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At some point in the next decade, if advances in biotechnology continue on their current path, clones of extinct species such as the passenger pigeon, Tasmanian tiger and wooly mammoth could once again live among us. But cloning lost species—or “de-extinction” as some scientists call it—presents us with myriad ethical, legal and regulatory questions that must be answered, such as which (if any) species should be brought back and whether or not such creatures could be allowed to return to the wild. Such questions are set to be addressed at the TEDx DeExtinction conference, a day-long event in Washington, D.C., organized by Stewart Brand’s Revive & Restore project. Brand previewed the topics for discussion last week at the TED2013 conference in Long Beach, Calif. Scientists are actively working on methods and procedures for bringing extinct species back to life, says Ryan Phelan, executive director of Revive & Restore and co-organizer of the TEDx event. “The technology is moving fast. What Stewart and I are trying to do with this meeting is for the first time to allow the public to start thinking about this. We’re going to hear from people who take it quite seriously. De-extinction is going to happen, and the questions are how does it get applied, when does it get used, what are the criteria which are going to be set?” Cloning extinct species has been tried before—with moderate success. An extinct Pyrenean ibex, or bucardo, (Capra pyrenaica pyrenaica) was born to a surrogate mother goat in 2009, nine years after the last member of its species was killed by a falling tree. The cloned animal lived for just seven minutes. Revive & Restore itself has launched a project to try to resurrect the passenger pigeon, which went extinct in 1914. More: http://www.wired.com/wiredscience/2013/03/passenger-pigeon-de-extinction/
Dr. Jennifer Peters’ and Dr. Michael Taylor’s winning image of the blood-brain barrier in a live zebrafish embryo perfectly demonstrates the intersection of art and science that drives the Nikon Small World Competition. The blood-brain barrier plays a critical role in neurological function and disease. Drs. Peters and Taylor, developed a transgenic zebrafish to visualize the development of this structure in a live specimen. By doing so, this model proves that not only can we image the blood-brain barrier, but we can also genetically and chemically dissect the signaling pathways that modulate the blood-brain barrier function and development. To achieve this image, Peters and Taylor used a maximum intensity projection of a series of images acquired in the z plane. The images were first pseudo-colored with a rainbow palette based on depth so that the coloring scheme would be both visually appealing and provide spatial information. In doing so, Peters and Taylor captured an image that Peters says“not only captures the beauty of nature, but is also topical and biomedically relevant.” Both Peters and Taylor have more than ten years of imaging experience. Peters is an imaging scientist in the St. Jude Children’s Research Hospital’s Light Microscopy Core Facility and Taylor is an Assistant Member in the Department of Chemical Biology and Therapeutics at St. Jude Children’s Research.
Researchers at Columbia Engineering have developed a new "plug-and-play" method to assemble complex cell microenvironments that is a scalable, highly precise way to fabricate tissues with any spatial organization or interest -- such as those found in the heart or skeleton or vasculature. The study reveals new ways to better mimic the enormous complexity of tissue development, regeneration, and disease.
"George Eng, an MD/PhD student in my lab who just received his doctoral degree, designed a lock-and-key technique to build cellular assemblies using a variety of shapes that lock into templates much the way you would use LEGO building blocks," says Gordana Vunjak-Novakovic, who led the study and is the Mikati Foundation Professor of Biomedical Engineering at Columbia Engineering and professor of medical sciences. "What is really important about this technique is that these shapes are tiny -- just a fraction of millimeter, the thickness of a human hair -- and that their precise arrangements are made using cell-friendly hydrogels."
Tissue cells in the human body form specific architectures that are critical for the function of each tissue. Cardiac cells, for example, are aligned to create maximum force acting in one direction. Cells without specific spatial organization may never become fully functional if they do not recapitulate their intrinsic organization found in the body. The Columbia Engineering technique enables researchers to construct unique and controlled cell patterns that allow precise studies of cell function, so that, Vunjak-Novakovic adds, "we can now ask some of the more complex questions about how the cells respond to the entire context of their environment. This will help us explore cellular behavior during the progression of disease and test the effects of drugs, stem cells, and various other therapeutic measures."
