Wednesday, April 3, 2013

An inside look at carnivorous plants

Wednesday, April 3, 2013

When we imagine drama playing out between predators and prey, most of us picture stealthy lions and restless gazelle, or a sharp-taloned hawk latched on to an unlucky squirrel. But Ben Baiser, a post-doctoral fellow at the Harvard Forest and lead author of a new study in Oikos, thinks on a more local scale. His inter-species drama plays out in the humble bogs and fens of eastern North America, home to the carnivorous pitcher plant, Sarracenia purpurea. "It's shocking, the complex world you can find inside one little pitcher plant," says Baiser.

A pitcher plant's work seems simple: their tube-shaped leaves catch and hold rainwater, which drowns the ants, beetles, and flies that stumble in.

But the rainwater inside a pitcher plant is not just a malevolent dunking pool. It also hosts a complex system of aquatic life, including wriggling mosquito, flesh fly, and midge larvae; mites; rotifers; copepods; nematodes; and multicellular algae. These tiny organisms are crucial to the pitcher plant's ability to process food. They create what scientists call a 'processing chain': when a bug drowns in the pitcher's rainwater, midge larvae swim up and shred it to smaller pieces, bacteria eat the shredded pieces, rotifers eat the bacteria, and the pitcher plant absorbs the rotifers' waste.

But that's not the whole story. Fly larvae are also eating the rotifers, midge larvae, and each other, and everybody eats bacteria. It's a complex food web that shifts on the order of seconds.

Aaron Ellison, a co-author on the new study and senior ecologist at the Harvard Forest, says the pitcher plant food web is an ideal model for understanding larger food webs?with top predators like wolves?that change over a longer period of time. He points out, "With pitcher plants, you can hold the whole food web in your hand. The vast number of pitcher plants in one bog provide endless opportunities for detailed experiments on how food webs work, not only in pitcher plants, but also in bigger ecosystems that are harder to manipulate, like ponds, lakes, or oceans."

With funding from the National Science Foundation, the research team traveled to bogs in British Columbia, Quebec City, and Georgia?the full extent of the plant's range?to analyze the aquatic food webs from 60 pitcher plants. They found 35 different types of organisms inside, with a large contingent of bacteria counting as just one type. Then, says Baiser, "We wanted to know: how did we get different food webs in individual pitchers from the same species pool? What caused these food webs to form the way they did?"

A few well-established scientific models predict how food webs form based on a ranked system of ecosystem factors. For the Oikos study, Baiser and his team checked their real-world observations against those models. He explains: "Say you've got a bunch of lakes. And you've got a big bucket holding all the species that can live in those lakes. When you dump out the bucket, which creatures end up in which lake? What matters more: the size of the lake, or the fact that predator species X is there, too? Or is it random? Those models help us tease those factors apart."

According to the Oikos study, the way pitcher plant food webs assemble is not random. In fact, it seems the predator-prey interactions are of key importance. "You take out one species, and that affects everything else," says Baiser.

###

Harvard University: http://www.harvard.edu

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The Buzz On Bees: Why Many Colonies Are Collapsing

Copyright ? 2013 NPR. For personal, noncommercial use only. See Terms of Use. For other uses, prior permission required.

NEAL CONAN, HOST:

This is TALK OF THE NATION. I'm Neal Conan.

Back in 2005, we started hearing about a phenomenon called colony collapse disorder. Unusual numbers of honeybees were dying off and nobody understood quite why. The problem never went away. This year, it seems much, much worse. And why there are lots of theories, from habitat loss to pesticides, we still don't know for sure what's to blame. We do know that these pollinate cherries, apples, almonds, onions and many other crops, an estimated one quarter of the American diet.

If you're a beekeeper, how are your hives doing? Give us a call, 800-989-8255. Email us: talk@npr.org. You can also join the conversation on our website. That's at npr.org, click on TALK OF THE NATION. Dan Charles is NPR's food and agriculture correspondent. He's reporting on this trend and joins us here in Studio 3A. Nice to have you back in the program, Dan.

DAN CHARLES, BYLINE: Nice to be here.

CONAN: So just how bad is it?

