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Like most microorganisms, Bacillus subtilis bacteria are single-celled creatures with one goal: to reproduce by making copies of themselves. But survival isn't always that simple. For example, when food gets scarce, B. subtilis must decide between two possible paths: shut down, form a dormant spore -- a process called "sporulation" -- and wait for better times or split into two cells and gamble that there is enough food for at least one more generation.
"The decision about whether to form a spore and when is a very important one for B. subtilis," said Oleg Igoshin, associate professor of bioengineering at Rice and one of the lead researchers on the new study. "If the organism waits too long, it can starve before it finishes transforming into a spore. If it acts too early and forms a spore too soon, it can be overwhelmed and out-reproduced by competitors."
Igoshin's lab specializes in describing the workings of the complex genetic regulatory networks that cells use to make such decisions. He said dozens of studies over the past 25 years have identified a network of more than 30 genes that B. subtilis uses to bring about sporulation. When food is plentiful, this network is largely silent. But during times of starvation the genes work in concert to form a spore.
B. subtilis is harmless to humans, but some dangerous bacteria like Bacillus anthracis, the organism that causes anthrax, also form spores by a similar mechanism. Scientists are keen to better understand the process, both to protect public health and to explore the evolution of complex genetic processes.
The exact workings of the sporulation network are complex. In 2012, Igoshin and graduate student Jatin Narula analyzed a genetic circuit downstream of the protein known as Spo0A, the "sporulation master regulator," to explain how the network filters out noisy fluctuations in Spo0A activity. By filtering out noise, cells are able to accurately determine if Spo0A activity is above the threshold that triggers sporulation.
In the new study, Narula, Igoshin and collaborators set out to explain how B. subtilis times its sporulation decision with its cell-division cycle, a programmed series of events that cells normally follow to reproduce.
"Successful sporulation requires two complete copies of the bacterial chromosome, so coordination between the sporulation decision and the completion of DNA replication is very important," Narula said. "A good analogy might be a semester-long course in biology. Lessons are presented in a particular order, and students are tested after they learn. If the final exam were given in the first week, students would almost certainly fail."
Igoshin said that when the researchers set out to find how sporulation decisions were timed to the cell cycle, several studies including prior work by team members, provided a significant clue: Under starvation conditions, the activity of the master regulator gene had been shown to spike once per cell cycle.
In investigating how this spike occurred, Narula pored through dozens of published studies and noticed a discrepancy between some experimental results and the widely accepted view of the interactions between two key players in the sporulation network, a protein called Spo0F and a kinase called KinA. To resolve this discrepancy, Narula built a mathematical model in which excess Spo0F inhibits KinA activity. The new model showed that changes in the ratio of KinA to Spo0F could produce the pulse similar to those seen in experiments.
"The inhibition of KinA by 0F results in a 'negative feedback loop,' which means the circuit output works to counteract the input that triggers it," said Narula, co-lead author of the study. "Such loops are common in engineered and biological systems and usually work to keep things relatively constant despite external perturbations. A simple example of negative feedback would be the thermostat on your house. When temperature drops it will keep your heater on until the temperature is back to normal. If there is a delay in the feedback loop, the system may overreact and produce a surge. With the thermostat, for example, if the heating unit continues to run for some time after the desired temperature is reached, the temperature can transiently spike before settling back to the desired level."
Igoshin and Narula said similar spikes appear to be a consequence of the delayed negative feedback loop in the network that controls the amount of the active Spo0A. Furthermore, these spikes were timed based upon the positions of the KinA and Spo0F genes on the bacterial genome.
To divide and reproduce, bacteria must make a duplicate copy of their DNA. Because replication of circular bacterial DNA always initiates at one particular point, Narula surmised that the location of the KinA and Spo0F genes could be crucial. If one were located near the point where DNA replication began, the cell would contain two copies of that gene -- doubling the rate of production of that protein -- throughout the DNA replication period. If the other gene were located on the part of the circle that was copied last, the ratio of KinA to Spo0F would be one-to-one only when DNA replication was nearly completed.
Igoshin and Narula used a mathematical model of the network to show that this type of gene arrangement could account for spikes in Spo0A activity after each round of DNA replication. To verify their idea, they teamed with experimental biologists Anna Kuchina, co-lead author of the study, and Gürol Süel, co-lead investigator, both of the University of California at San Diego.
Experiments showed that the spikes of Spo0A activity always followed completion of DNA replication as the model predicted. In addition, Kuchina and colleagues used biotechnology to engineer mutant forms of B. subtilis in which the two critical genes were located near one another. The Spo0A spike from the delayed negative feedback loop was not observed in the mutants, and they failed to produce spores. In another engineered strain, the feedback loop between Spo0A and Spo0F was eliminated. This led to a gradual increase in Spo0A activity as opposed to a spike, and such cells were several times more likely to fail or die during sporulation.
"We found that the relative location of sporulation genes on the DNA circle were similar in more than 30 species of spore-forming bacteria, including Bacillus anthracis," Igoshin said. "This evidence suggests that the DNA timing mechanism is highly conserved, and it is possible that other time-critical functions related to the cell cycle may be regulated in a similar way.

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The above post is reprinted from materials provided by Rice University. The original item was written by Jade Boyd. Note: Materials may be edited for content and length.

Vesicles are responsible for transporting molecules between the different compartments within a cell and also for bringing material into cells from outside. There are several types of vesicle: each has a specific type of coat which is made up of different proteins and assembles onto a membrane surrounding the vesicle.
The EMBL team has been taking a close look at a coat called COPI. This surrounds vesicles that move material around within the Golgi apparatus and to the endoplasmic reticulum (ER) -- these are regions of the cell where proteins are made and modified in preparation for transport to the cell surface.
Using a technique called cryo-electron tomography, in which samples can be frozen at very low temperatures to avoid fixing or staining them chemically, the researchers combined data from hundreds of vesicles to build up a 3D image of the COPI coat. This enabled them to produce the most detailed pictures yet obtained of a vesicle coat assembled on the vesicle membrane.
This imaging technique is still in its infancy and although scientists have been able to gather structural information about parts of the membrane coats in other types of vesicle, this is the first time a model of a complete assembled vesicle coat has been produced.
What the images revealed was surprising: unlike other types of vesicle, where the coat is thought to be made from proteins assembled in different layers -- each with a specific function -- around the vesicle membrane, the EMBL team observed that the proteins in the COPI coat all intertwine together in one big layer, which is curved to fit around the membrane. More precisely, the COPI coat is made of a repetition of building blocks, called "triads," that contain all the important functional elements organised in a precise 3D structure.
"Until now we could see different elements of the vesicle coat, but not get a complete and detailed picture of the coat assembled onto the vesicle membrane. This is an important step forward for our understanding of intracellular transportation," explains John Briggs who led the study.
"Our images showed us how the proteins that make up the coat are arranged and it was surprising to discover how different COPI is from, for example, clathrin or COPII coated vesicles," adds Svetlana Dodonova, co-author of the paper. "Our next step will be to try to find out how this coat forms and binds to the vesicle membrane and how it arranges itself into such complex shapes."