"We used a LEGO-like lock-and-key docking system to spatially localize different cell populations with high specificity and precision," Eng explains. "And, since each shape is docking independent of each other, large tissues can be organized simultaneously, instead of having to create a sequential, brick-by-brick type of organization. With this method, we can design and create better tissues for potential organ replacement." "The beauty of this method is that complex configurations of living cellular material -- many different types of cells, molecules, and extracellular materials -- emerge in the lab in precise three-dimensional geometries in a way that can be used by anyone, as no special equipment is involved," Vunjak-Novakovic adds. Eng is excited about leveraging the microtechnologies used to make computer chips with biomedical engineering techniques to make cells to fabricate new organs. "We develop new ideas and methods to try and alleviate disease by assembling tiny subunits of cells into larger, more functional organs," he says. "It's really like a scene from science fiction! To be on the frontier of scientific discovery, developing new methods and products that we hope will have therapeutic benefit for people is quite fulfilling and motivating. And there's such an exciting element of discovery in designing new cellular microenvironments, studying the rules that define cell communication and organization." Next steps in the application of this new technique include fabrication of different types of functional tissues, such as well-organized cardiac muscle, a tissue whose function critically depends on its architecture and cell alignment, incorporating blood vessel networks along with organized cardiac cells. The method will also be extended to the design of pathological microenvironments of interest, such as tumor models. "Our lab has worked for many years in building 'human-on-a-chip' systems that will allow us to see cellular responses representative of those of whole body physiology," says Vunjak-Novakovic. "We're also very interested in developing technologies that can advance biological experimentation and allow us to ask more complex questions. This study, which was conducted over the last four years, is contributing to both of these areas and helping us advance our methods for screening of therapeutic cells and factors."
Algae-like structures inside a Sri Lankan meteorite are clear evidence of panspermia, the idea that life exists throughout the Universe, say astrobiologists On 29 December 2012, a fireball lit up the early evening skies over the Sri Lankan province of Polonnaruwa. Hot, sparkling fragments of the fireball rained down across the countryside and witnesses reported the strong odour of tar or asphalt. Over the next few days, the local police gathered numerous examples of these stones and sent them to the Sri Lankan Medical Research Institute of the Ministry of Health in Colombo. After noticing curious features inside these stones, officials forwarded the samples to a team of astrobiologists at Cardiff University in the UK for further analysis. The results of these tests, which the Cardiff team reveal today, are extraordinary. They say the stones contain fossilised biological structures fused into the rock matrix and that their tests clearly rule out the possibility of terrestrial contamination. In total, the Jamie Wallis at Cardiff University and a few buddies received 628 stone fragments collected from rice fields in the region. However, they were able to clearly identify only three as possible meteorites. The general properties of these three stones immediately mark them out as unusual. One stone, for example, had a density of less than 1 gram per cubic centimetre, less than all known carbonaceous meteorites. It had a partially fused crust, good evidence of atmospheric heating, a carbon content of up to 4 per cent and contained an abundance of organic compounds with a high molecular weight, which is not unknown in meteorites. On this evidence, Wallis and co think the fireball was probably a small comet. The most startling claims, however, are based on electron microscope images of structures within the stones (see above). Wallis and co say that one image shows a complex, thick-walled, carbon-rich microfossil about 100 micrometres across that bares similarities with a group of largely extinct marine dinoflagellate algae. They say another image shows well-preserved flagella that are 2 micrometres in diameter and 100 micrometres long. By terrestrial standards, that’s extremely long and thin, which Wallis and co interpret as evidence of formation in a low-gravity, low-pressure environment. Wallis and co also measured the abundance of various elements in the samples to determine their origin. They say that low levels of nitrogen in particular rule out the possibility of contamination by modern organisms which would have a much higher nitrogen content. The fact that these samples are also buried within the rock matrix is further evidence, they say. Wallis and co are convinced that the lines of evidence they have gathered are powerful and persuasive. “This provides clear and convincing evidence that these obviously ancient remains of extinct marine algae found embedded in the Polonnaruwa meteorite are indigenous to the stones and not the result of post-arrival microbial contaminants,” they conclude. There’s no question that a claim