing Climate for Prediction
Peter Cox and David Stephenson
The latest report by the Intergovernmental Panel on Climate
Change (IPCC) makes it clear that recent global warming is
significant in the context of natural climate variations, and
that human activities are very likely to be the cause of this
climate change. As a result, businesses, policy-makers, and
members of the public are seeking the advice of climate
scientists on what they should do to prepare for the inevitable
further climate change over the next few decades (adaptation) and
how they can help to avoid dangerous climate change in the longer
term (mitigation).
Current climate change projections produce a wide range of
estimates of global warming by 2100. These projections are useful
for stressing the consequences of different greenhouse gas
emission scenarios, but too long-term and uncertain to guide
regional adaptation to climate change. Standard climate
projections are also insufficiently focused on quantifying the
risk of dangerous climate change to properly inform mitigation
policy under the United Nations Framework Convention on Climate
Change. (The UNFCCC is an international treaty joined by most
countries; the Kyoto Protocol is an addendum to that treaty.) How
can projections be designed so that they better inform policy?
Uncertainties in climate predictions vary with the averaging
period over which the climate is defined and with the lead time
of the prediction. Consider, for example, the prediction of the
global mean decadal temperature over the next century, with
forecast lead times varying between 1 and 100 years. On lead
times of less than 10 years, the signal of anthropogenic climate
change is relatively small compared to natural decadal climate
variability, and uncertainties in initial conditions dominate the
overall uncertainty of the prediction (see the first figure) (1).
By contrast, climate predictions on time scales of a century are
much less sensitive to initial conditions, because the signal of
anthropogenic climate change is typically much larger at longer
time scales and because most elements of the climate system have
a "memory" of past climate-forcing factors that is shorter than a
few decades. The major source of uncertainty here lies in the
future anthropogenic emissions of greenhouse gases and aerosols
(see the first figure) (2). This uncertainty can be seen as
humankind's free will concerning future climate change.
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2.
Science 13 July 2007: Vol. 317. no. 5835, pp. 209 - 210 DOI:
10.1126/science.1146072
Molecular Biology: How and When the Genome Sticks Together
Erwan Watrin and Jan-Michael Peters
Before a eukaryotic cell divides, it generates a copy of its
genome by DNA replication. As a result, each chromosome in a
postreplicative cell contains two identical DNA molecules, the
sister chromatids. These DNA molecules are physically connected
to each other, a phenomenon known as sister-chromatid cohesion.
Cohesion is essential for the symmetrical segregation of
chromosomes during cell division (1). Not surprisingly, cohesion
is normally established when sister chromatids are synthesized
during S phase of the cell division cycle (see the figure). But
cohesion also helps to repair damaged DNA after S phase has been
completed (2). Two papers in this issue, by Ström et al. (3) on
page 242 and Ünal et al. (4) on page 245, show that cohesion can
be established in response to DNA damage independently of DNA
replication. This overturns a long-held belief that cohesion is
strictly coupled to DNA synthesis. The papers also imply that DNA
damage may have a broader impact than previously thought,
triggering genomewide protection of chromosome integrity.
Sister-chromatid cohesion is thought to be mediated by ring-
shaped protein structures called cohesin complexes (1). In normal
cells, cohesin can connect sister chromatids only in S phase,
even though newly synthesized cohesin complexes can associate
with DNA in the subsequent G2 phase (5, 6). Until recently, it
was generally assumed that sister-chromatid cohesion can only be
generated at replication forks where DNA is synthesized. This
view was first challenged by the finding that cohesion can also
occur in G2 phase if DNA is damaged by double-strand breaks (7,
8). In this case, large amounts of cohesin are recruited to the
damaged DNA, forming new connections between the sister
chromatids (7, 9). However, repair of damaged DNA also typically
depends on DNA, synthesis. It therefore remained quite possible
that establishment of cohesion after DNA damage is also
mechanistically coupled to DNA synthesis, just as the two
processes are linked during S phase.
To address this issue, Ström et al. and Ünal et al. analyzed
budding yeast mutants that are deficient in an enzyme (Rad52)
that is needed for DNA synthesis, specifically during DNA repair.