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The above post is reprinted from materials provided by European Molecular Biology Laboratory (EMBL). Note: Materials may be edited for content and length.

For the first time a structure called 'the mesh' has been identified which helps to hold together cells. This discovery, which has been published in the online journal eLife, changes our understanding of the cell's internal scaffolding.
This also has implications for researchers' understanding of cancer cells as the mesh is partly made of a protein which is found to change in certain cancers, such as those of the breast and bladder.
The finding was made by a team led by Dr Stephen Royle, associate professor and senior Cancer Research UK Fellow at the division of biomedical cell biology at Warwick Medical School. Dr Royle said: "As a cell biologist you dream of finding a new structure in cells but it's so unlikely. Scientists have been looking at cells since the 17th Century and so to find something that no-one has seen before is amazing."
Researchers at the University's Warwick Medical School made the discovery by accident while looking at gaps between microtubules which are part of the cells' 'internal skeleton'. In dividing cells, these gaps are incredibly small at just 25 nanometres wide -- 3,000 times thinner than a human hair.
One of Dr Royle's PhD students was examining structures called mitotic spindles in dividing cells using a technique called tomography which is like a hospital CAT scan but on a much smaller scale. This meant that they could see the structure which they later named the mesh.
Mitotic spindles are the cell's way of making sure that when they divide each new cell has a complete genome. Mitotic spindles are made of microtubules and the mesh holds the microtubules together, providing support. While "inter-microtubule bridges" in the mitotic spindle had been seen before, the researchers were the first to view the mesh.
The study received funding and support from Cancer Research UK and North West Cancer Research.
Dr Royle said: "We had been looking in 2D and this gave the impression that 'bridges' linked microtubules together. This had been known since the 1970s. All of a sudden, tilting the fibre in 3D showed us that the bridges were not single struts at all but a web-like structure linking all the microtubules together."
The discovery impacts on the research into cancerous cells. A cell needs to share chromosomes accurately when it divides otherwise the two new cells can end up with the wrong number of chromosomes. This is called aneuploidy and this has been linked to a range of tumours in different body organs.
The mitotic spindle is responsible for sharing the chromosomes and the researchers at the University believe that the mesh is needed to give structural support. Too little support from the mesh and the spindle will be too weak to work properly, however too much support will result in it being unable to correct mistakes. It was found that one of the proteins that make up the mesh, TACC3, is over-produced in certain cancers. When this situation was mimicked in the lab, the mesh and microtubules were altered and cells had trouble sharing chromosomes during division.
Dr Emma Smith, senior science communications officer at Cancer Research UK, said: "Problems in cell division are common in cancer -- cells frequently end up with the wrong number of chromosomes. This early research provides the first glimpse of a structure that helps share out a cell's chromosomes correctly when it divides, and it might be a crucial insight into why this process becomes faulty in cancer and whether drugs could be developed to stop it from happening."
North West Cancer Research (NWCR) has funded the research as part of a collaborative project between the University of Warwick and the University of Liverpool, where part of the research is being carried out.
Anne Jackson, CEO at NWCR, said: "Dr Royle and Professor Ian Prior at the University of Liverpool have made significant inroads into our understanding of the way in which cancer cells behave, which could potentially better inform future cancer therapies.
"As a charity we fund only the highest standard of research, as evidenced by Dr Royle's work.
"All our funded projects undergo a thorough peer review process, before they are considered by our scientific committee. Our specially selected scientific committee includes some of the UK's leading professors, award-winning scientists and pioneering professionals."

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The above post is reprinted from materials provided by University of Warwick. Note: Materials may be edited for content and length.

In collaboration with the farming community of the Indian Creek Watershed in central Illinois, these researchers are finding ways to simultaneously meet three objectives: maximize a farmer's production, grow feedstock for bioenergy and protect the environment. These goals, as it turns out, are not necessarily mutually exclusive.
All it takes is a multifunctional landscape, where resources are allocated efficiently and crops are situated in their ideal soil and landscape position. Planting bioenergy crops like willows or switchgrass in rows where commodity crops are having difficulty growing could both provide biomass feedstock and also limit the runoff of nitrogen fertilizer into waterways -- all without hurting a farmer's profits. This is what a group of Argonne scientists has discovered through careful data collection and modeling at a cornfield in Fairbury.
"The issue we're working to address is how to design bioenergy systems that are sustainable" said Cristina Negri, principal agronomist and environmental engineer at Argonne. "It's not idealistic. We wanted to show that it's doable; if we design for specific outcomes, we'll see real results."
So Negri and her team created a pilot farm site that balances the priorities of economic feasibility, bioenergy and environmental health.
Meeting this challenge called for a change in perspective. Rather than looking at whole fields as the unit of planting decisions, researchers analyzed subareas of the cornfield. They found that subareas with the lowest yield also had the lowest nitrogen retention. These sections of land are doubly taxing -- unprofitable for the farmer and damaging to the environment.
Negri explained what happens in the underproductive land: "Imagine pouring a nice, nutrient-rich solution through a fertile soil with plants growing in it," she said. These nutrients would be retained by the soil long enough to be taken up by plants, minimizing any leakage. "Now imagine pouring this same solution through a colander: If nutrients filter through the soil too quickly, they're no longer available for plants. The corn grows less, and more nitrogen is leached into groundwater."
But planting bioenergy crops in the colander-like soil could solve both problems -- environmental and economic -- as the Argonne team showed with the Denitrification Decomposition simulation.
Willows and switchgrass are perennial bioenergy crops, meaning their life cycle spans multiple years. These plants have a more extensive root system than annual plants, which start their growth from scratch every year. Deeper roots are better able to absorb nitrogen as it seeps deeper into the soil.
The loss of nitrogen from agricultural land is a major environmental concern. If not retained by soil or taken up by plants, nitrogen escapes into air or water. It is released into the atmosphere as nitrous oxide, a greenhouse gas with 310 times the warming potential of carbon dioxide. Nitrate leaking into water spurs oxygen depletion that harms aquatic ecosystems and can lead to toxic algal blooms, as seen in Lake Erie. The Fairbury cornfield is located within the Indian Creek Watershed, draining to the Vermilion River and eventually to the Gulf of Mexico, which for years has been suffering from oxygen depletion caused by nutrient runoff.
While scientists may be invested in energy and environment, the team recognized that farmers -- the true agents of change -- have to think first and foremost about their economic bottom line.
"Across the entire field your farm might be profitable, but by collecting more specific data we can identify subareas where the farmer is not recovering his or her investment," said Argonne postdoctoral researcher Herbert Ssegane.
The money lost comes from farmers cropping and applying expensive nitrogen fertilizers to patches of the field that are just not producing enough. Inserting rows of bioenergy crops where there is low corn yield means the farmer is not sacrificing substantial profit from row crops. As a cost-saving bonus, the deep-rooted bioenergy crops naturally accumulate the lost nitrogen as a free fertilizer.
Argonne scientists planted willows at the Fairbury site in 2013 and will continue collecting data through next year to see how results compare to their predictions. "We've already reached a 28 percent reduction in nitrate, even with two full growing seasons still ahead of us," Ssegane said. Willow growth has also been good, without the researchers applying any fertilizer.
According to Ssegane, this project is about proving a concept. It shows farmers that strategic planting of bioenergy crops can increase productivity and save money, while demonstrating to the scientific community that bioenergy will be sustainable if we match plants to their optimal position within a landscape.
"Before this work, the popular idea was 'dedicated fields,' where you might convert a large area from corn to switchgrass," Ssegane said. "But dedicated fields of bioenergy crops are currently inviable in an agricultural setting where the economy is tied to grain. What does pass the cost-benefit test is converting underproductive subareas to an alternative crop."
A multifunctional landscape finds the happy, efficient medium between a dedicated bioenergy field and a farm growing continuous acres of the same cash crop.
The scientists are exploring how these design principles can be scaled up to the entire watershed. Eventually, they hope this research informs agricultural planning for scientists and farmers alike.

