/page/2
neurosciencestuff:

(Image caption: Granule cells connect with other cells via long projections (dendrites). The actual junctions (synapses) are located on thorn-like protuberances called “spines”. Spines are shown in green in the computer reconstruction. Credit: DZNE/Michaela Müller)
A protein couple controls flow of information into the brain’s memory center
Neuroscientists in Bonn and Heidelberg have succeeded in providing new insights into how the brain works. Researchers at the DZNE and the German Cancer Research Center (DKFZ) analyzed tissue samples from mice to identify how two specific proteins, ‘CKAMP44’ and ‘TARP Gamma-8’, act upon the brain’s memory center. These molecules, which have similar counterparts in humans, affect the connections between nerve cells and influence the transmission of nerve signals into the hippocampus, an area of the brain that plays a significant role in learning processes and the creation of memories. The results of the study have been published in the journal Neuron.
Brain function depends on the active communication between nerve cells, known as neurons. For this purpose, neurons are woven together into a dense network where they constantly relay signals to one another. However, neurons do not form direct contacts with each other. Instead they are separated by an extremely narrow gap, known as the synapse. This gap is bridged by ‘neurotransmitters’, which carry nerve signals from one cell to the next.
Docking stations

Specific molecular complexes in the cell’s outer shell, so-called ‘receptors’, receive the signal by binding the neurotransmitters. This triggers an electrical impulse in the receptor-bearing cell and thus the nerve signal has moved on one neuron further.
In the current study, a team led by Dr Jakob von Engelhardt focused on the AMPA receptors. These bind the neurotransmitter glutamate and are particularly common in the brain. “We looked at AMPA receptors in an area of the brain, which constitutes the main entrance to the hippocampus,” explains von Engelhardt, who works for the DZNE and DKFZ. “The hippocampus is responsible for learning and memory formation. Among other things it processes and combines sensory perception. We therefore asked ourselves how the flow of information into the hippocampus is controlled.”
A pair of helpers
Dr von Engelhardt’s research team specifically focused on two protein molecules: ‘CKAMP44’ and ‘TARP Gamma-8’. These proteins are present, along with AMPA receptors, in the ‘granule’ cells, which are neurons that receive signals from areas outside of the hippocampus. It was already known that these proteins form protein complexes with AMPA receptors. “We have now found out that they exert a significant influence on the functioning of glutamate receptors. Each in its own way, as chemically they are completely different,” says the neuroscientist. “We identified that the ability of a nerve cell to receive signals doesn’t depend solely on the actual receptors; CKAMP44 and TARP Gamma-8 are just as important. Their function cannot be separated from that of the receptors.”
This was the result of an analysis in which the researchers compared brain tissue from mice with a natural genotype with brain tissue from genetically modified mice. Neurons in the genetically modified animals were not able to produce either CKAMP44 or TARP Gamma-8 or both.
Long-term effect
The researchers discovered, among other things, that both proteins promote the transportation of glutamate receptors to the cell surface. “This means they influence how receptive the nerve cell is to incoming signals,” says von Engelhardt.
However, the number of receptors and thus the signal reception can be altered by neuronal activity. The von Engelhardt group found that in this regard the auxiliary molecules have different effects: TARP Gamma-8 is essential to ensure that more AMPA receptors are integrated into the synapse following a plasticity induction protocol, whereas CKAMP44 plays no role in this context. “Synapses alter their communication depending on their activity. This ability is called plasticity. Some of the changes involved are only temporary, others may last longer,” explains von Engelhardt. “TARP Gamma-8 influences long-term plasticity. It makes the cell able to strengthen synaptic communication for a prolonged time-period. The larger the number of receptors on the receiving side of the synapse, the better the neuronal connection.”
The number of receptors doesn’t change suddenly, but remains largely stable for a certain amount of time. “This condition may last for hours, days or even longer. This long-term effect is essential for the creation of memories. We can only remember things if the connections between neurons undergo a long-lasting change,” says the scientist.
Fast sequence of signals
However, CKAMP44 and TARP Gamma-8 also act over shorter periods of time. The research team discovered that the molecules affect how quickly the AMPA receptors return to a receptive state. “If glutamate has docked on to a receptor, it takes a while until the receptor can react to the next neurotransmitter. CKAMP44 lengthens this period. In contrast, TARP Gamma-8 helps the receptor to recover more quickly,” says von Engelhardt.
Hence, CKAMP44 temporarily weakens the synaptic connection, while TARP Gamma-8 strengthens it. Through the interplay of these proteins the synapse is able to tune its sensitivity to a specific level. This condition can last from milliseconds to a few seconds before the strength of the connection is again adapted. Specialists refer to this as “short-term plasticity”.
“These molecules ultimately influence how well the nerve cell is able to react to a rapid succession of signals,” the scientist summarises the findings. “Such a rapid firing enables neuronal networks to synchronize their activity, which is a common process in the brain.”
Sensitive balance
Much to the researchers’ surprise, it turned out that the two proteins influence not only the synapse but also the shape of the nerve cells. In the absence of these auxiliary molecules, the neurons have fewer dendrites to establish contact with other nerve cells. “The organism can use CKAMP44 and TARP Gamma-8 molecules to regulate neuronal connections in a number of ways,” von Engelhardt says. “This ability depends on the balance between the partners, as to some extent they have a contrary effect. The way in which the neurons of the hippocampus react to signals from other regions of the brain is therefore highly dependent on the presence and the expression ratio of these molecules.”
Since the two molecules act directly on the structure and function of synapses of granule cells, Jakob von Engelhardt considers it probable that they also have an influence on learning and memory.

neurosciencestuff:

(Image caption: Granule cells connect with other cells via long projections (dendrites). The actual junctions (synapses) are located on thorn-like protuberances called “spines”. Spines are shown in green in the computer reconstruction. Credit: DZNE/Michaela Müller)

A protein couple controls flow of information into the brain’s memory center

Neuroscientists in Bonn and Heidelberg have succeeded in providing new insights into how the brain works. Researchers at the DZNE and the German Cancer Research Center (DKFZ) analyzed tissue samples from mice to identify how two specific proteins, ‘CKAMP44’ and ‘TARP Gamma-8’, act upon the brain’s memory center. These molecules, which have similar counterparts in humans, affect the connections between nerve cells and influence the transmission of nerve signals into the hippocampus, an area of the brain that plays a significant role in learning processes and the creation of memories. The results of the study have been published in the journal Neuron.

