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Laughing gas set to deplete the ozone layer
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EMILY KAY
DEER mice have pulled off the same trick as the famous peppered moth, but in reverse, by evolving a light coat to disguise themselves from predators. What’s more, they did it without having any genes for light fur in their original population. When the pale-coloured Sand Hills of Nebraska formed, about 10,000 years ago, they were colonised by dark-furred deer mice, which would have stood out vividly against the sand. Genetic analysis performed by Catherine Linnen of Harvard University and colleagues has revealed that, back then, the deer mouse genome did not contain the genes for light fur. That means the trait arose from a novel mutation, which rapidly spread through the mouse population (Science, DOI: 10.1126/science.1175826). The mutation was found in a gene called Agouti, which helps control coat colour in many mammals. Linnen says the small amount of genetic variation seen in the new version of Agouti suggests that the mutation occurred less than 10,000 years ago, fitting with the Sand Hills’ formation. Normally, to achieve such a rapid evolutionary shift, a species needs to start with an alternative version of a gene already in circulation, giving natural selection more to work with, but in deer mice the new version of Agouti spread rapidly from a standing start.
Rogue proteins spread prion diseases all by themselves A ROGUE, misfolded protein really is enough to trigger prion diseases such as mad cow disease, laying to rest the notion that a virus has to be involved as well. Prion diseases seem to start with changes in the shape of the prion protein found in mammalian brains, which, mysteriously, prompt other identical prions to change shape too. These misfolded proteins build up leading to brain damage and often death, the theory goes. Since no one is sure how a rogue prion can persuade others to
follow suit, some researchers have insisted a virus must also be involved. To investigate, Walker Jackson of the Whitehead Institute in Boston, Massachusetts, and his colleagues created mice with a mutation associated with the human prion disease Fatal Familial Insomnia and injected some of their brain tissue into the brains of mice without the mutation. Crucially, both sets of mice also had a second genetic alteration, which would have made the mice resistant to FFI
if the disease is triggered by a virus. The researchers found that the first set of mice developed FFI symptoms, suggesting that the FFI mutation alone causes the prion to misfold, and the second set of mice also developed symptoms, showing that the protein change alone is enough to transmit the infection (Neuron, DOI: 10.1016/j. neuron.2009.07.026). The result should finally settle the question of whether proteins act alone to cause prion diseases, says Jackson. NASA
Deer mice lightened up fast
Martian meteorite may have held life MORE than a decade after the furore over a Martian meteorite that some claimed contained fossil microbes, a new analysis suggests the rock’s environment on Mars was conducive to life. In 1996, some scientists argued that ALH 84001, a Martian rock found in Antarctica, contained complex carbon-based molecules and some microscopic markings shaped like bacteria. Sceptics said that the shapes were ambiguous and that the molecules could have been formed at temperatures of 650 °C or so. Even the hardiest known microbes on Earth die above about 120 °C. But an analysis of the other mineral deposits in ALH 84001 – such as those containing calcium and iron – by Paul Niles of NASA’s Johnson Space Center in Houston, Texas, and his team suggests that water surrounded the rock and had been cool enough for life to thrive. “These minerals were formed in what is very likely to have been a habitable environment,” says Niles. This keeps open the possibility that the meteorite does indeed contain fossils (Earth and Planetary Science Letters, DOI: 10.1016/j.epsl.2009.06.039).
No laughing matter for Earth’s ozone NITROUS oxide – also known as laughing gas – is the new villain in the fight to save the ozone layer. Ever since the 1987 Montreal protocol phased out the use of chlorofluorocarbons (CFCs) and other ozone-depleting gases, Earth’s damaged ozone layer has been on the mend. But nitrous oxide (N2O), whose emissions are not regulated, could reverse those gains, reports A. R. Ravishankara of the US National Oceanic and Atmospheric Administration in Boulder, Colorado. N2O reacts with oxygen atoms in the stratosphere to produce nitric oxide, which in turn destroys ozone.
Bacteria release N2O when they consume the nitrogen in soil or water, but human activity now accounts for nearly 40 per cent of N2O emissions (Science, DOI: 10.1126/ science.1176985). N2O could become 50 per cent more destructive as stratospheric CFCs return to pre-industrial levels. That’s because nitrogen and chlorine compounds counteract each other’s effects on ozone: the more chlorine there is, the less destructive nitrogen is, and vice versa. “N2O is the most important ozone-depleting gas that’s being emitted,” says Ravishankara.