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The above post is reprinted from materials provided by DOE/Argonne National Laboratory. The original item was written by Payal Marathe. Note: Materials may be edited for content and length.

The study, which has just been published in the well known American Journal of Clinical Nutrition, is based on the Copenhagen General Population Study.
As part of the study, the researchers had access to data about 100,000 Danes and their intake of fruit and vegetables as well as their DNA. "We can see that those with the highest intake of fruit and vegetables have a 15% lower risk of developing cardiovascular disease and a 20% lower risk of early death compared with those who very rarely eat fruit and vegetables. At the same time, we can see that the reduced risk is related to high vitamin C concentrations in the blood from the fruit and vegetables," says Camilla Kobylecki, a medical doctor and PhD student at the Department of Clinical Biochemistry, Herlev and Gentofte Hospital.
Vitamin C from food rather than supplements
Among other things, vitamin C helps build connective tissue which supports and connects different types of tissues and organs in the body. Vitamin C is also a potent antioxidant which protects cells and biological molecules from the damage which causes many diseases, including cardiovascular disease. The human body is not able to produce vitamin C, which means that we must get the vitamin from our diet.
"We know that fruit and vegetables are healthy, but now our research is pinpointing more precisely why this is so. Eating a lot of fruit and vegetables is a natural way of increasing vitamin C blood levels, which in the long term may contribute to reducing the risk of cardiovascular disease and early death. You can get vitamin C supplements, but it is a good idea to get your vitamin C by eating a healthy diet, which will at the same time help you to develop a healthier lifestyle in the long term, for the general benefit of your health," says Boerge Nordestgaard, a clinical professor at the Faculty of Health and Medical Sciences, University of Copenhagen, and a consultant at Herlev and Gentofte Hospital.
The researchers are now continuing their work to determine which other factors, combined with vitamin C, have an impact on cardiovascular disease and death.

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The above post is reprinted from materials provided by University of Copenhagen The Faculty of Health and Medical Sciences. Note: Materials may be edited for content and length.

In the natural world, sense of taste controls many behavioral decisions. For many animals, pheromones, which are chemical signals used for communication, influence the choice to mate. However, very little is known about how taste pheromones are processed in the brain.
The recent work by Joanne Yew, assistant researcher at the Pacific Biosciences Research Center (PBRC), a newly integrated research unit of the School of Ocean and Earth Science and Technology (SOEST) at the University of Hawai'i - Mānoa, and colleagues explicitly tracked this process - identifying the taste cells on the fruitfly's legs which detect the pheromone, locating the neurons in the brain which respond to the pheromone, and mapping the connection between the two populations of cells.
The pheromone, named CH503, is produced by males, passed to females during mating, and stops other males from mating with the female - it is an anti-aphrodisiac for other males.
Many taste cells are found on the forelegs of flies, so Yew and colleagues used genetic manipulation to turn off activity in individual classes of these taste cells. They then tested whether males could still respond to the pheromone. Using this strategy, they were able to identify one class of taste receptors, called Gr68a, that is responsible for detecting the pheromone.
"Normally, males are repulsed by females that have been perfumed with the pheromone. However, when activity in Gr68a neurons is turned off, males will actively try to mate with females perfumed with the pheromone," said Yew.
Next, the researchers turned off activity in different groups of cells in the central brain to determine whether males could still respond to the pheromone. One group of cells which produces the chemical Tachykinin appeared to be essential for detecting the pheromone.
Finally, the scientists established that the Gr68a neurons in the leg connect with the Tachykinin neurons in the brain. To do this, they introduced 2 sensors into the Gr68a and Tachykinin neuron populations. The sensors light up when neurons in the region are close enough to form connections. The researchers were able to detect connectivity between the two populations of neurons.
"This work identifies a molecular signal, Tachykinin, that controls the perception of taste pheromones and provides an anatomical map of where this information is processed in the brain," said Yew. "By understanding the cellular basis of how taste information is encoded, we will be able to study how sensory signals shape programmed behaviors and influence complex social decisions such as the choice to mate. Potentially, we could devise a way to manipulate Tachykinin in pest populations to control reproduction."
In the future, Yew and colleagues intend to further map the connections of Tachykinin neurons and examine how physiological state (e.g., hunger, stress) can influence the choice to mate via the Tachykinin pathway.

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The above post is reprinted from materials provided by University of Hawaii at Manoa. Note: Materials may be edited for content and length.