Brain function depends on the active communication between nerve cells, known as neurons. For this purpose, neurons are woven together into a dense network where they constantly relay signals to one another. However, neurons do not form direct contacts with each other. Instead they are separated by an extremely narrow gap, known as the synapse. This gap is bridged by ‘neurotransmitters’, which carry nerve signals from one cell to the next.

Docking stations

Specific molecular complexes in the cell’s outer shell, so-called ‘receptors’, receive the signal by binding the neurotransmitters. This triggers an electrical impulse in the receptor-bearing cell and thus the nerve signal has moved on one neuron further.

In the current study, a team led by Dr Jakob von Engelhardt focused on the AMPA receptors. These bind the neurotransmitter glutamate and are particularly common in the brain. “We looked at AMPA receptors in an area of the brain, which constitutes the main entrance to the hippocampus,” explains von Engelhardt, who works for the DZNE and DKFZ. “The hippocampus is responsible for learning and memory formation. Among other things it processes and combines sensory perception. We therefore asked ourselves how the flow of information into the hippocampus is controlled.”

A pair of helpers

Dr von Engelhardt’s research team specifically focused on two protein molecules: ‘CKAMP44’ and ‘TARP Gamma-8’. These proteins are present, along with AMPA receptors, in the ‘granule’ cells, which are neurons that receive signals from areas outside of the hippocampus. It was already known that these proteins form protein complexes with AMPA receptors. “We have now found out that they exert a significant influence on the functioning of glutamate receptors. Each in its own way, as chemically they are completely different,” says the neuroscientist. “We identified that the ability of a nerve cell to receive signals doesn’t depend solely on the actual receptors; CKAMP44 and TARP Gamma-8 are just as important. Their function cannot be separated from that of the receptors.”

This was the result of an analysis in which the researchers compared brain tissue from mice with a natural genotype with brain tissue from genetically modified mice. Neurons in the genetically modified animals were not able to produce either CKAMP44 or TARP Gamma-8 or both.

Long-term effect

The researchers discovered, among other things, that both proteins promote the transportation of glutamate receptors to the cell surface. “This means they influence how receptive the nerve cell is to incoming signals,” says von Engelhardt.

However, the number of receptors and thus the signal reception can be altered by neuronal activity. The von Engelhardt group found that in this regard the auxiliary molecules have different effects: TARP Gamma-8 is essential to ensure that more AMPA receptors are integrated into the synapse following a plasticity induction protocol, whereas CKAMP44 plays no role in this context. “Synapses alter their communication depending on their activity. This ability is called plasticity. Some of the changes involved are only temporary, others may last longer,” explains von Engelhardt. “TARP Gamma-8 influences long-term plasticity. It makes the cell able to strengthen synaptic communication for a prolonged time-period. The larger the number of receptors on the receiving side of the synapse, the better the neuronal connection.”

The number of receptors doesn’t change suddenly, but remains largely stable for a certain amount of time. “This condition may last for hours, days or even longer. This long-term effect is essential for the creation of memories. We can only remember things if the connections between neurons undergo a long-lasting change,” says the scientist.

Fast sequence of signals

However, CKAMP44 and TARP Gamma-8 also act over shorter periods of time. The research team discovered that the molecules affect how quickly the AMPA receptors return to a receptive state. “If glutamate has docked on to a receptor, it takes a while until the receptor can react to the next neurotransmitter. CKAMP44 lengthens this period. In contrast, TARP Gamma-8 helps the receptor to recover more quickly,” says von Engelhardt.

Hence, CKAMP44 temporarily weakens the synaptic connection, while TARP Gamma-8 strengthens it. Through the interplay of these proteins the synapse is able to tune its sensitivity to a specific level. This condition can last from milliseconds to a few seconds before the strength of the connection is again adapted. Specialists refer to this as “short-term plasticity”.

“These molecules ultimately influence how well the nerve cell is able to react to a rapid succession of signals,” the scientist summarises the findings. “Such a rapid firing enables neuronal networks to synchronize their activity, which is a common process in the brain.”

Sensitive balance

Much to the researchers’ surprise, it turned out that the two proteins influence not only the synapse but also the shape of the nerve cells. In the absence of these auxiliary molecules, the neurons have fewer dendrites to establish contact with other nerve cells. “The organism can use CKAMP44 and TARP Gamma-8 molecules to regulate neuronal connections in a number of ways,” von Engelhardt says. “This ability depends on the balance between the partners, as to some extent they have a contrary effect. The way in which the neurons of the hippocampus react to signals from other regions of the brain is therefore highly dependent on the presence and the expression ratio of these molecules.”

Since the two molecules act directly on the structure and function of synapses of granule cells, Jakob von Engelhardt considers it probable that they also have an influence on learning and memory.

ifonlywewereamoungstfriends:

nilenna:


Kryolan HD, BodyArt and Special FX make-up at IMATS LA.

Looks like something out of ‘Farescape’ :)

SFX make up game so strong. This is one of my all time favourites. The paint job alone is magnificent. 

ifonlywewereamoungstfriends:

nilenna:

Kryolan HD, BodyArt and Special FX make-up at IMATS LA.

Looks like something out of ‘Farescape’ :)

SFX make up game so strong. This is one of my all time favourites. The paint job alone is magnificent. 

(Source: cosplaysleepeatplay, via mushroooms)

neurosciencestuff:

Choice bias: A quirky byproduct of learning from reward
The price of learning from rewarding choices may be just a touch of self-delusion, according to a new study in Neuron.
The research by Brown University brain scientists links a fundamental problem in neuroscience called “credit assignment” — how the brain reinforces learning only in the exact circuits that caused the rewarding choice — to an oft-observed quirk of behavior called “choice bias” – we value the rewards we choose more than equivalent rewards we don’t choose. The researchers used computational modeling and behavioral and genetic experiments to discover evidence that choice bias is essentially a byproduct of credit assignment.
“We weren’t looking to explain anything about choice bias to start off with,” said lead author Jeffrey Cockburn, a graduate student in the research group of senior author Michael Frank, associate professor of cognitive, linguistic, and psychological sciences. “This just happened to be the behavioral phenomenon we thought would emerge out of this credit assignment model.”
So the next time a friend raves about the movie he chose and is less enthusiastic about the just-as-good one that you chose, you might be able to chalk it up to his basic learning circuitry and a genetic difference that affects it.
Modeled mechanism
The model, developed by Frank, Cockburn, and co-author Anne Collins, a postdoctoral researcher, was based on prior research on the function of the striatum, a part of the brain’s basal ganglia (BG) that is principally involved in representing reward values of actions and picking one. “An interaction between three key BG regions moderates that decision-making process. When a rewarding choice has been made, the substantia nigra pars compacta (SNc) releases dopamine into the striatum to reinforce connections between cortex and striatum, so that rewarded actions are more likely to be repeated. But how does the SNc reinforce just the circuits that made the right call? The authors proposed a mechanism by which another part of the subtantia nigra, the SNr, detects when actions are worth choosing and then simultaneously amplifies any dopamine signal coming from the SNc.”
“The novel part here is that we have proposed a mechanism by which the BG can detect when it has selected an action and should therefore amplify the dopamine reinforcing event specifically at that time,” Frank said. “When the SNr decides that striatal valuation signals are strong enough for one action, it releases the brakes not only on downstream structures that allow actions to be executed, but also on the SNc dopamine system, so any unexpected rewards are amplified.”
Specifically, dopamine provides reinforcement by enhancing the responsiveness of connections between cells so that a circuit can more easily repeat its rewarding behavior in the future. But along with that process of reinforcing the action of choosing, the value placed on the resulting reward becomes elevated compared to rewards not experienced this way.
Experimental evidence
That prediction seemed intriguing, but it still had to be tested. The authors identified both behavioral and genetic tests that would be telling.
They recruited 80 people at Brown and elsewhere in Providence to play a behavioral game and to donate some saliva for genetic testing.
The game first presented the subjects pictures of arbitrary Japanese characters that would have different probabilities of rewards if chosen ranging from a 20 percent to 80 percent chance of winning a point or losing a point. For some characters, the player could choose a character to discover its resulting reward or penalty, whereas for others, its result was simply given to them. After that learning phase, the subjects were then presented the characters in pairs and instructed to pick the one they thought had the highest chance of winning based on what they had learned.
The researchers built the game so that for every character a player could choose, there was an equally rewarding one that had merely been given to them. On average, players showed a clear choice bias in that they were more likely to prefer rewarding characters that they had chosen over equally rewarding characters they had been given.
Notably, they exhibited no choice bias between unrewarding characters suggesting that choice bias emerges only in relation to reward, one of the key predictions of their model. But they wanted to test further whether the impact of reward on choice bias was related to the proposed biological mechanism, that striatal dopaminergic learning is enhanced to chosen rewards.
The genetic tests focused on single-letter differences in a gene called DARPP-32, which governs how well cells in the striatum respond to the reinforcing influence of dopamine.
People with one version of the gene have been shown in previous research to be less able to learn from rewards, while people with other versions were less driven by reward in learning.
“The reason why this gene is interesting is because we know something about the biology of what it does and where it is expressed in the brain,” Frank said. “It’s predominant in the striatum and specifically affects synaptic plasticity induced by dopamine signaling. It’s related to the imbalance by which you learn from really good things or not so good things.
“The logic was if the mechanism that we think describes this choice bias and credit assignment problem is accurate then that gene should predict the impact of how good something was on this choice bias phenomenon,” he said.
Indeed, that’s what the data showed. People with the form of the gene that predisposed them to be responsive to big rewards also showed more choice bias from the most strongly rewarded characters. Interestingly, the other people also showed choice bias, but more strongly for those characters that were more mediocre. This pattern was mirrored by the authors’ model when it simulated the effects of DARPP-32 on reward learning imbalances from positive vs. negative outcomes.
For some people, the plums are sweeter if they picked them.

neurosciencestuff:

Choice bias: A quirky byproduct of learning from reward

The price of learning from rewarding choices may be just a touch of self-delusion, according to a new study in Neuron.

The research by Brown University brain scientists links a fundamental problem in neuroscience called “credit assignment” — how the brain reinforces learning only in the exact circuits that caused the rewarding choice — to an oft-observed quirk of behavior called “choice bias” – we value the rewards we choose more than equivalent rewards we don’t choose. The researchers used computational modeling and behavioral and genetic experiments to discover evidence that choice bias is essentially a byproduct of credit assignment.

“We weren’t looking to explain anything about choice bias to start off with,” said lead author Jeffrey Cockburn, a graduate student in the research group of senior author Michael Frank, associate professor of cognitive, linguistic, and psychological sciences. “This just happened to be the behavioral phenomenon we thought would emerge out of this credit assignment model.”

So the next time a friend raves about the movie he chose and is less enthusiastic about the just-as-good one that you chose, you might be able to chalk it up to his basic learning circuitry and a genetic difference that affects it.

Modeled mechanism

The model, developed by Frank, Cockburn, and co-author Anne Collins, a postdoctoral researcher, was based on prior research on the function of the striatum, a part of the brain’s basal ganglia (BG) that is principally involved in representing reward values of actions and picking one. “An interaction between three key BG regions moderates that decision-making process. When a rewarding choice has been made, the substantia nigra pars compacta (SNc) releases dopamine into the striatum to reinforce connections between cortex and striatum, so that rewarded actions are more likely to be repeated. But how does the SNc reinforce just the circuits that made the right call? The authors proposed a mechanism by which another part of the subtantia nigra, the SNr, detects when actions are worth choosing and then simultaneously amplifies any dopamine signal coming from the SNc.”

“The novel part here is that we have proposed a mechanism by which the BG can detect when it has selected an action and should therefore amplify the dopamine reinforcing event specifically at that time,” Frank said. “When the SNr decides that striatal valuation signals are strong enough for one action, it releases the brakes not only on downstream structures that allow actions to be executed, but also on the SNc dopamine system, so any unexpected rewards are amplified.”

Specifically, dopamine provides reinforcement by enhancing the responsiveness of connections between cells so that a circuit can more easily repeat its rewarding behavior in the future. But along with that process of reinforcing the action of choosing, the value placed on the resulting reward becomes elevated compared to rewards not experienced this way.

Experimental evidence

That prediction seemed intriguing, but it still had to be tested. The authors identified both behavioral and genetic tests that would be telling.

They recruited 80 people at Brown and elsewhere in Providence to play a behavioral game and to donate some saliva for genetic testing.

The game first presented the subjects pictures of arbitrary Japanese characters that would have different probabilities of rewards if chosen ranging from a 20 percent to 80 percent chance of winning a point or losing a point. For some characters, the player could choose a character to discover its resulting reward or penalty, whereas for others, its result was simply given to them. After that learning phase, the subjects were then presented the characters in pairs and instructed to pick the one they thought had the highest chance of winning based on what they had learned.