CHARLES: Well, you know, the reports are - the - what happens is the honeybees, you know, they go through the winter, and they come out in the spring, and that's when sort of some of the big commercial pollination events happen. And that's when you really sort of figure out, OK, did they get through the winter OK? And apparently, this year may have been the worst ever. The big - the really big pollination event is the almond pollination that happens in February. You know, something like half of all the honeybees in the entire country go to California to...

CONAN: On trucks. They don't...

CHARLES: On trucks. You know, they box up the hives. They send them on big, big trucks out to California, and they had a shortage. You know, a lot of people opened up the hives, a lot of beekeepers, and found that they had, you know, a big lost rates this year.

CONAN: And, obviously, that is a problem. You need X many hives per acre to achieve the pollination.

CHARLES: Two hives per acre, they say, in the almond groves of California. Yeah, that's right. And - I mean, they got through it. They, you know, some people were paying high prices to try to get some extra hives in and so forth. But this is a long-term problem, and they're still trying to figure out what of the, you know, the various suspects in this mystery, you know, this mystery story. You know, is it the mites? You know, there - clearly, there is a mite problem that's infected - these parasites that infect the hives. Is it, you know, diseases? There have been, you know, some viruses that were implicated. Is it simply loss of good habitat? You know, bees need flowers through the summer, lots and lots of different kinds of flowers to, you know, be healthy. Is it, you know, all this, like, transportation across the country that's stressing them out too much? Or is it, you know, the increase in use of some pesticides on some of the major crops in the country?

CONAN: And Neonics, as I understand, are getting a lot of the blame.

This is kind of the new - for some people, prime suspect. So there's a class of pesticides - you've mentioned the name, neonicotinoids or...

You mentioned the name. I mentioned the nickname.

(LAUGHTER)

CHARLES: Neonics for short. They became widely used in the 1990s. They're typically applied to the seeds of the crop and the biggest crop is corn, but there are other crops, too - canola, sunflower. I mentioned those because those are crops that produce flowers that bees like. Although corn, you know, pollen also bees feed on. So, you know, the pesticide is applied to the seed which goes into the ground. So you would, think, OK, no problem. Bees aren't exposed to it. They aren't insecticides and bees are insects, right? So bees are very, very sensitive to these pesticides.

The thing is there's two - there are sort of different ways in which bees actually could be exposed to these. One, is at planting time, you know, there can be dust that goes off the plant or, you know, from these seeds, these pesticide-coated seeds. That's one way in which bees, you know, can actually be exposed to, you know, high amounts, enough to kill them, in isolated cases. But the pesticide actually goes with the growing plant, from the seed. As the plant grows, the pesticide - small amounts - go with the plant, and that's what makes them effective. Insects, like, you know, feed on the plant and die. Bees feed on the pollen, and could also be exposed to very low amounts.

CONAN: And it could build up over time and cause - as the name suggests, these are derived from tobacco. These are nicotine.

CHARLES: You know, the chemistry of them is similar. Yeah. Yeah. And they have - so, you know, here's the thing. It's not enough to kill a bee, right? And that's - the toxicology is fairly clear. The bees survive these low amounts of exposure. But last summer, there were some scientific studies that came out that indicated that it might actually change their behavior in subtle ways. So there was a study done with bumblebees, where the bumblebees stop making queens. And there was a study with honeybees, where they seem to lose direction. They seem to get lost more. Now, these were sort of controlled, almost laboratory-type studies. And, you know, these are not proof, but they seem to demonstrate that there might be subtle effects on bees.

CONAN: And there seem to be researchers in Europe who are more convinced that these pesticides are to blame.

CHARLES: The researchers - there was a move by the European commission to ban neonics in Europe. That actually got slapped down by the larger kind of European governing body. So, you know, we'll see where this goes. I mean, there's clearly a lot more research that's going to be done on neonics.

CONAN: We're talking about the collapse of so many beehives over this past winter, especially 40, maybe even 50 percent. We want to hear from beekeepers. 800-989-8255. How are your hives doing? Email: talk@npr.org. Michelle is on the line with us from the Black Hills of South Dakota.

MICHELLE: Hello.

CONAN: Hi, Michelle. You're on the air. Go ahead, please.