Both groups observed cohesion even if the DNA of these mutant
cells was damaged during G2 phase, indicating that cohesion can
be fully uncoupled from DNA synthesis. Beyond this surprise, the
discovery could also prove technically useful to address another
long-standing question: Do DNA replication factors also function
in sister-chromatid cohesion? Replication defects inevitably lead
to the absence of cohesion. The discovery that cohesion can,
under certain conditions, occur without DNA replication may
enable reinvestigation of this question.
Ünal et al. and Ström et al. made a second unexpected discovery
when they analyzed yeast cells in which only one chromosome had
been damaged by a double-strand break. Surprisingly, cohesin
complexes could establish cohesion on both damaged and undamaged
chromosomes during G2 phase. This implies that the presence of
DNA double-strand breaks somehow reactivates the molecular
machinery that normally forges cohesion only during S phase.
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3.
Science 13 July 2007: Vol. 317. no. 5835, pp. 210 - 211 DOI:
10.1126/science.1140909
Computer Science: Happy Birthday, Dear Viruses
Richard Ford and Eugene H. Spafford
Birthdays and other anniversaries are often a time for
celebration, as we reflect on milestones passed. In the world of
computing, we have quite a few happy anniversaries: for example,
the first computer (arguably, Babbage's design of 1822) and the
first e-mail message sent (1965).
Some remembrances, however, are less positive, and 2007 marks the
silver anniversary of a darker sort--the genesis of malicious
computer viruses (1-3). In 1982, a virus written by a high-school
student in Pittsburgh began appearing on Apple II systems. This
virus--known as "Elk Cloner"--infected the operating system,
copied itself to floppy discs, and displayed bad poetry.
Primarily intended to be irritating, the virus came and went with
little notice. Few people spent time worrying about the beastie,
and almost nobody predicted that it was a harbinger of the
current multibillion dollar antivirus industry.
From such humble beginnings, computer viruses--and, more broadly,
"malware" programs--are now so ingrained in popular culture that
they've become the butt of jokes in ads and talk shows. Although
the malware problem grew slowly in the early 1980s, not much time
passed before it really made the news. In 1988, the infamous
"Morris Worm" spread worldwide, causing outages across the
fledgling Internet. There was also the media storm surrounding
the Michelangelo virus, which was set to trigger on 6 March 1992,
threatening to destroy data on infected machines. Since then,
SQL.Slammer, Code Red, Nimda, Concept, and Melissa all had their
15 minutes of fame and, in the process, collectively caused
billions of dollars in damage.
The most talked-about risks from today's malware have a
distinctly financial flavor. If the viruses and worms of the past
decade were the online equivalent of graffiti artists, malware is
now like criminals who wish to steal your wallet and forge your
checks. This has led to much quieter attacks, because too much
visibility would cut down on profits. Instead of displaying a
message or erasing your hard drive, modern malware is more
insidious, turning your machine into a relay for spam, a staging
ground to attack other systems, or a spy capturing your bank
account and credit card information--or all three.
Spyware, phishing, rootkits, and bots--the cutting-edge malware
of today--are truly nasty, and considerable effort has been
invested in their creation. It has become a significant criminal
enterprise and supports a thriving underground economy.
Surely the scientific community has simply been too preoccupied
to deal with this challenge and a good solution is available.
Sadly, even after decades, it appears that no end is in sight.
This stems partly from a subtle computational twist: Building a
computer program that can tell with absolute certainty whether
any other program contains a virus is equivalent to a famous
computer science conundrum called the "halting problem." It has
no solution in the general case and has no approximate solution
for our current computing environments without also generating
too many false results (4).
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4.
Science 13 July 2007: Vol. 317. no. 5835, pp. 190 - 191 DOI:
10.1126/science.317.5835.190
Neuroscience: Autism's Cause May Be Abnormal Synapses
Ken Garber
New genetic evidence is leading researchers to home in on the
cleft separating neurons as the site where the disorder may
originate.
No one knows what causes autism, which in its broad definition
affects about 1 in every 150 children. The impaired social
interaction, communication deficits, and restricted and
repetitive behaviors seen in people with the condition have
confounded scientists since it was first identified in 1943.
Because only a minority of autistic persons have severe
intellectual disability, and some show exceptional cognitive
talents, relatively subtle changes in the brain are probably
responsible. Now a flurry of new discoveries is pointing to one
possible site of autism's origin: the synapse.
Synapses are junctions across which neurons communicate. They are
essential for sensory perception, movement coordination,
learning, and memory--virtually all brain function. "The synapse
is like the soul of the brain," says Huda Zoghbi, a pediatric
neurologist at the Baylor College of Medicine in Houston, Texas.