A new study by Northeastern physicist Dmitri Krioukov and his colleagues suggests an answer: to expedite the transfer of information from one brain region to another, enabling us to operate at peak capacity.
The paper, published in the July 3 issue of Nature Communications, reveals that the structure of the human brain has an almost ideal network of connections--the links that permit information to travel from, say, the auditory cortex (responsible for hearing) to the motor cortex (responsible for movement) so we can do everything from raise our hand in class in response to a question to rock out to the beat of The 1975.
The findings represent more than a confirmation of our evolutionary progress. They could have important implications for pinpointing the cause of neurological disorders and eventually developing therapies to treat them.
"An optimal network in the brain would have the smallest number of connections possible, to minimize cost, and at the same time it would have maximum navigability--that is, the most direct pathways for routing signals from any possible source to any possible destination," says Krioukov. It's a balance, he explains, raising and lowering his hands to indicate a scale. The study presents a new strategy to find the connections that achieve that balance or, as he puts it, "the sweet spot."
Krioukov, an associate professor in the Department of Physics, studies networks, from those related to massive Internet datasets to those defining our brains. In the new research, he and his co-authors used sophisticated statistical analyses based on Nobel laureate John Nash's contributions to game theory to construct a map of an idealized brain network--one that optimized the transfer of information. They then compared the idealized map of the brain to a map of the brain's real network and asked the question "How close are the two?"
Remarkably so. They were surprised to learn that 89 percent of the connections in the idealized brain network showed up in the real brain network as well. "That means the brain was evolutionarily designed to be very, very close to what our algorithm shows," says Krioukov.
The scientists' strategy bucks tradition: It lets function--in this case, navigability--drive the structure of the idealized network, thereby showing which links are essential for optimal navigation. Most researchers in the field, says Krioukov, build models of the real network first, and only then address function, an approach that does not highlight the most crucial links.
The new strategy is also transferable to a variety of disciplines. The study, whose co-authors are at the Budapest University of Technology and Economics, mapped six diverse navigable networks in total, including that of the Internet, U.S. air¬ports, and Hungarian roads. The Hungarian road network, for example, gave travelers the "luxury to go on a road trip without a map," the authors wrote.
Future applications of the research cross disciplines, too. Knowing what links in a network are the most critical for navigation tells you where to focus protective measures, whether the site is the Internet, roadways, train routes, or flight patterns.
"Conversely, if you're a good guy facing a terrorist network, you know what links to attack first," says Krioukov. A systems designer could locate the missing connections necessary to maximize the navigability of a computer network and add them.
In the brain, the links existing in the idealized network are likely those required for normal brain function, says Krioukov. He points to a maze of magenta and turquoise tangles coursing through a brain illustration in his paper and traces the magenta trail, which is present in both the ideal and real brains.
"So we suspect that they are the primary candidates to look at if some disease develops--to see if they are dam-aged or broken."
Looking to the future, he speculates that once such links are identified, new drugs or surgical techniques could perhaps be developed to target them and repair, or circumvent, the damage.
"At the end of the day, what we are trying to do is to fix the diseased network so that it can resume its normal function," says Krioukov.

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The above post is reprinted from materials provided by Northeastern University. The original item was written by Thea Singer. Note: Materials may be edited for content and length.

A new study published in Nature Communications by researchers from the MRC Centre for Developmental Neurobiology (MRC CDN) at IoPPN, carried out in collaboration with the Tian lab at the Rutgers New Jersey Medical School (USA), unravels how this synchrony is achieved at the molecular level. The researchers found that many RNA messengers encoding neuronal proteins contain specialized sequences that can promote their destabilization in the presence of an RNA-binding protein called tristetraprolin, or TTP. This protein is expressed at relatively high levels in proliferating precursors and non-neuronal cells but down-regulated in developing neurons by a brain-enriched regulatory RNA called miR-9. The TTP/miR-9 pair functions as a switch limiting unscheduled accumulation of neuronal messengers in non-neuronal cells and ensuring coordinated accumulation of these molecules in neurons. "Coherent regulation of multiple genes can pose substantial logistical problems, akin running a successful business employing thousands of people or controlling the vast Galactic Empire from the Star Wars movies" remarks Dr. Eugene Makeyev, a senior author of the study from the MRC CDN. "Our work suggests that fine-tuning messenger stability is an important mechanism orchestrating gene expression changes during normal brain development."
Defective regulation of messenger stability, cellular localization and translation into corresponding protein products often leads to serious medical conditions including neurodegenerative diseases and cancer. A subset of the TTP/miR-9 target genes have been previously linked to these disorders and it will be important to determine whether deregulation of TTP or/and miR-9 plays a causative role in such pathological contexts. Moreover, by uncovering a hitherto unknown mechanism mediating neuronal differentiation, the study by Makeyev and co-authors should facilitate development of novel cell replacement therapies for neurological and neurodegenerative diseases. "Natural renewal of neurons in the adult brain is notoriously inefficient and it likely becomes virtually non-existent as we grow older. With a continued increase in the average life expectancy neuron replacement might become a common medical procedure at some point in the future. Luke Skywalker and his aging father would certainly relate to this idea."
The study was supported by grants from the Biotechnology and Biosciences Research Council (BBSRC), National Institutes of Health (NIH) and National Medical Research Council (NMRC).

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The above post is reprinted from materials provided by King's College London. Note: Materials may be edited for content and length.

In recent years, scientists have used various techniques to determine the structure of the capsid protein, which is the building block of an inner shell of HIV. Until now, the clearest image had been of a mutated protein. Stefan Sarafianos, an associate professor of molecular microbiology and immunology and the Chancellor's Chair of Excellence in molecular virology in the University of Missouri School of Medicine, and his team captured long sought detailed images of the capsid protein in its natural state.
"The capsid shell acts as an 'invisibility cloak' that hides the virus' genetic information, the genome, while it is being copied in a hostile environment for the virus," said Sarafianos, who also holds an appointment in the Department of Biochemistry in the College of Agriculture, Food and Natural Resources and serves as a researcher at the Bond Life Sciences Center. "Fine-tuned capsid stability is critical for successful infection: too stable a capsid shell and the cargo is never delivered properly; not stable enough and the contents are detected by our immune defenses, triggering an antiviral response. Capsid stability is a key to the puzzle, and you have to understand its structure to solve it."
Sarafianos and his team created the most complete model yet of an HIV capsid protein. The research team used a technique called X-ray crystallography to unravel the protein's secrets. By taking many copies of the protein, they coaxed them into forming a patterned, crystalline lattice (see photo).
"With X-ray crystallography, the biggest challenge is to get protein crystals of good quality that will allow researchers to accurately study the protein," said Anna Gres, an MU graduate student in the Department of Chemistry and first author of the study. "Sometimes this process can take years, but by using advanced techniques, we were able to cut that down considerably."
Next they shot high-powered X-ray beams at the crystal. By interpreting how the X-rays scattered when they ricocheted off the proteins, the researchers made a 3-D map of the protein. "But the 3-D map doesn't make sense until we make an atomic model of the protein to fit in that map," said Karen Kirby, a research scientist at Bond LSC and co-author of the study. "The map is just a grid that you can't really interpret unless you put a model into it to see 'Ok, it looks like this part is here, and that part is there, and this is how the protein is put together.'"
Gres constructed the model, which surprisingly revealed "ordered" water molecules at areas between the viral proteins.
"We thought, 'How could some simple water molecules really be of consequence?'" Sarafianos said. "But when we looked carefully, we realized there are thousands of waters that help stabilize the complex capsid scaffold. We hypothesized that this is an essential part of the stability of the whole capsid assembly."
To test that hypothesis, they dehydrated the crystals using chemicals and noticed that the proteins in them changed shape. This change suggested that water molecules help the capsid shell to be flexible and assume different forms, which is critical for the life cycle of the virus, Sarafianos said.
The National Institutes of Health recently awarded the team a grant of $2.28 million over five years to continue their study. Future studies using the newly developed model will assist Sarafianos and his team as they work toward developing antiviral drugs that combat the disease by taking advantage of the new findings.