MICHELLE: Oh, thank you. I'm really excited to get through. I'm a hobby beekeeper. We have a hobbyist bee club in Rapid City, South Dakota called the Wannabees. You can find us online. But I'm calling because I - about four, five years ago, I had met one of the biggest beekeepers in our state. And he said that we know very well what's causing colony collapse disorder, and it's systemics. And kind of like your guest was explaining, this beekeeper, a commercial beekeeper, he told me that the analogy would be like that it gets in the blood of the plants. So it's in the seed and all throughout the growing process - in the stem, the leaves, the flowers, the pollen.

And they tried to sue, and they had a group, a collective of beekeepers that tried to sue this particular company, I won't mention. And their attorneys eventually just walked away from it. They couldn't do anything about it.

CONAN: Dan Charles, as I understand it, some have also tried to sue the - or at least appeal to the Environmental Protection Agency, saying, we need help here.

CHARLES: A group of beekeepers and environmental groups have, in fact, sued the EPA, saying the law requires you to take some action against neonics. So we'll see what happens with that lawsuit. Since, you know, the caller is from South Dakota, I should mention, people may not know this, but the Dakotas, you know, the - and Montana and parts of Minnesota, this is where - when you're talking about honeybees, this is where a huge proportion of the honeybees in the country spend their summer. And there's an issue there with changing land use, changing habitat. As corn has become more profitable, as soy beans have become more profitable, much more land has been devoted to those crops, as opposed to, say, range land or crops like sunflowers, you know, which are much better habitat for bees.

CONAN: How are you hives doing, Michelle?

MICHELLE: Well, I lost what I had. As a hobby beekeeper, I don't have very much. And quite a few of the people in our club lost bees last year due to the drought. But we don't have corn in western South Dakota. It's mostly range land, pasture, and there's really nothing for bees to eat on pasture, either. You know, it's grass and wheat. So we depend on the clover. And when the drought came, the clover just died off. It was looking like a really good year for us last year, and the drought came and a lot of bees starved.

CONAN: Sorry to hear that, Michelle.

MICHELLE: Thank you so much for addressing this topic.

CONAN: Thank you for the call. Let's see if we can go next to Mansah(ph), Mansah with us from Menomonie in Wisconsin.

MARSAH: Yes. It's actually Marsah(ph).

CONAN: Marsah, excuse me.

MARSAH: That's OK.

CONAN: I got Menomonie right.

MARSAH: Yeah, you sure did. Very good. Well done. Interesting, I love this topic. I've been following it. We have bees. We had them for years at our horse farm in Minnesota and never had a problem. That was alfalfa country, so - where there was a lot of food for the bees. Now we're in western Wisconsin, dairy land, a lot of corn and alfalfa crops. And two years ago, we went out to check the bees and - in the spring, and they were just gone. It was eerie. It was strange. They had been doing OK, and we'd been real concerned about them. And there wasn't a bee body, dead carcass anywhere. They were just gone, completely wiped out. And no sign of where they went, no sign of trauma, just spooky, spooky, strange. So we just don't know.

We're keeping - we keep ordering queens every year and trying again. And this year, it doesn't look good. My husband just went out this morning, and they're all dead. So we don't know what to think.

CONAN: I'm sorry to hear that, Marsah. Dan, let me ask you. If these commercial - big commercial companies where they are eating, feeding on crops that have are - been with these pesticides and, again, traveling and going through that kind of stress, what about wild bees? Are they suffering the same kind of fate?

CHARLES: Well, it's good that you bring that up, actually, because we focus a lot on the honeybees, because they're the ones we know and they make the honey for us, and these are the ones that are easily managed and that get, you know, sort of transported around and provide commercial, what they call pollination services. But honeybees, you know, they are - they're foreign to this continent. They were brought here from Europe, originated, probably, you know, in Africa. But they're useful for agriculture. You know, sort of extensive, intensive agriculture requires, in some cases - in the case of almonds, certainly, also - intensive pollination, and you bring in lots and lots of hives of honeybees to do that.

But there are native pollinators, native bees here: bumblebees, leafcutter bees, carpenter bees. And, you know, there's been some interesting research lately on their sort of health. And there's sort of two things to keep in mind. One is that they are also very affected by the things that we're talking about - for instance, the changing use of land and the declining sort of prevalence of flowers in the landscape.

But the other side is people didn't realize how important they were also for pollination of crops. And there was some research done, and if there are lots of native bees around, no matter how many honeybees you put into your orchard, the native bees actually make a better crop for you, for unknown reasons. Maybe they just sort of are attracted to different kinds of flowers in a different way. But the native bees that you don't manage, that just are there because of the landscape, are contributing significantly to agricultural production.