"It's at the root of everything."
Zoghbi was the first to propose, in 2003, that altered synapses
might be responsible for autism. But direct evidence was thin.
Now "there seems to be a confluence of data flowing," says
Stephen Scherer, a geneticist at the Hospital for Sick Children
in Toronto, Ontario.
Until the mid-1980s, experts considered autism a strictly
environmental disorder, with most of the blame falling on faulty
parenting. Now we know that "autistic spectrum disorder," the
term specialists prefer, is overwhelmingly genetic. Based mostly
on studies of fraternal and identical twins, University of
Illinois at Chicago autism researcher Edwin Cook concludes that
genetic factors contribute about 90% to autism, with
environmental factors contributing no more than 10%. Autism is
"the most heritable of neurodevelopmental disorders that are
complex in origin," says Scherer. (Biology is not destiny, of
course, because the environment affects the form any genetic
disorder takes, and autistic children often improve if placed in
the right learning setting.)
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5.
Nature 448, 143-145 (12 July 2007) | doi:10.1038/448143a;
Published online 11 July 2007
Extrasolar Planets: Water on Distant Worlds
Heather A. Knutson
Is the presence of water a feature common to all gas-giant
planets? The first convincing detection of water vapour in the
atmosphere of such a planet from outside our Solar System
indicates that the answer is yes.
Gas-giant planets - Jupiter, Saturn, Uranus and Neptune in our
own Solar System - generally form at large distances from their
parent star. Here, radiation is less intense, and so water and
other low-mass elements and compounds, such as methane, can be
more easily accreted in the form of ices onto the newly formed
protoplanet. This process explains why the Solar System's gas
giants contain significantly larger quantities of water than does
the relatively rocky planet we call home. The rule is expected to
hold for gas giants outside our Solar System, which we presume
formed through similar processes. Until recently, however, the
only planets we were able to study in the necessary detail were
those in our own backyard.
On page 169 of this issue, Tinetti and colleagues1 provide the
first convincing evidence for water vapour in the atmosphere of
an extrasolar planet. The hot gas-giant planet, or 'hot Jupiter',
that they studied, known as HD 189733b, is too far away to be
imaged directly. Instead, the authors took advantage of the
unusual geometry of the system, which is oriented such that the
planet eclipses its parent star once every orbit. This transiting
geometry of HD 189733b was exploited most recently to produce the
first-ever infrared 'map' of the temperatures in an extrasolar
planet's atmosphere2, 3. Because, unlike the giants of our Solar
System, HD 189733b orbits extremely close to its parent star - at
less than 3% of the Earth-Sun distance - these temperatures range
from a toasty 1,200 kelvin on the dayside of the planet to a
relatively balmy 970 kelvin on the nightside.
Tinetti et al. used NASA's powerful Spitzer Space Telescope to
look for the signal of water absorption in starlight transmitted
through the edges of the planet's atmosphere during transit. This
method was applied successfully a few years ago to detect sodium
in the atmosphere of a hot Jupiter4. The authors find that the
effective light-blocking area of HD 189733b is slightly larger
when measured at a wavelength of 5.8 microm than at 3.6 microm.
This difference, they conclude, is the effect of water vapour in
the planet's atmosphere, which will absorb more light at the
longer wavelength and transmit more at the shorter wavelength.
The detection comes as a relief for the theorists who had
predicted5, 6, 7, 8 that water vapour should be a significant
component of the atmospheres of hot Jupiters. But it contradicts
previous studies of the same planet9 and of another hot
Jupiter10, both of which found no evidence for water. The earlier
study of HD 189733b involved looking for evidence of water
absorption in the spectrum of light emitted by the hot dayside of
the planet9 (HD 189733b always presents the same face to its
parent star).
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6.
Nature 448, 147-148 (12 July 2007) | doi:10.1038/448147a;
Published online 11 July 2007
Neurophysiology: Channelling Cold Reception
Bernd Nilius & Thomas Voets
Perception of cold and hot is one of life's essentials. Three
research teams find that, when a temperature-sensing receptor is
deleted in mice, the animals lose their response to a range of
cold temperatures.