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The above post is reprinted from materials provided by University of Missouri-Columbia. Note: Materials may be edited for content and length.

"The leading cause of death worldwide is complications of atherosclerosis, and the most common end-stage disease is when an atherosclerotic plaque ruptures. If this occurs in one of your large coronary arteries, it's a catastrophic event," said Gary K. Owens, PhD, of UVA's Robert M. Berne Cardiovascular Research Center. "Once a plaque ruptures, it can induce formation of a large clot that can block blood flow to the downstream regions. This is what causes most heart attacks. The clot can also dislodge and cause a stroke if it lodges in a blood vessel in the brain. As such, understanding what controls the stability of plaques is extremely important. "
Until now, doctors have believed that smooth muscle cells -- the cells that help blood vessels contract and dilate -- were the good guys in the body's battle against atherosclerotic plaque. They were thought to migrate from their normal location in the blood vessel wall into the developing atherosclerotic plaque, where they would attempt to wall off the accumulating fats, dying cells and other nasty components of the plaque. The dogma has been that the more smooth muscle cells in that wall -- particularly in the innermost layer referred to as the "fibrous cap" -- the more stable the plaque is and the less danger it poses.
UVA's research reveals those notions are woefully incomplete at best. Scientists have grossly misjudged the number of smooth muscle cells inside the plaques, the work shows, suggesting the cells are not just involved in forming a barrier so much as contributing to the plaque itself. "We suspected there was a small number of smooth muscle cells we were failing to identify using the typical immunostaining detection methods. It wasn't a small number. It was 82 percent," Owens said. "Eighty-two percent of the smooth muscle cells within advanced atherosclerotic lesions cannot be identified using the typical methodology since the lesion cells down-regulate smooth muscle cell markers. As such, we have grossly underestimated how many smooth muscle cells are in the lesion."
Suddenly, the role of smooth muscle cells is much more complex, much less black-and-white. Are they good or bad? Should treatments try to encourage more? It's no longer that simple, and the problem is made all the more complicated by the fact that some smooth muscle cells were being misidentified as immune cells called macrophages, while some macrophage-derived cells were masquerading as smooth muscle cells. It's very confusing, even for scientists, and it has led to what Owens called "complete ambiguity as to which cell is which within the lesion." (The research also shows other subsets of smooth muscle cells were transitioning to cells resembling stem cells and myofibroblasts.)
Researcher Laura S. Shankman, a PhD student in the Owens lab, was able to overcome the limitations of the traditional methodology for detecting smooth muscle cells in the plaque. Her approach was to genetically tag smooth muscle cells early in their development, so she could follow them and their descendants even if they changed their stripes. "This allowed us to mark smooth muscle cells when we were confident that they were actually smooth muscle cells," she said. "Then we let the atherosclerosis develop and progress [in mice] in order to see where those cells were later in disease."
Further, Shankman identified a key gene, Klf4, that appears to regulate these transitions of smooth muscle cells. Remarkably, when she genetically knocked out Klf4 selectively in smooth muscle cells, the atherosclerotic plaques shrank dramatically and exhibited features indicating they were more stable -- the ideal therapeutic goal for treating the disease in people. Of major interest, loss of Klf4 in smooth muscle cells did not reduce the number of these cells in lesions but resulted in them undergoing transitions in their functional properties that appear to be beneficial in disease pathogenesis. That is, it switched them from being "bad" guys to "good" guys.
Taken together, Shankman's findings raise many critical questions about previous studies built on techniques that failed to assess the composition of the lesions accurately. Moreover, her studies are the first to indicate that therapies targeted at controlling the properties of smooth muscle cells within lesions may be highly effective in treating a disease that is the leading cause of death worldwide.
The discoveries have been outlined in a paper published online by the journal Nature Medicine.

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Various kinds of damage can happen to DNA, making it unstable, which is a hallmark of cancer. One common way that our genetic material can be harmed is from a phenomenon called oxidative stress. When our bodies process certain chemicals or even by simply breathing, one of the products is a form of oxygen that can acutely damage DNA bases, predominantly the Gs. In order to stay cancer-free, our bodies must repair this DNA. Interestingly, where it counts -- in a regulatory DNA structure called a G-quadruplex -- the damaged G is not repaired via the typical repair mechanisms. However, people somehow do not develop cancers at the high rate that these insults occur. Cynthia Burrows, Susan Wallace and colleagues sought to unravel this conundrum.
The researchers scanned the sequences of known human oncogenes associated with cancer, and found that many contain the four G-stretches necessary for quadruplex formation and a fifth G-stretch one or more bases downstream. The team showed that these extra Gs could act like a "spare tire," getting swapped in as needed to allow damage removal by the typical repair machinery. When they exposed these quadruplex-forming sequences to oxidative stress in vitro, a series of different tests indicated that the extra Gs allowed the damages to fold out from the quadruplex structure, and become accessible to the repair enzymes. They further point out that G-quadruplexes are highly conserved in many genomes, indicating that this could be a factory-installed safety feature across many forms of life.