CONAN: So, again, are the natural bees suffering the same colony collapse?

CHARLES: Well, not colony collapse, as such, but their numbers certainly are down - maybe not for the same reasons, except for the important reason of habitat change. They may also be affected if they - you know, if the honeybees are being affected by the pesticides, the native bees probably are, as well. They may not be afflicted so much by the mites in the hives that are affecting honeybees. I'm not sure about that, actually. I'm not a big bee expert. But they certainly are affected by sort of the declining habitat.

CONAN: And we've just heard that there will be more corn planted this year than ever before in our history. Dan Charles, thank you very much, and we'll hope for the recovery of the bees.

CHARLES: Thank you.

CONAN: Dan Charles, NPR food and agriculture correspondent, joined us here in Studio 3A. You're listening to TALK OF THE NATION, from NPR News.

Copyright ? 2013 NPR. All rights reserved. No quotes from the materials contained herein may be used in any media without attribution to NPR. This transcript is provided for personal, noncommercial use only, pursuant to our Terms of Use. Any other use requires NPR's prior permission. Visit our permissions page for further information.

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Source: http://www.npr.org/2013/04/02/176037645/the-buzz-on-bees-why-many-colonies-are-collapsing?ft=1&f=1007

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Tuesday, April 2, 2013

Florida bill would create ?innovation schools? (tbo)

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How cells distinguish friend from foe

Mar. 31, 2013 ? Researchers at UC Davis have shown how the innate immune system distinguishes between dangerous pathogens and friendly microbes. Like burglars entering a house, hostile bacteria give themselves away by breaking into cells. However, sensing proteins instantly detect the invasion, triggering an alarm that mobilizes the innate immune response. This new understanding of immunity could ultimately help researchers find new targets to treat inflammatory disorders.

The paper was published in Nature on March 31.

The immune system has a number of difficult tasks, including differentiating between cells and microbes. However, the body, particularly the digestive tract, contains trillions of beneficial microbes, which must be distinguished from dangerous pathogens.

"We are colonized by microbes. In fact, there are more bacteria in the body than cells," said senior author Andreas B?umler, professor and vice chair of research in the UC Davis Department of Medical Microbiogy and Immunology. "The immune system must not overreact to these beneficial microbes. On the other hand it must react viciously when a pathogen invades."

The key to distinguishing between pathogenic and beneficial bacteria are their differing goals. Ordinary digestive bacteria are content to colonize the gut, while their more virulent cousins must break into cells to survive. Salmonella achieves this by activating enzymes that rearrange the actin in a cell's cytoskeleton. Fortunately, cellular proteins sense the active enzymes, leading to a rapid immune response.

In the study, the researchers investigated a strain of Salmonella, in both cell lines and animal models, to determine how the innate immune system singles out the bacteria for attack. Salmonella uses a secretion system, a type of molecular syringe, to inject pathogenic proteins, such as SopE, into the cell. SopE activates human GTPase enzymes RAC1 and CDC42, which break down the surrounding actin, allowing the bacteriuminside.

But breaking and entering has consequences. Sensing the active GTPase enzymes, and recognizing their pathogenic nature, a protein called NOD1 sends the alarm, signaling other proteins, such as RIP2, that the cell is in danger. Ultimately, this signaling pathway reaches the protein NF-?B, a transcription factor that instructs the genome to mount an immune response, activating genes associated with inflammation, neutrophils and other immune functions.

Though it had been hypothesized that GTPase activation might trigger an immune response to attacking bacteria, prior to this study, no one had identified the pathway to NF-?B. These results were somewhat surprising, as NOD1had been thoroughly studied; leading many researchers to conclude it had no further mysteries to divulge. No one expected it to play such a significant role in alerting the innate immune system that cells were under attack.

These results could help researchers find new targets to combat inflammatory diseases. For example, NF-?B is known to be involved in a variety of conditions, such as inflammatory bowel disease, arthritis, sepsis and others. By understanding the pathways that activate inflammation, scientists and clinicians can develop ways to inhibit it.

"These pathways might be triggered erroneously because the host thinks there's an infection," said B?umler. "Knowing the pathways and how they are activated is critical to controlling them."