In his description of the five senses, Aristotle described visus
(sight) as the most supreme sense, yielding the highest pleasure,
and contactus (touch and sensing temperature) as the most
rudimentary sense, required for sheer survival1. Indeed, to
maintain a healthy core body temperature of 37 °C, humans - like
other animals that can retain a relatively constant internal body
temperature - need to be able to 'feel' the ambient temperature
and show a suitable physiological or behavioural response to
drastic fluctuations in it.
Ambient temperatures are sensed by cells of the peripheral
nervous system, which convey thermal information from the skin
and peripheral tissues to the brain (for reviews see refs 2,3).
Three papers4, 5, 6, including one by Bautista et al. in this
issue, now report the consequences of deleting the gene encoding
a peripheral cold sensor called TRPM8. These researchers find
that mice that do not have the TRPM8 cation channel - a member of
the transient receptor potential (TRP) family - have severe
deficiencies in sensing cold and in cold-induced behaviour.
It is not surprising that the deletion of the TRPM8 gene leads to
reduced cold sensitivity. Previous studies had shown that TRPM8
is a temperature-sensitive TRP channel that is activated by
moderate cooling and by 'cool' substances such as menthol,
eucalyptol and icilin3. It is expressed in the free nerve endings
of a subset of small-diameter sensory neurons7; the nerve fibres
of these neurons, which are not covered by the myelin sheath,
carry sensory information from the skin to the brain (Fig. 1a).
Consequently, TRPM8 had been proposed as the source of non-
painful and painful reactions to cold3 and as the molecular
mediator of cold-induced pain relief8.
The results of studies4, 5, 6 on TRPM8-deficient mice mainly
endorse these earlier views. At a cellular level, all three
studies4, 5, 6 showed that sensory neurons of these mice show a
drastically blunted response to cold stimuli - for example, a
drop in temperature from around 30 °C to below 20 °C - and to
menthol. Behavioural studies4, 5, 6 illustrate the consequences
of such severe deficits in cold sensation. When given the freedom
of choice, mice with their TRPM8 gene intact prefer to reside in
a warm (around 30 °C) rather than a cool (20 °C or lower) zone.
By contrast, those without TRPM8 do not discriminate against cool
temperatures, cheerfully walking into the cold. Moreover, these
mice no longer exhibit the typical 'wet-dog-shake' response to
injections of icilin, and show a reduced sensitivity to extreme
and painful cold stimuli. Finally, Colburn et al.4 find that
TRPM8 might participate in hypersensitivity to cold, which is
observed after inflammation or nerve injury9.
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7.
Nature 448, 122-125 (12 July 2007) | doi:10.1038/448122a;
Published online 11 July 2007
Mass Extinctions: Reading the Book of Death
Nick Lane
Studies of mass extinctions tend to emphasize the sheer scope of
the carnage. But subtle differences between the species that died
and those that survived can be crucial, finds Nick Lane.
The extinction at the end of the Permian period, some 251 million
years ago, is the most fascinating mass-murder mystery in Earth's
history. Simply put, a party or parties unknown killed off up to
96% of all species then alive. Palaeontologists and Earth-system
scientists have suggested any number of possible culprits, from a
comet or asteroid collision to a collapse of the ozone layer,
from a dramatic suite of volcanic eruptions to ocean waters
bubbling with sulphurous fumes.
Given that the evidence for an impact, although championed by
some, seems sketchy and inconclusive to the majority, the most
dramatic of these suspects is volcanism - the sequence of
eruptions that gave rise to the basalts of the Siberian Traps.
The scale of the eruptions was vast, with something like 3
million cubic kilometres of basalt flowing on to the surface, and
the main lava flows took place at almost exactly at the same time
as the end-Permian extinction itself, give or take a few hundred
thousand years. The vast clouds of gas and ash they spewed out
look like the smoke from a very large gun indeed1.
But if the erupting traps look increasingly like the trigger for
the great die-off, how did they actually do their damage? The
fiery birth of a small continent's worth of new landscape can
change everything from the brightness of the sky to the chemistry
of the oceans. How can scientists work out which of these effects
were inconveniences, and which were fatal?
One answer is to study not the volcanoes, nor their victims, but
the creatures that survived. A mortality rate of 96% sounds
pretty indiscriminate - but recent physiological comparisons
between the creatures that died and those that survived reveal
intriguing patterns2. And these patterns do not just provide
clues as to how the great dying actually unfurled. They also
reveal how the extinctions at the end of the Permian period
shaped the subsequent history of the world that the survivors
inherited.
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