The researchers built the game so that for every character a player could choose, there was an equally rewarding one that had merely been given to them. On average, players showed a clear choice bias in that they were more likely to prefer rewarding characters that they had chosen over equally rewarding characters they had been given.

Notably, they exhibited no choice bias between unrewarding characters suggesting that choice bias emerges only in relation to reward, one of the key predictions of their model. But they wanted to test further whether the impact of reward on choice bias was related to the proposed biological mechanism, that striatal dopaminergic learning is enhanced to chosen rewards.

The genetic tests focused on single-letter differences in a gene called DARPP-32, which governs how well cells in the striatum respond to the reinforcing influence of dopamine.

People with one version of the gene have been shown in previous research to be less able to learn from rewards, while people with other versions were less driven by reward in learning.

“The reason why this gene is interesting is because we know something about the biology of what it does and where it is expressed in the brain,” Frank said. “It’s predominant in the striatum and specifically affects synaptic plasticity induced by dopamine signaling. It’s related to the imbalance by which you learn from really good things or not so good things.

“The logic was if the mechanism that we think describes this choice bias and credit assignment problem is accurate then that gene should predict the impact of how good something was on this choice bias phenomenon,” he said.

Indeed, that’s what the data showed. People with the form of the gene that predisposed them to be responsive to big rewards also showed more choice bias from the most strongly rewarded characters. Interestingly, the other people also showed choice bias, but more strongly for those characters that were more mediocre. This pattern was mirrored by the authors’ model when it simulated the effects of DARPP-32 on reward learning imbalances from positive vs. negative outcomes.

For some people, the plums are sweeter if they picked them.

catmota:

Bottle Brush Trees
Jian Chong Min

catmota:

Bottle Brush Trees

Jian Chong Min

(via thunorsdottir)

scienceyoucanlove:

Why Has This Really Common Virus Only Just Been Discovered?
by Ed Yong

The most common viruses in your body don’t make you ill. Instead, they infect the legions of microbes that live in your gut. These bacteriophages, or phages for short, number in their trillions. And the most common of them might be a newly discovered virus called crAssphage.
No one has seen crAssphage under the microscope, but we know what its genome looks like—Bas Dutilh from Radboud University Medical Centre pieced it together using fragments of DNA from the stools of 12 individuals. He found crAssphage in all of them. Then, he found it in hundreds more.
To study the microbes that live in a person’s guts, scientists will typically collect a stool sample, break all the DNA within into small fragments, and sequence these pieces. The result is a metagenome: a mish-mashed collection of DNA from all the local bacteria, viruses and other microbes.
Dutilh’s team, led by Rob Edwards at San Diego State University, analysed 466 metagenomes that have been added to public databases and found crAssphage in three-quarters of them. It’s there in stool samples from people in the USA, Europe and South Korea. It actually accounted for 1.7 percent of all the sequences that the team analysed—six times more than all the other known phages put together. You probably have it inside you right now.
The work highlights just how much we don’t know about the viruses in our guts and “what exciting times these are for viral discovery”, says Lesley Ogilvie from the Max Planck Institute for Molecular Genetics.
But how could such a common virus go undiscovered for so long, especially considering how popular the study of gut microbes has become? It’s as if zookeepers suddenly realised that most of their zoos contain a giant grey animal with tusks and a trunk, which no one had noticed before.
For one thing, the viruses in our guts are hard to study.  “To study a virus, normally you have to make heaps of it, which isn’t possible if you can’t grow the host,” says Martha Clokiefrom the University of Leicester.And since mostgut bacteria won’t grow easily in a lab, the viruses that infect them are similarly hard to rear.
The alternative is to use metagenomics to analyse a microbe’s genes without having to grow it. But first, you have to assemble your mish-mash of sequences, which come from different organisms, into a complete genome. It’s a bit like putting all the pieces of a thousand jigsaw puzzles into one bag, and trying to solve just one.
The usual strategy is to work off what you know by aligning these new sequences to those in databases. But this approach doesn’t work very well for our inner viruses because most of them are unknown. The sequences in the databases represent the tip of the iceberg. According to Dutilh, around 75 percent of the DNA from any new stool sample—and as much as 99 percent—won’t match any of these known sequences.
So what’s in that other 75 percent?
Well, crAssphage for starters.
Dutilh’s team found it by using a different approach based on a simple idea: that fragments which repeatedly turn up in the same samples are more likely to be parts of the same genome. They used a technique called cross-assembly to identify one such group of co-occurring sequences, in stool samples from 12 people. They then assembled these sequences into a single genome.
The genome had several distinctive features which told the researchers that it belonged to a phage, albeit one that’s very different to any we currently know of. They called it crAssphage after the cross-assembly method that revealed its existence.
They used the same technique to work out what the virus infects: if there’s lots of crAssphage DNA in a sample, there should also be lots of DNA from its host. Based on this logic, the most likely hosts are a group of bacteria called Bacteroides.
The team checked this result with a second technique. They looked at CRISPR sequences—a kind of bacterial immune system that recognises DNA from infecting phages. The team scanned all known bacterial genomes for CRISPR sequences that matched crAssphage and found that the closest matches came from two groups of gut bacteria, one of which wasBacteroides.
Bacteroides are major players in our guts. They help us break down our food, control the development of our immune system, and protect us from disease-causing bacteria. Their numbers change depending on the food we eat, and they correlate with our risk of different diseases. If crAssphage infects these microbes, it could also be an important player in our daily dramas.
It’s too early to speculate what its role might be, says Dutihl. Still, we know that phages are generally important. By killing off the most abundant bacteria in the gut, they ensure that no single species can monopolise the space. And last year, Jeremy Barr, who was involved of this new study,  showed that phages could even act as part of our own immune system.
Many scientists had assumed that viruses in the gut are caught up in fast-paced evolutionary battles with local bacteria. This leaves people with very different collections, and explains why most of the viral sequences that we find don’t match anything in the databases. But the existence of crAssphage challenges this concept: it was part of the pool of unknowns but it’s alsoincredibly common. “It definitely changes the idea we had about viruses being very individual-specific,” says Dutihl. The study of human gut bacteria followed a similar path: early studies highlighted the differences between us but important similarities started emerging as our techniques became more sophisticated.
read the rest on Nat Geo’s website 

scienceyoucanlove:

Why Has This Really Common Virus Only Just Been Discovered?

papermagazine:

Happy birthday to Queen Iman.

papermagazine:

Happy birthday to Queen Iman.