5 September 2009 | NewScientist | 17
EMILY KAY
DEER mice have pulled off the same trick as the famous peppered moth, but in reverse, by evolving a light coat to disguise themselves from predators. What’s more, they did it without having any genes for light fur in their original population. When the pale-coloured Sand Hills of Nebraska formed, about 10,000 years ago, they were colonised by dark-furred deer mice, which would have stood out vividly against the sand. Genetic analysis performed by Catherine Linnen of Harvard University and colleagues has revealed that, back then, the deer mouse genome did not contain the genes for light fur. That means the trait arose from a novel mutation, which rapidly spread through the mouse population (Science, DOI: 10.1126/science.1175826). The mutation was found in a gene called Agouti, which helps control coat colour in many mammals. Linnen says the small amount of genetic variation seen in the new version of Agouti suggests that the mutation occurred less than 10,000 years ago, fitting with the Sand Hills’ formation. Normally, to achieve such a rapid evolutionary shift, a species needs to start with an alternative version of a gene already in circulation, giving natural selection more to work with, but in deer mice the new version of Agouti spread rapidly from a standing start.
Rogue proteins spread prion diseases all by themselves A ROGUE, misfolded protein really is enough to trigger prion diseases such as mad cow disease, laying to rest the notion that a virus has to be involved as well. Prion diseases seem to start with changes in the shape of the prion protein found in mammalian brains, which, mysteriously, prompt other identical prions to change shape too. These misfolded proteins build up leading to brain damage and often death, the theory goes. Since no one is sure how a rogue prion can persuade others to
follow suit, some researchers have insisted a virus must also be involved. To investigate, Walker Jackson of the Whitehead Institute in Boston, Massachusetts, and his colleagues created mice with a mutation associated with the human prion disease Fatal Familial Insomnia and injected some of their brain tissue into the brains of mice without the mutation. Crucially, both sets of mice also had a second genetic alteration, which would have made the mice resistant to FFI
if the disease is triggered by a virus. The researchers found that the first set of mice developed FFI symptoms, suggesting that the FFI mutation alone causes the prion to misfold, and the second set of mice also developed symptoms, showing that the protein change alone is enough to transmit the infection (Neuron, DOI: 10.1016/j. neuron.2009.07.026). The result should finally settle the question of whether proteins act alone to cause prion diseases, says Jackson. NASA
Deer mice lightened up fast
Martian meteorite may have held life MORE than a decade after the furore over a Martian meteorite that some claimed contained fossil microbes, a new analysis suggests the rock’s environment on Mars was conducive to life. In 1996, some scientists argued that ALH 84001, a Martian rock found in Antarctica, contained complex carbon-based molecules and some microscopic markings shaped like bacteria. Sceptics said that the shapes were ambiguous and that the molecules could have been formed at temperatures of 650 °C or so. Even the hardiest known microbes on Earth die above about 120 °C. But an analysis of the other mineral deposits in ALH 84001 – such as those containing calcium and iron – by Paul Niles of NASA’s Johnson Space Center in Houston, Texas, and his team suggests that water surrounded the rock and had been cool enough for life to thrive. “These minerals were formed in what is very likely to have been a habitable environment,” says Niles. This keeps open the possibility that the meteorite does indeed contain fossils (Earth and Planetary Science Letters, DOI: 10.1016/j.epsl.2009.06.039).
No laughing matter for Earth’s ozone NITROUS oxide – also known as laughing gas – is the new villain in the fight to save the ozone layer. Ever since the 1987 Montreal protocol phased out the use of chlorofluorocarbons (CFCs) and other ozone-depleting gases, Earth’s damaged ozone layer has been on the mend. But nitrous oxide (N2O), whose emissions are not regulated, could reverse those gains, reports A. R. Ravishankara of the US National Oceanic and Atmospheric Administration in Boulder, Colorado. N2O reacts with oxygen atoms in the stratosphere to produce nitric oxide, which in turn destroys ozone.
Bacteria release N2O when they consume the nitrogen in soil or water, but human activity now accounts for nearly 40 per cent of N2O emissions (Science, DOI: 10.1126/ science.1176985). N2O could become 50 per cent more destructive as stratospheric CFCs return to pre-industrial levels. That’s because nitrogen and chlorine compounds counteract each other’s effects on ozone: the more chlorine there is, the less destructive nitrogen is, and vice versa. “N2O is the most important ozone-depleting gas that’s being emitted,” says Ravishankara.
5 September 2009 | NewScientist | 17