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"Patients who received the gene therapy showed a significant, if modest, benefit in tests of lung function compared with the placebo group and there were no safety concerns," said senior author Professor Eric Alton from the National Heart and Lung Institute at Imperial College London. "Whilst the effect was inconsistent, with some patients responding better than others, the results are encouraging."
Cystic fibrosis is a rare inherited disease caused by mutations in a single gene called cystic fibrosis transmembrane conductance regulator (CFTR) and affects 1 in every 2500 newborns in the UK and over 90000 people worldwide. Scientists have discovered around 2000 CFTR mutations so far. These mutations make the lining of the lungs secrete unusually thick mucus. This leads to recurrent life-threatening lung infections, which result in lung damage that causes 90% of deaths in people with cystic fibrosis.
Since the discovery of the genetic basis for cystic fibrosis in 1989, scientists have developed a variety of viral and non-viral vector systems for delivering a corrected CFTR gene back into lung cells. Despite expectations of a rapid breakthrough, no cystic fibrosis gene therapy trial so far has been able to show long-term clinical improvement.
Coordinated by the UK Cystic Fibrosis Gene Therapy Consortium, the two-year study involved 136 CF patients aged 12 years or older from across the UK. Participants were randomly assigned to either 5ml of nebulised (inhaled) pGM169/GL67A (gene therapy) or saline (placebo) at monthly intervals over 1 year. Lung function was evaluated using a common clinical measure of the volume of air forcibly exhaled in one second (FEV1).
After a year of treatment, in the 62 patients who received the gene therapy, FEV1 was 3.7% greater compared to placebo.* This was a result of stabilisation of respiratory function rather than an improvement. However, the effects were inconsistent, with some patients responding better than others. In particular, in the half of patients with the worst lung function at the start of the study, there was a doubling of the treatment effect, with changes in FEV1 of 6.4%.
Overall, the gene therapy was well tolerated and patients in the treatment and placebo groups experienced similar rates of adverse events.
According to senior co-author Professor Stephen Hyde from the Gene Medicine Research Group at the University of Oxford, "Stabilisation of lung disease in itself is a worthwhile goal. We are actively pursuing further studies of non-viral gene therapy looking at different doses and combinations with other treatments, and more efficient vectors."
Senior co-author Dr Alastair Innes from Western General Hospital, Edinburgh, UK adds, "Publication of this trial is a landmark for cystic fibrosis patients and we are particularly grateful to the many patients across the UK who gave their time and effort to participate and make this collaborative venture a success."
This study was funded by a partnership between the UK Medical Research Council (MRC) and the National Institute for Health Research (NIHR).
*The 95% confidence interval for the effect size is 0.1% to 7.3%. Thus, although the best estimate of the effect size is 3.7%, the data are consistent with the true effect size lying anywhere in the range 0.1% to 7.3%. This interval straddles values from no effect to clear clinical relevance.

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"Because the young mice (less than 2 weeks-old) are being fed milk while being exposed to the odour, they experience positive reinforcement," says Dr Vera Voznessenskaya, one of the lead researchers behind this study. "So they don't escape the cats when exposed to cat odour later on."
The researchers have identified the molecule in the urine responsible for these effects as L-Felinine.
"We already knew that odour affects reproduction in mice: in fact, this molecule (L-Felinine) is capable of blocking pregnancy in females and reducing the size of the litter," explains Dr Voznessenskaya.
Interestingly, while the mice don't escape from the odour later in life, they still experience hormonal changes throughout their life. "Early exposure to cat odour changes behavioral reactions to, but not physiological (hormonal) responses in the mice, which remain elevated. In fact, mice that had experienced the odour showed stress response (elevated corticosterone) to cat odours in the same way as controls."
This research was presented at the Society for Experimental Biology 2015 conference.

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Certain types of stem cells use microscopic, threadlike nanotubes to communicate with neighboring cells, like a landline phone connection, rather than sending a broadcast signal, researchers at University of Michigan Life Sciences Institute and University of Texas Southwestern Medical Center have discovered.
The findings, which are scheduled for online publication July 1 in Nature, offer new insights on how stem cells retain their identities when they divide to split off a new, specialized cell.
The fruit-fly research also suggests that short-range, cell-to-cell communication may rely on this type of direct connection more than was previously understood, said co-senior author Yukiko Yamashita, a U-M developmental biologist whose lab is located at the Life Sciences Institute.
"There are trillions of cells in the human body, but nowhere near that number of signaling pathways," she said. "There's a lot we don't know about how the right cells get just the right messages to the right recipients at the right time."
The nanotubes had actually been hiding in plain sight.
The investigation began when a postdoctoral researcher in Yamashita's lab, Mayu Inaba, approached her mentor with questions about tiny threads of connection she noticed in an image of fruit fly reproductive stem cells, which are also known as germ line cells. The projections linked individual stem cells back to a central hub in the stem cell "niche." Niches create a supportive environment for stem cells and help direct their activity.
Yamashita, a Howard Hughes Medical Institute investigator, MacArthur Fellow and an associate professor at the U-M Medical School, looked through her old image files and discovered that the connections appeared in numerous images.
"I had seen them, but I wasn't seeing them," Yamashita said. "They were like a little piece of dust on an otherwise normal picture. After we presented our findings at meetings, other scientists who work with the same cells would say, 'We see them now, too.'"
It's not surprising that the minute structures went overlooked for so long. Each one is about 3 micrometers long; by comparison, a piece of paper is 100 micrometers thick.
While the study looked specifically at reproductive cells in male Drosophila fruit flies, there have been indications of similar structures in other contexts, including mammalian cells, Yamashita said.
Fruit flies are an important model for this type of investigation, she added. If one was to start instead with human cells, one might find something, but the system's greater complexity would make it far more difficult to tease apart the underlying mechanisms.
The findings shed new light on a key attribute of stem cells: their ability to make new specialized cells while still retaining their identity as stem cells.
Germ line stem cells typically divide asymmetrically. In the male fruit fly, when a stem cell divides, one part stays attached to the hub and remains a stem cell. The other part moves away from the hub and begins differentiation into a fly sperm cell.
Until the discovery of the nanotubes, scientists had been puzzled as to how cellular signals guiding identity could act on one of the cells but not the other, said collaborator Michael Buszczak, an associate professor of molecular biology at UT Southwestern, who shares corresponding authorship of the paper and currently co-mentors Inaba with Yamashita.
The researchers conducted experiments that showed disruption of nanotube formation compromised the ability of the germ line stem cells to renew themselves.
The work was supported by the Howard Hughes Medical Institute and the MacArthur Foundation.