(Source: saloandseverine, via aanubis)

neurosciencestuff:

(Image caption: Granule cells connect with other cells via long projections (dendrites). The actual junctions (synapses) are located on thorn-like protuberances called “spines”. Spines are shown in green in the computer reconstruction. Credit: DZNE/Michaela Müller)
A protein couple controls flow of information into the brain’s memory center
Neuroscientists in Bonn and Heidelberg have succeeded in providing new insights into how the brain works. Researchers at the DZNE and the German Cancer Research Center (DKFZ) analyzed tissue samples from mice to identify how two specific proteins, ‘CKAMP44’ and ‘TARP Gamma-8’, act upon the brain’s memory center. These molecules, which have similar counterparts in humans, affect the connections between nerve cells and influence the transmission of nerve signals into the hippocampus, an area of the brain that plays a significant role in learning processes and the creation of memories. The results of the study have been published in the journal Neuron.
Brain function depends on the active communication between nerve cells, known as neurons. For this purpose, neurons are woven together into a dense network where they constantly relay signals to one another. However, neurons do not form direct contacts with each other. Instead they are separated by an extremely narrow gap, known as the synapse. This gap is bridged by ‘neurotransmitters’, which carry nerve signals from one cell to the next.
Docking stations

Specific molecular complexes in the cell’s outer shell, so-called ‘receptors’, receive the signal by binding the neurotransmitters. This triggers an electrical impulse in the receptor-bearing cell and thus the nerve signal has moved on one neuron further.
In the current study, a team led by Dr Jakob von Engelhardt focused on the AMPA receptors. These bind the neurotransmitter glutamate and are particularly common in the brain. “We looked at AMPA receptors in an area of the brain, which constitutes the main entrance to the hippocampus,” explains von Engelhardt, who works for the DZNE and DKFZ. “The hippocampus is responsible for learning and memory formation. Among other things it processes and combines sensory perception. We therefore asked ourselves how the flow of information into the hippocampus is controlled.”
A pair of helpers
Dr von Engelhardt’s research team specifically focused on two protein molecules: ‘CKAMP44’ and ‘TARP Gamma-8’. These proteins are present, along with AMPA receptors, in the ‘granule’ cells, which are neurons that receive signals from areas outside of the hippocampus. It was already known that these proteins form protein complexes with AMPA receptors. “We have now found out that they exert a significant influence on the functioning of glutamate receptors. Each in its own way, as chemically they are completely different,” says the neuroscientist. “We identified that the ability of a nerve cell to receive signals doesn’t depend solely on the actual receptors; CKAMP44 and TARP Gamma-8 are just as important. Their function cannot be separated from that of the receptors.”
This was the result of an analysis in which the researchers compared brain tissue from mice with a natural genotype with brain tissue from genetically modified mice. Neurons in the genetically modified animals were not able to produce either CKAMP44 or TARP Gamma-8 or both.
Long-term effect
The researchers discovered, among other things, that both proteins promote the transportation of glutamate receptors to the cell surface. “This means they influence how receptive the nerve cell is to incoming signals,” says von Engelhardt.
However, the number of receptors and thus the signal reception can be altered by neuronal activity. The von Engelhardt group found that in this regard the auxiliary molecules have different effects: TARP Gamma-8 is essential to ensure that more AMPA receptors are integrated into the synapse following a plasticity induction protocol, whereas CKAMP44 plays no role in this context. “Synapses alter their communication depending on their activity. This ability is called plasticity. Some of the changes involved are only temporary, others may last longer,” explains von Engelhardt. “TARP Gamma-8 influences long-term plasticity. It makes the cell able to strengthen synaptic communication for a prolonged time-period. The larger the number of receptors on the receiving side of the synapse, the better the neuronal connection.”
The number of receptors doesn’t change suddenly, but remains largely stable for a certain amount of time. “This condition may last for hours, days or even longer. This long-term effect is essential for the creation of memories. We can only remember things if the connections between neurons undergo a long-lasting change,” says the scientist.
Fast sequence of signals
However, CKAMP44 and TARP Gamma-8 also act over shorter periods of time. The research team discovered that the molecules affect how quickly the AMPA receptors return to a receptive state. “If glutamate has docked on to a receptor, it takes a while until the receptor can react to the next neurotransmitter. CKAMP44 lengthens this period. In contrast, TARP Gamma-8 helps the receptor to recover more quickly,” says von Engelhardt.
Hence, CKAMP44 temporarily weakens the synaptic connection, while TARP Gamma-8 strengthens it. Through the interplay of these proteins the synapse is able to tune its sensitivity to a specific level. This condition can last from milliseconds to a few seconds before the strength of the connection is again adapted. Specialists refer to this as “short-term plasticity”.
“These molecules ultimately influence how well the nerve cell is able to react to a rapid succession of signals,” the scientist summarises the findings. “Such a rapid firing enables neuronal networks to synchronize their activity, which is a common process in the brain.”
Sensitive balance
Much to the researchers’ surprise, it turned out that the two proteins influence not only the synapse but also the shape of the nerve cells. In the absence of these auxiliary molecules, the neurons have fewer dendrites to establish contact with other nerve cells. “The organism can use CKAMP44 and TARP Gamma-8 molecules to regulate neuronal connections in a number of ways,” von Engelhardt says. “This ability depends on the balance between the partners, as to some extent they have a contrary effect. The way in which the neurons of the hippocampus react to signals from other regions of the brain is therefore highly dependent on the presence and the expression ratio of these molecules.”
Since the two molecules act directly on the structure and function of synapses of granule cells, Jakob von Engelhardt considers it probable that they also have an influence on learning and memory.

neurosciencestuff:

(Image caption: Granule cells connect with other cells via long projections (dendrites). The actual junctions (synapses) are located on thorn-like protuberances called “spines”. Spines are shown in green in the computer reconstruction. Credit: DZNE/Michaela Müller)

A protein couple controls flow of information into the brain’s memory center

Neuroscientists in Bonn and Heidelberg have succeeded in providing new insights into how the brain works. Researchers at the DZNE and the German Cancer Research Center (DKFZ) analyzed tissue samples from mice to identify how two specific proteins, ‘CKAMP44’ and ‘TARP Gamma-8’, act upon the brain’s memory center. These molecules, which have similar counterparts in humans, affect the connections between nerve cells and influence the transmission of nerve signals into the hippocampus, an area of the brain that plays a significant role in learning processes and the creation of memories. The results of the study have been published in the journal Neuron.

Brain function depends on the active communication between nerve cells, known as neurons. For this purpose, neurons are woven together into a dense network where they constantly relay signals to one another. However, neurons do not form direct contacts with each other. Instead they are separated by an extremely narrow gap, known as the synapse. This gap is bridged by ‘neurotransmitters’, which carry nerve signals from one cell to the next.