Other authors include A. Marijke Keestra, Maria G.Winter, Josef J. Auburger, Simon P. Fr??le, Mariana N. Xavier, Sebastian E. Winter, Anita Kim, Victor Poon, Mari?tta M. Ravesloot, Julian F. T. Waldenmaier, Ren?e M. Tsolis and Richard A. Eigenheer.

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The above story is reprinted from materials provided by University of California - Davis Health System.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


Journal Reference:

  1. A. Marijke Keestra, Maria G. Winter, Josef J. Auburger, Simon P. Fr??le, Mariana N. Xavier, Sebastian E. Winter, Anita Kim, Victor Poon, Mari?tta M. Ravesloot, Julian F. T. Waldenmaier, Ren?e M. Tsolis, Richard A. Eigenheer, Andreas J. B?umler. Manipulation of small Rho GTPases is a pathogen-induced process detected by NOD1. Nature, 2013; DOI: 10.1038/nature12025

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

Source: http://feeds.sciencedaily.com/~r/sciencedaily/top_news/~3/88moH7jNzi8/130401101025.htm

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Congestion in Earth's mantle: Mineralogists explain why plate tectonics stagnates in some places

Mar. 31, 2013 ? Earth is dynamic. What we perceive as solid ground beneath our feet, is in reality constantly changing. In the space of a year Africa and America are drifting apart at the back of the Middle Atlantic for some centimeters while the floor of the Pacific Ocean is subducted underneath the South American Continent. "In 100 million years' time Africa will be pulled apart and North Australia will be at the equator," says Prof. Dr. Falko Langenhorst from the Friedrich Schiller University Jena (Germany). Plate tectonics is leading to a permanent renewal of the ocean floors, the mineralogist explains. The gaps between the drifting slabs are being filled up by rising melt, solidifying to new oceanic crust. In other regions the slabs dive into the deep interior of Earth and mix with the surrounding Earth's mantle.

Earth is the only planet in our solar system, conducting such a 'facelift' on a regular basis. But the continuous up and down on Earth's crust doesn't run smoothly everywhere. "Seismic measurements show that in some mantle regions, where one slab is subducted underneath another one, the movement stagnates, as soon as the rocks have reached a certain depth," says Prof. Langenhorst. The causes of the 'congestion' of the subducted plate are still unknown. In the current issue of Nature Geoscience, Prof. Langenhorst and earth scientists of Bayreuth University now explain the phenomenon for the first time.

According to this, the rocks of the submerging ocean plate pond at a depth of 440 to 650 kilometers -- in the transition zone between the upper and the lower Earth mantle. "The reason for that can be found in the slow diffusion and transformation of mineral components," mineralogist Langenhorst explains. On the basis of high pressure experiments the scientists were able to clarify things: under the given pressure and temperature in this depth, the exchange of elements between the main minerals of the subducted ocean plate -- pyroxene and garnet -- is slowed down to an extreme extent. "The diffusion of a pyroxene-component in garnet is so slow, that the submerging rocks don't become denser and heavier, and therefore stagnate," the Jena scientist says.

Interestingly there is congestion in Earth's mantle exactly where the ocean floor submerges particularly fast into the interior of Earth. "In the Tonga rift off Japan for example, the speed of subduction is very high," Prof. Langenhorst states. Thereby the submerging rocks of the oceanic plate stay relatively cold up to great depth, which makes the exchange of elements between the mineral components exceptionally difficult. "It takes about 100 Million years for pyroxene crystals which are only 1 mm in size to diffuse into the garnet. For this amount of time the submerging plate stagnates," Langenhorst describes the rock congestion. It can probably only diffuse at the boundary of the lower Earth mantle. Because then pyroxene changes into the mineral akimotoite due to the higher pressure in the depth of 650 kilometers. "This could lead to an immediate rise in the rock density and would enable the submerging into greater depths."

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The above story is reprinted from materials provided by Friedrich-Schiller-Universitaet Jena.

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Journal Reference:

  1. W. L. van Mierlo, F. Langenhorst, D. J. Frost, D. C. Rubie. Stagnation of subducting slabs in the transition zone due to slow diffusion in majoritic garnet. Nature Geoscience, 2013; DOI: 10.1038/NGEO1772

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Disclaimer: Views expressed in this article do not necessarily reflect those of ScienceDaily or its staff.