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Now researchers from the University of Wisconsin-Madison have come up with a new solution to alleviate the environmental burden of discarded electronics. They have demonstrated the feasibility of making microwave biodegradable thin-film transistors from a transparent, flexible biodegradable substrate made from inexpensive wood, called cellulose nanofibrillated fiber (CNF). This work opens the door for green, low-cost, portable electronic devices in future.
In a paper published this week in the Applied Physics Letters from AIP Publishing, the researchers describe the biodegradable device.
"We found that cellulose nanofibrillated fiber based transistors exhibit superior performance as that of conventional silicon-based transistors," said Zhenqiang Ma, the team leader and a professor of electrical and computer engineering at the UW-Madison. "And the bio-based transistors are so safe that you can put them in the forest, and fungus will quickly degrade them. They become as safe as fertilizer."
Nowadays, the majority of portable electronics are built on non-renewable, non-biodegradable materials such as silicon wafers, which are highly purified, expensive and rigid substrates, but cellulose nanofibrillated fiber films have the potential to replace silicon wafers as electronic substrates in environmental friendly, low-cost, portable gadgets or devices of the future.
Cellulose nanofibrillated fiber is a sustainable, strong, transparent nanomaterial made from wood. Compared to other polymers like plastics, the wood nanomaterial is biocompatible and has relatively low thermal expansion coefficient, which means the material won't change shape as the temperature changes. All these superior properties make cellulose nanofibril an outstanding candidate for making portable green electronics.
To create high-performance devices, Ma's team employed silicon nanomembranes as the active material in the transistor -- pieces of ultra-thin films (thinner than a human hair) peeled from the bulk crystal and then transferred and glued onto the cellulose nanofibrill substrate to create a flexible, biodegradable and transparent silicon transistor.
But to make portable electronics, the biodegradable transistor needed to be able to operate at microwave frequencies, which is the working range of most wireless devices. The researchers thus conducted a series of experiments such as measuring the current-voltage characteristics to study the device's functional performance, which finally showed the biodegradable transistor has superior microwave-frequency operation capabilities comparable to existing semiconductor transistors.
"Biodegradable electronics provide a new solution for environmental problems brought by consumers' pursuit of quickly upgraded portable devices," said Ma. "It can be anticipated that future electronic chips and portable devices will be much greener and cheaper than that of today."
Next, Ma and colleagues plan to develop more complicated circuit system based on the biodegradable transistors.

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The researchers, whose findings have been published online today in research journal PLOS ONE, hope that some of the coral pigments could be developed into new imaging tools for medical applications.
The team studied corals at depths of more than 50 metres and found that many of them glow brightly with fluorescent colours, ranging from green over yellow to red. The encounter of such a rainbow of coral colours in deep waters was unexpected, since their shallow-water counterparts in the same reef contain only green fluorescent pigments.
Jörg Wiedenmann, Professor of Biological Oceanography and Head of the University of Southampton's Coral Reef Laboratory, explains: "These fluorescent pigments are proteins. When they are illuminated with blue or ultraviolet light, they give back light of longer wavelengths, such as reds or greens.
"Their optical properties potentially make them important tools for biomedical imaging applications, as their fluorescent glow can be used to highlight living cells or cellular structures of interest under the microscope. They could also be applied to track cancer cells or as tools to screen for new drugs."
Gal Eyal, PhD candidate at the IUI, says: "Corals from these so-called mesophotic reefs are less well studied since they are beyond the depth limits of standard Scuba diving techniques. Advances in technical diving have enabled us to explore coral communities from these deeper waters.
"Since only the blue parts of the sunlight penetrate to depths greater than 50 metres, we were not expecting to see any red coloration around. To our surprise, we found a number of corals showing an intense green or orange glow. This could only be due to the presence of fluorescent pigments."
Such pigments are often found in shallow water corals, where they can act as sunscreens for the corals and their symbiotic algae. Finding them in depths where corals are struggling to collect enough light to sustain the photosynthesis of their algal symbionts (a vital energy source for the corals) is therefore unexpected.
Dr Cecilia D'Angelo, Senior Research Fellow at Southampton, has studied corals commonly found in mesophotic depths in the experimental aquarium of the University's Coral Reef Laboratory: "In many shallow water corals, the production of the pigments is tightly controlled by the amount and colour of the incidental light. In the majority of our deep water species, the pigment production is essentially independent from the light exposure of the coral animals.
"We found, however, that some of the pigments of these corals require violet light to switch from their nascent green colour to the red hue of the mature pigment. This is a particularly interesting property to develop markers for advanced microscopic imaging applications."
The team now are now exploring which other biological functions these fluorescent pigments may fulfil.
Substantial parts of the research were conducted during the International Mesophotic Workshop 2014 held at the IUI in Eilat. Dr Yossi Loya, Professor of Zoology at Tel Aviv University and organiser of the workshop, concludes: "This study clearly shows the potential of interdisciplinary and international collaborations. We are delighted that the workshop has opened up such exiting new research avenues."

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That's the upshot of a study published this week in the Proceedings of the National Academy of Sciences (PNAS). The findings have meaning for fields as diverse as mining and the search for life in space.
Clark Johnson, a professor of geoscience at the University of Wisconsin-Madison, and former postdoctoral researcher Weiqiang Li examined samples from the banded iron formation in Western Australia. Banded iron is the iron-rich rock found in ore deposits worldwide, from the proposed iron mine in Northern Wisconsin to the enormous mines of Western Australia.
These ancient deposits, up to 150 meters deep, were begging for explanation, says Johnson.
Scientists thought the iron had entered the ocean from hot, mineral-rich water released at mid-ocean vents that then precipitated to the ocean floor. Now Johnson and Li, who is currently at Nanjing University in China, show that half of the iron in banded iron was metabolized by ancient bacteria living along the continental shelves.
The banding was thought to represent some sort of seasonal changes. The UW-Madison researchers found long-term swings in the composition, but not variations on shorter periods like decades or centuries.
The study began with precise measurements of isotopes of iron and neodymium using one of the world's fastest lasers, housed in the UW-Madison geoscience department. (Isotopes, forms of an atom that differ only by weight, are often used to "fingerprint" the source of various samples.)
Bursts of light less than one-trillionth of a second long vaporized thin sections of the sample without heating the sample itself. "It's like taking an ice cream scoop and quickly pulling out material before it gets heated," Johnson explains.
"Heating with traditional lasers gave spurious results."
It took three years to perfect the working of the laser and associated mass spectrometry instruments, Li says.
Previous probes of the source of banded iron had focused on iron isotopes. "There has been debate about what the iron isotopes were telling us about the source," Li says. "Adding neodymium changed that picture and gave us an independent measure of the amount coming from shallow continental waters that carried an isotopic signature of life."
The idea that an organism could metabolize iron may seem strange today, but Earth was very different 2.5 billion years ago. With little oxygen in the atmosphere, many organisms derived energy by metabolizing iron instead of oxygen.
Biologists say this process "is really deep in the tree of life, but we've had little evidence from the rock record until now," Johnson says. "These ancient microbes were respiring iron just like we respire oxygen. It's a hard thing to wrap your head around, I admit."
The current study is important in several ways, Johnson says. "If you are an exploration geologist, you want to know the source of the minerals so you know where to explore."
The research also clarifies the evolution of our planet -- and of life itself -- during the "iron-rich" era 2.5 billion years ago. "What vestiges of the iron-rich world remain in our metabolism?" Johnson asks. "It's no accident that iron is an important part of life, that early biological molecules may have been iron-based."
NASA has made the search for life in space a major focus and sponsors the UW-Madison Astrobiology Institute, which Johnson directs. Recognizing unfamiliar forms of life is a priority for the space agency.
The study reinforces the importance of microbes in geology. "This represents a huge change," Johnson says. "In my introductory geochemistry textbook from 1980, there is no mention of biology, and so every diagram showing what minerals are stable at what conditions on the surface of the Earth is absolutely wrong."
Research results like these affect how classes are taught, Johnson says. "If I only taught the same thing, I would be teaching things that are absolutely wrong. If you ever wonder why we combine teaching and research at this university, geomicrobiology gives you the answer. It has completely turned geoscience on its ear."