Docking stations

Specific molecular complexes in the cell’s outer shell, so-called ‘receptors’, receive the signal by binding the neurotransmitters. This triggers an electrical impulse in the receptor-bearing cell and thus the nerve signal has moved on one neuron further.

In the current study, a team led by Dr Jakob von Engelhardt focused on the AMPA receptors. These bind the neurotransmitter glutamate and are particularly common in the brain. “We looked at AMPA receptors in an area of the brain, which constitutes the main entrance to the hippocampus,” explains von Engelhardt, who works for the DZNE and DKFZ. “The hippocampus is responsible for learning and memory formation. Among other things it processes and combines sensory perception. We therefore asked ourselves how the flow of information into the hippocampus is controlled.”

A pair of helpers

Dr von Engelhardt’s research team specifically focused on two protein molecules: ‘CKAMP44’ and ‘TARP Gamma-8’. These proteins are present, along with AMPA receptors, in the ‘granule’ cells, which are neurons that receive signals from areas outside of the hippocampus. It was already known that these proteins form protein complexes with AMPA receptors. “We have now found out that they exert a significant influence on the functioning of glutamate receptors. Each in its own way, as chemically they are completely different,” says the neuroscientist. “We identified that the ability of a nerve cell to receive signals doesn’t depend solely on the actual receptors; CKAMP44 and TARP Gamma-8 are just as important. Their function cannot be separated from that of the receptors.”

This was the result of an analysis in which the researchers compared brain tissue from mice with a natural genotype with brain tissue from genetically modified mice. Neurons in the genetically modified animals were not able to produce either CKAMP44 or TARP Gamma-8 or both.

Long-term effect

The researchers discovered, among other things, that both proteins promote the transportation of glutamate receptors to the cell surface. “This means they influence how receptive the nerve cell is to incoming signals,” says von Engelhardt.

However, the number of receptors and thus the signal reception can be altered by neuronal activity. The von Engelhardt group found that in this regard the auxiliary molecules have different effects: TARP Gamma-8 is essential to ensure that more AMPA receptors are integrated into the synapse following a plasticity induction protocol, whereas CKAMP44 plays no role in this context. “Synapses alter their communication depending on their activity. This ability is called plasticity. Some of the changes involved are only temporary, others may last longer,” explains von Engelhardt. “TARP Gamma-8 influences long-term plasticity. It makes the cell able to strengthen synaptic communication for a prolonged time-period. The larger the number of receptors on the receiving side of the synapse, the better the neuronal connection.”

The number of receptors doesn’t change suddenly, but remains largely stable for a certain amount of time. “This condition may last for hours, days or even longer. This long-term effect is essential for the creation of memories. We can only remember things if the connections between neurons undergo a long-lasting change,” says the scientist.

Fast sequence of signals

However, CKAMP44 and TARP Gamma-8 also act over shorter periods of time. The research team discovered that the molecules affect how quickly the AMPA receptors return to a receptive state. “If glutamate has docked on to a receptor, it takes a while until the receptor can react to the next neurotransmitter. CKAMP44 lengthens this period. In contrast, TARP Gamma-8 helps the receptor to recover more quickly,” says von Engelhardt.

Hence, CKAMP44 temporarily weakens the synaptic connection, while TARP Gamma-8 strengthens it. Through the interplay of these proteins the synapse is able to tune its sensitivity to a specific level. This condition can last from milliseconds to a few seconds before the strength of the connection is again adapted. Specialists refer to this as “short-term plasticity”.

“These molecules ultimately influence how well the nerve cell is able to react to a rapid succession of signals,” the scientist summarises the findings. “Such a rapid firing enables neuronal networks to synchronize their activity, which is a common process in the brain.”

Sensitive balance

Much to the researchers’ surprise, it turned out that the two proteins influence not only the synapse but also the shape of the nerve cells. In the absence of these auxiliary molecules, the neurons have fewer dendrites to establish contact with other nerve cells. “The organism can use CKAMP44 and TARP Gamma-8 molecules to regulate neuronal connections in a number of ways,” von Engelhardt says. “This ability depends on the balance between the partners, as to some extent they have a contrary effect. The way in which the neurons of the hippocampus react to signals from other regions of the brain is therefore highly dependent on the presence and the expression ratio of these molecules.”

Since the two molecules act directly on the structure and function of synapses of granule cells, Jakob von Engelhardt considers it probable that they also have an influence on learning and memory.

(Source: heroingranola)

ifonlywewereamoungstfriends:

nilenna:


Kryolan HD, BodyArt and Special FX make-up at IMATS LA.

Looks like something out of ‘Farescape’ :)

SFX make up game so strong. This is one of my all time favourites. The paint job alone is magnificent. 

ifonlywewereamoungstfriends:

nilenna:

Kryolan HD, BodyArt and Special FX make-up at IMATS LA.

Looks like something out of ‘Farescape’ :)

SFX make up game so strong. This is one of my all time favourites. The paint job alone is magnificent. 

(Source: cosplaysleepeatplay, via mushroooms)

(Source: unit-02, via 80sanime)

neurosciencestuff:

Choice bias: A quirky byproduct of learning from reward
The price of learning from rewarding choices may be just a touch of self-delusion, according to a new study in Neuron.
The research by Brown University brain scientists links a fundamental problem in neuroscience called “credit assignment” — how the brain reinforces learning only in the exact circuits that caused the rewarding choice — to an oft-observed quirk of behavior called “choice bias” – we value the rewards we choose more than equivalent rewards we don’t choose. The researchers used computational modeling and behavioral and genetic experiments to discover evidence that choice bias is essentially a byproduct of credit assignment.
“We weren’t looking to explain anything about choice bias to start off with,” said lead author Jeffrey Cockburn, a graduate student in the research group of senior author Michael Frank, associate professor of cognitive, linguistic, and psychological sciences. “This just happened to be the behavioral phenomenon we thought would emerge out of this credit assignment model.”
So the next time a friend raves about the movie he chose and is less enthusiastic about the just-as-good one that you chose, you might be able to chalk it up to his basic learning circuitry and a genetic difference that affects it.
Modeled mechanism
The model, developed by Frank, Cockburn, and co-author Anne Collins, a postdoctoral researcher, was based on prior research on the function of the striatum, a part of the brain’s basal ganglia (BG) that is principally involved in representing reward values of actions and picking one. “An interaction between three key BG regions moderates that decision-making process. When a rewarding choice has been made, the substantia nigra pars compacta (SNc) releases dopamine into the striatum to reinforce connections between cortex and striatum, so that rewarded actions are more likely to be repeated. But how does the SNc reinforce just the circuits that made the right call? The authors proposed a mechanism by which another part of the subtantia nigra, the SNr, detects when actions are worth choosing and then simultaneously amplifies any dopamine signal coming from the SNc.”
“The novel part here is that we have proposed a mechanism by which the BG can detect when it has selected an action and should therefore amplify the dopamine reinforcing event specifically at that time,” Frank said. “When the SNr decides that striatal valuation signals are strong enough for one action, it releases the brakes not only on downstream structures that allow actions to be executed, but also on the SNc dopamine system, so any unexpected rewards are amplified.”
Specifically, dopamine provides reinforcement by enhancing the responsiveness of connections between cells so that a circuit can more easily repeat its rewarding behavior in the future. But along with that process of reinforcing the action of choosing, the value placed on the resulting reward becomes elevated compared to rewards not experienced this way.
Experimental evidence
That prediction seemed intriguing, but it still had to be tested. The authors identified both behavioral and genetic tests that would be telling.
They recruited 80 people at Brown and elsewhere in Providence to play a behavioral game and to donate some saliva for genetic testing.
The game first presented the subjects pictures of arbitrary Japanese characters that would have different probabilities of rewards if chosen ranging from a 20 percent to 80 percent chance of winning a point or losing a point. For some characters, the player could choose a character to discover its resulting reward or penalty, whereas for others, its result was simply given to them. After that learning phase, the subjects were then presented the characters in pairs and instructed to pick the one they thought had the highest chance of winning based on what they had learned.
The researchers built the game so that for every character a player could choose, there was an equally rewarding one that had merely been given to them. On average, players showed a clear choice bias in that they were more likely to prefer rewarding characters that they had chosen over equally rewarding characters they had been given.
Notably, they exhibited no choice bias between unrewarding characters suggesting that choice bias emerges only in relation to reward, one of the key predictions of their model. But they wanted to test further whether the impact of reward on choice bias was related to the proposed biological mechanism, that striatal dopaminergic learning is enhanced to chosen rewards.
The genetic tests focused on single-letter differences in a gene called DARPP-32, which governs how well cells in the striatum respond to the reinforcing influence of dopamine.
People with one version of the gene have been shown in previous research to be less able to learn from rewards, while people with other versions were less driven by reward in learning.
“The reason why this gene is interesting is because we know something about the biology of what it does and where it is expressed in the brain,” Frank said. “It’s predominant in the striatum and specifically affects synaptic plasticity induced by dopamine signaling. It’s related to the imbalance by which you learn from really good things or not so good things.
“The logic was if the mechanism that we think describes this choice bias and credit assignment problem is accurate then that gene should predict the impact of how good something was on this choice bias phenomenon,” he said.
Indeed, that’s what the data showed. People with the form of the gene that predisposed them to be responsive to big rewards also showed more choice bias from the most strongly rewarded characters. Interestingly, the other people also showed choice bias, but more strongly for those characters that were more mediocre. This pattern was mirrored by the authors’ model when it simulated the effects of DARPP-32 on reward learning imbalances from positive vs. negative outcomes.
For some people, the plums are sweeter if they picked them.

neurosciencestuff:

Choice bias: A quirky byproduct of learning from reward

The price of learning from rewarding choices may be just a touch of self-delusion, according to a new study in Neuron.

The research by Brown University brain scientists links a fundamental problem in neuroscience called “credit assignment” — how the brain reinforces learning only in the exact circuits that caused the rewarding choice — to an oft-observed quirk of behavior called “choice bias” – we value the rewards we choose more than equivalent rewards we don’t choose. The researchers used computational modeling and behavioral and genetic experiments to discover evidence that choice bias is essentially a byproduct of credit assignment.

“We weren’t looking to explain anything about choice bias to start off with,” said lead author Jeffrey Cockburn, a graduate student in the research group of senior author Michael Frank, associate professor of cognitive, linguistic, and psychological sciences. “This just happened to be the behavioral phenomenon we thought would emerge out of this credit assignment model.”

So the next time a friend raves about the movie he chose and is less enthusiastic about the just-as-good one that you chose, you might be able to chalk it up to his basic learning circuitry and a genetic difference that affects it.

Modeled mechanism

The model, developed by Frank, Cockburn, and co-author Anne Collins, a postdoctoral researcher, was based on prior research on the function of the striatum, a part of the brain’s basal ganglia (BG) that is principally involved in representing reward values of actions and picking one. “An interaction between three key BG regions moderates that decision-making process. When a rewarding choice has been made, the substantia nigra pars compacta (SNc) releases dopamine into the striatum to reinforce connections between cortex and striatum, so that rewarded actions are more likely to be repeated. But how does the SNc reinforce just the circuits that made the right call? The authors proposed a mechanism by which another part of the subtantia nigra, the SNr, detects when actions are worth choosing and then simultaneously amplifies any dopamine signal coming from the SNc.”

“The novel part here is that we have proposed a mechanism by which the BG can detect when it has selected an action and should therefore amplify the dopamine reinforcing event specifically at that time,” Frank said. “When the SNr decides that striatal valuation signals are strong enough for one action, it releases the brakes not only on downstream structures that allow actions to be executed, but also on the SNc dopamine system, so any unexpected rewards are amplified.”

Specifically, dopamine provides reinforcement by enhancing the responsiveness of connections between cells so that a circuit can more easily repeat its rewarding behavior in the future. But along with that process of reinforcing the action of choosing, the value placed on the resulting reward becomes elevated compared to rewards not experienced this way.

Experimental evidence

That prediction seemed intriguing, but it still had to be tested. The authors identified both behavioral and genetic tests that would be telling.

They recruited 80 people at Brown and elsewhere in Providence to play a behavioral game and to donate some saliva for genetic testing.

The game first presented the subjects pictures of arbitrary Japanese characters that would have different probabilities of rewards if chosen ranging from a 20 percent to 80 percent chance of winning a point or losing a point. For some characters, the player could choose a character to discover its resulting reward or penalty, whereas for others, its result was simply given to them. After that learning phase, the subjects were then presented the characters in pairs and instructed to pick the one they thought had the highest chance of winning based on what they had learned.

The researchers built the game so that for every character a player could choose, there was an equally rewarding one that had merely been given to them. On average, players showed a clear choice bias in that they were more likely to prefer rewarding characters that they had chosen over equally rewarding characters they had been given.