Source: http://feeds.sciencedaily.com/~r/sciencedaily/~3/lA2XiL0tTGo/130331165559.htm

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Monday, April 1, 2013

High court poised to upend civil rights policies (The Arizona Republic)

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Sorting out Parkinson's protein structure: Computer modeling may offer hints for new drug-design strategies

Apr. 1, 2013 ? Clumps of proteins that accumulate in brain cells are a hallmark of neurological diseases such as dementia, Parkinson's disease and Alzheimer's disease. Over the past several years, there has been much controversy over the structure of one of those proteins, known as alpha synuclein.

MIT computational scientists have now modeled the structure of that protein, most commonly associated with Parkinson's, and found that it can take on either of two proposed states -- floppy or rigid. The findings suggest that forcing the protein to switch to the rigid structure, which does not aggregate, could offer a new way to treat Parkinson's, says Collin Stultz, an associate professor of electrical engineering and computer science at MIT.

"If alpha synuclein can really adopt this ordered structure that does not aggregate, you could imagine a drug-design strategy that stabilizes these ordered structures to prevent them from aggregating," says Stultz, who is the senior author of a paper describing the findings in a recent issue of the Journal of the American Chemical Society.

For decades, scientists have believed that alpha synuclein, which forms clumps known as Lewy bodies in brain cells and other neurons, is inherently disordered and floppy. However, in 2011 Harvard University neurologist Dennis Selkoe and colleagues reported that after carefully extracting alpha synuclein from cells, they found it to have a very well-defined, folded structure.

That surprising finding set off a scientific controversy. Some tried and failed to replicate the finding, but scientists at Brandeis University, led by Thomas Pochapsky and Gregory Petsko, also found folded (or ordered) structures in the alpha synuclein protein.

Stultz and his group decided to jump into the fray, working with Pochapsky's lab, and developed a computer-modeling approach to predict what kind of structures the protein might take. Working with the structural data obtained by the Brandeis researchers, Stultz created a model that calculates the probabilities of many different possible structures, to determine what set of structures would best explain the experimental data.

The calculations suggest that the protein can rapidly switch among many different conformations. At any given time, about 70 percent of individual proteins will be in one of the many possible disordered states, which exist as single molecules of the alpha synuclein protein. When three or four of the proteins join together, they can assume a mix of possible rigid structures, including helices and beta strands (protein chains that can link together to form sheets).

"On the one hand, the people who say it's disordered are right, because a majority of the protein is disordered," Stultz says. "And the people who would say that it's ordered are not wrong; it's just a very small fraction of the protein that is ordered."

"This paper seems to bridge the gap" between the two camps, says Trevor Creamer, an associate professor of molecular and cellular biochemistry at the University of Kentucky who was not involved in this research. Also important is the model's prediction of new structures for the protein that experimental biologists can now look for, Creamer adds.

The MIT researchers also found that when alpha synuclein adopts an ordered structure, similar to that described by Selkoe and co-workers, the portions of the protein that tend to aggregate with other molecules are buried deep within the structure, explaining why those ordered forms do not clump together.

Stultz is now working to figure out what controls the protein's configuration. There is some evidence that other molecules in the cell can modify alpha synuclein, forcing it to assume one conformation or another.

"If this structure really does exist, we have a new way now of potentially designing drugs that will prevent aggregation of alpha synuclein," he says.

Lead author of the paper is Thomas Gurry, an MIT graduate student in computational and systems biology. Other authors are Orly Ullman, an MIT graduate student in chemistry; Pochapsky, a professor of chemistry and biochemistry at Brandeis; Iva Perovic, a graduate student in Pochapsky's lab; and Charles Fisher, a Harvard graduate student in biophysics.

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The above story is reprinted from materials provided by Massachusetts Institute of Technology. The original article was written by Anne Trafton.

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Journal Reference:

  1. Thomas Gurry, Orly Ullman, Charles K. Fisher, Iva Perovic, Thomas Pochapsky, Collin M. Stultz. The Dynamic Structure of ?-Synuclein Multimers. Journal of the American Chemical Society, 2013; 135 (10): 3865 DOI: 10.1021/ja310518p

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

Source: http://feeds.sciencedaily.com/~r/sciencedaily/top_news/top_health/~3/kvkaYuWaeuo/130401111638.htm

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