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Associate Professor Steve Chenoweth from The University of Queensland's School of Biological Sciences said the study showed that male harassment of females hampered the species' ability to adapt to new environmental conditions.
"We found that sexually attractive females were overwhelmed by male suitors," he said.
"Female fruit flies with superior genes that allow them to lay more eggs were so attractive to male suitors they spent most of the time fending off male suitors rather than actually laying eggs.
"The end result was that these supposedly 'superior' genes could not be passed on to the next generation."
The genetic study found a large number of genes appeared to be a double-edged sword for females.
The genes increased their egg-laying ability but with the unfortunate side effect of boosting sexual attractiveness to a level where males wouldn't leave them alone.
The researchers allowed different groups of flies to adapt to a new environment in the lab for 13 generations.
They manipulated the number of potential mates that males and females had in each group, thereby controlling the potential harassment rate.
At the end of the experiment, researchers sequenced the genomes of the flies and found a number of genes that became more common when harassment was not allowed, but these same genes became rare when male harassment was allowed to occur as usual.
As such, increased male attention held the population back and stopped the flies from adapting as well as they could.
Associate Professor Chenoweth said the study's results were significant.
"We have known for some time of these harmful interactions between males and females," he said.
"However, we hadn't realised there may be a large number of genes fueling the interactions, or that these types of genes hamper a species' ability to adapt to new conditions."
Associate Professor Chenoweth heads a laboratory in UQ that uses new genomic technology to answer questions of evolutionary behaviour.
He said future directions for the study included pinpointing the exact types of gene functions involved and to understanding the broader consequences of male-female interactions and their relevance to the evolutionary history of other species.

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The researchers studied cats from two UK villages, Mawnan Smith in Cornwall and Thornhill near Stirling. They found that although cat owners were broadly aware of whether their cat was predatory or not, those with a predatory cat had little idea of how many prey items it typically caught.
Regardless of the amount of prey returned by their cats, the majority of cat owners did not agree that cats are harmful to wildlife and were against suggestions that they should keep their cat inside as a control measure. They were however willing to consider neutering which is generally associated with cat welfare.
The results, which are published in Ecology and Evolution, indicate that management options to control cat predation are likely to be unsuccessful unless they focus on cat welfare.
Dr Jenni McDonald from the Centre for Ecology and Conservation at the University of Exeter's Penryn Campus in Cornwall said: "Our study shows that cat owners do not accept that cats are a threat to wildlife, and oppose management strategies with the exception of neutering. There is a clear need to directly address the perceptions and opinions of cat owners.
"If we are to successfully reduce the number of wildlife deaths caused by domestic cats, the study suggests that we should use cat welfare as a method of encouraging cat owners to get involved."
Co-author Professor Matthew Evans, Professor of Ecology at Queen Mary University of London, said: "In this paper we examined how aware cat owners were of the predatory behaviour of their pet. Owners proved to be remarkably unaware of the predatory behaviour of their cat, they also did not agree with any measures that might limit the impact that cats have on local wildlife. This study illustrates how difficult it would be to change the behaviour of cat owners if they are both unaware of how many animals are killed by their pet and resistant to control measures. This presents conservationists who might be attempting to reduce cat predation with serious difficulties, as owners disassociate themselves from any conservation impacts of their cat and take the view that cat predation is a natural part of the ecosystem."
A total of 58 households, with 86 cats, took part in the study. Owners' views regarding their cats' predatory behaviour was assessed by comparing predictions of the number of prey their cat returns with the actual numbers bought home. A questionnaire was given to 45 owners at Mawnan Smith to determine whether the predatory behaviour of cats influences the attitudes of their owners.
In the UK, 23% of households share a population of over ten million domestic cats.
Previous studies have shown that although the majority of cats only return a small amount of prey, one or two items per month, it is the cumulative effect of high densities of cats that is likely to have an overall negative effect on the environment.

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The researchers monitored brain activity in rats, first as the animals viewed food in a location they could not reach, then as they rested in a separate chamber, and finally as they were allowed to walk to the food. The activity of specialised brain cells involved in navigation suggested that during the rest the rats simulated walking to and from food that they had been unable to reach.
The study, published in the open access journal eLife, could help to explain why some people with damage to a part of the brain called the hippocampus are unable to imagine the future.
"During exploration, mammals rapidly form a map of the environment in their hippocampus," says senior author Dr Hugo Spiers (UCL Experimental Psychology). "During sleep or rest, the hippocampus replays journeys through this map which may help strengthen the memory. It has been speculated that such replay might form the content of dreams. Whether or not rats experience this brain activity as dreams is still unclear, as we would need to ask them to be sure! Our new results show that during rest the hippocampus also constructs fragments of a future yet to happen. Because the rat and human hippocampus are similar, this may explain why patients with damage to their hippocampus struggle to imagine future events."
In the experiment, animals were individually placed on a straight track with a T-junction ahead. Access to the junction as well as the left and right hand arms beyond it was prevented by a transparent barrier. One of the arms had food at the end, the other side was empty. After observing the food the rats were put in a sleep chamber for an hour. Finally after the barrier was removed, the animals were returned to the track and allowed to run across the junction and on to the arms.
During the rest period, the data showed that place cells that would later provide an internal map of the food arm were active. Cells representing the empty arm were not activated in this way. This indicates that the brain was simulating or preparing future paths leading to a desired goal.
"What's really interesting is that the hippocampus is normally thought of as being important for memory, with place cells storing details about locations you've visited," explains co-lead author Dr Freyja Ólafsdóttir (UCL Biosciences). "What's surprising here is that we see the hippocampus planning for the future, actually rehearsing totally novel journeys that the animals need to take in order to reach the food."
The results suggest that the hippocampus plans routes that have not yet happened as well as recording those that have already happened, but only when there is a motivational cue such as food. This may also imply the ability to imagine future events is not a uniquely human ability.
"What we don't know at the moment is what these neural simulations are actually for," says co-lead author Dr Caswell Barry (UCL Biosciences). "It seems possible this process is a way of evaluating the available options to determine which is the most likely to end in reward, thinking it through if you like. We don't know that for sure though and something we'd like to do in the future is try to establish a link between this apparent planning and what the animals do next."

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