Notably, they exhibited no choice bias between unrewarding characters suggesting that choice bias emerges only in relation to reward, one of the key predictions of their model. But they wanted to test further whether the impact of reward on choice bias was related to the proposed biological mechanism, that striatal dopaminergic learning is enhanced to chosen rewards.

The genetic tests focused on single-letter differences in a gene called DARPP-32, which governs how well cells in the striatum respond to the reinforcing influence of dopamine.

People with one version of the gene have been shown in previous research to be less able to learn from rewards, while people with other versions were less driven by reward in learning.

“The reason why this gene is interesting is because we know something about the biology of what it does and where it is expressed in the brain,” Frank said. “It’s predominant in the striatum and specifically affects synaptic plasticity induced by dopamine signaling. It’s related to the imbalance by which you learn from really good things or not so good things.

“The logic was if the mechanism that we think describes this choice bias and credit assignment problem is accurate then that gene should predict the impact of how good something was on this choice bias phenomenon,” he said.

Indeed, that’s what the data showed. People with the form of the gene that predisposed them to be responsive to big rewards also showed more choice bias from the most strongly rewarded characters. Interestingly, the other people also showed choice bias, but more strongly for those characters that were more mediocre. This pattern was mirrored by the authors’ model when it simulated the effects of DARPP-32 on reward learning imbalances from positive vs. negative outcomes.

For some people, the plums are sweeter if they picked them.

catmota:

Bottle Brush Trees
Jian Chong Min

catmota:

Bottle Brush Trees

Jian Chong Min

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20aliens:

untitledby aveces

20aliens:

untitled
by aveces

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scienceyoucanlove:

Why Has This Really Common Virus Only Just Been Discovered?
by Ed Yong

The most common viruses in your body don’t make you ill. Instead, they infect the legions of microbes that live in your gut. These bacteriophages, or phages for short, number in their trillions. And the most common of them might be a newly discovered virus called crAssphage.
No one has seen crAssphage under the microscope, but we know what its genome looks like—Bas Dutilh from Radboud University Medical Centre pieced it together using fragments of DNA from the stools of 12 individuals. He found crAssphage in all of them. Then, he found it in hundreds more.
To study the microbes that live in a person’s guts, scientists will typically collect a stool sample, break all the DNA within into small fragments, and sequence these pieces. The result is a metagenome: a mish-mashed collection of DNA from all the local bacteria, viruses and other microbes.
Dutilh’s team, led by Rob Edwards at San Diego State University, analysed 466 metagenomes that have been added to public databases and found crAssphage in three-quarters of them. It’s there in stool samples from people in the USA, Europe and South Korea. It actually accounted for 1.7 percent of all the sequences that the team analysed—six times more than all the other known phages put together. You probably have it inside you right now.
The work highlights just how much we don’t know about the viruses in our guts and “what exciting times these are for viral discovery”, says Lesley Ogilvie from the Max Planck Institute for Molecular Genetics.
But how could such a common virus go undiscovered for so long, especially considering how popular the study of gut microbes has become? It’s as if zookeepers suddenly realised that most of their zoos contain a giant grey animal with tusks and a trunk, which no one had noticed before.
For one thing, the viruses in our guts are hard to study.  “To study a virus, normally you have to make heaps of it, which isn’t possible if you can’t grow the host,” says Martha Clokiefrom the University of Leicester.And since mostgut bacteria won’t grow easily in a lab, the viruses that infect them are similarly hard to rear.
The alternative is to use metagenomics to analyse a microbe’s genes without having to grow it. But first, you have to assemble your mish-mash of sequences, which come from different organisms, into a complete genome. It’s a bit like putting all the pieces of a thousand jigsaw puzzles into one bag, and trying to solve just one.
The usual strategy is to work off what you know by aligning these new sequences to those in databases. But this approach doesn’t work very well for our inner viruses because most of them are unknown. The sequences in the databases represent the tip of the iceberg. According to Dutilh, around 75 percent of the DNA from any new stool sample—and as much as 99 percent—won’t match any of these known sequences.
So what’s in that other 75 percent?
Well, crAssphage for starters.
Dutilh’s team found it by using a different approach based on a simple idea: that fragments which repeatedly turn up in the same samples are more likely to be parts of the same genome. They used a technique called cross-assembly to identify one such group of co-occurring sequences, in stool samples from 12 people. They then assembled these sequences into a single genome.
The genome had several distinctive features which told the researchers that it belonged to a phage, albeit one that’s very different to any we currently know of. They called it crAssphage after the cross-assembly method that revealed its existence.
They used the same technique to work out what the virus infects: if there’s lots of crAssphage DNA in a sample, there should also be lots of DNA from its host. Based on this logic, the most likely hosts are a group of bacteria called Bacteroides.
The team checked this result with a second technique. They looked at CRISPR sequences—a kind of bacterial immune system that recognises DNA from infecting phages. The team scanned all known bacterial genomes for CRISPR sequences that matched crAssphage and found that the closest matches came from two groups of gut bacteria, one of which wasBacteroides.
Bacteroides are major players in our guts. They help us break down our food, control the development of our immune system, and protect us from disease-causing bacteria. Their numbers change depending on the food we eat, and they correlate with our risk of different diseases. If crAssphage infects these microbes, it could also be an important player in our daily dramas.
It’s too early to speculate what its role might be, says Dutihl. Still, we know that phages are generally important. By killing off the most abundant bacteria in the gut, they ensure that no single species can monopolise the space. And last year, Jeremy Barr, who was involved of this new study,  showed that phages could even act as part of our own immune system.
Many scientists had assumed that viruses in the gut are caught up in fast-paced evolutionary battles with local bacteria. This leaves people with very different collections, and explains why most of the viral sequences that we find don’t match anything in the databases. But the existence of crAssphage challenges this concept: it was part of the pool of unknowns but it’s alsoincredibly common. “It definitely changes the idea we had about viruses being very individual-specific,” says Dutihl. The study of human gut bacteria followed a similar path: early studies highlighted the differences between us but important similarities started emerging as our techniques became more sophisticated.
read the rest on Nat Geo’s website 

scienceyoucanlove:

Why Has This Really Common Virus Only Just Been Discovered?

papermagazine:

Happy birthday to Queen Iman.

papermagazine:

Happy birthday to Queen Iman.

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smallspacesblog:

Axel Vervoodt 

smallspacesblog:

Axel Vervoodt 

(via sealmaiden)

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