of this kind is likely to generate controversy. Critics have already pointed out that the stones could have been formed by lightning strikes on Earth although Wallis and co counter by saying there was no evidence of lightning at the time of the fireball and that in any case, the stones do not bear the usual characteristics of this kind of strike. What’s more, the temperatures generated by lightning would have destroyed any biological content. Nevertheless, extraordinary claims require extraordinary evidence and Wallis and co will need to make their samples and evidence available to the scientific community for further study before the claims will be taken seriously. If the paper is taken at face value, one obvious question that arises is where these samples came from. Wallis and co have their own ideas: “The presence of fossilized biological structures provides compelling evidence in support of the theory of cometary panspermia first proposed over thirty years ago,” they say. This is an idea put forward by Fred Hoyle and Chandra Wickramasinghe, the latter being a member of the team who has carried out this analysis. There are other explanations, of course. One is that the fireball was of terrestrial origin, a remnant of one of the many asteroid impacts in Earth’s history that that have ejected billions of tonnes of rock and water into space, presumably with biological material inside. Another is that the structures are not biological and have a different explanation. Either way, considerably more work will have to be done before the claims from this team can be broadly accepted. Exciting times ahead! Original paper is here: Ref: http://arxiv.org/abs/1303.1845: The Polonnaruwa Meteorite: Oxygen isotope, Crystalline and Biological Composition
Our world is quite literally lousy with parasites. We are hosts to hundreds of them, and they are so common that in some ecosystems, the total mass of them can outweigh top predators by 20 fold. Even parasites have parasites. It’s such a good strategy that over 40% of all known species are parasitic. They steal genes from their hosts, take over other animals’ bodies, and generally screw with their hosts’ heads. But there’s one thing that we believed they couldn’t do: stop being parasites. Once the genetic machinery set the lifestyle choice in motion, there’s supposed to be no going back to living freely. Once a parasite, always a parasite - unless you’re a mite. In evolutionary biology, the notion of irreversibility is known as Dollo’s Law after the Belgian paleontologist that first hypothesized it in 1893. He stated that once a lineage had lost or modified organs or structures, that they couldn’t turn back the clock and un-evolve those changes. Or, as he put it, “an organism is unable to return, even partially, to a previous stage already realized in the ranks of its ancestors.” While some animals seem to challenge Dollo’s Law, it has long been a deeply held belief in the field of parasitology. Parasitism is, in general, a process of reduction. Adjusting to survival on or in another animal is a severe evolutionary undertaking, and many parasites lose entire organs or even body systems, becoming entirely dependent on their hosts to perform biological tasks like breaking down food or locomotion. Parasitology textbooks often talk about the irreversibility of becoming a parasite in very finite terms. “Parasites as a whole are worthy examples of the inexorable march of evolution into blind alleys” says Noble & Noble’s 1976 Parasitology: the Biology of Animal Parasites. Robert Poulin is even more direct: “Once they are dependent on the host there is no going back. In other words, early specialisation for a parasitic life commits a lineage forever.” Now, parasites are proving that not only can they evade immune systems, trick other animals, and use their hosts’ bodies in hundreds of nefarious ways, some can go back to living on their own. This is exactly what scientists now believed happened in the Pyroglyphidae — the dust mites. Mites, as a whole, are a frighteningly successful if often overlooked group of organisms. More than 48,000 species have been described. These minuscule relatives of spiders can be found worldwide in just about every habitat you can imagine. Many are free-living, but there are also a number of parasitic species, including all-too-familiar pests like Sarcoptes scabiei, the mite which causes scabies. Exactly how the different groups of mites are related to each other, however, has been a hot topic of debate amongst mite biologists. Though the closest relatives of dust mites are the Psoroptidia, a large and diverse parasitic group of mites, many have argued that dust mites came from free-living ancestors — ‘living fossils’ of a sort, the only surviving line of ancestral free-living mites that later gave rise to parasites. In fact, Pavel Klimov and Barry O’Connor from the University of Michigan were able to find 62 different hypothesis as to how the free-living the dust mites fit into the mite family tree. Sixty-two, the team decided, was simply too many. So, they turned to the mites’ genes. To test which of the hypotheses had the most merit, Klimov and O’Conner conscripted a team of 64 biologists in 19 countries to obtain over 700 mite specimens, which they then used to construct a mite family tree. They sequenced five nuclear genes from each species, then applied statistical analyses to construct a tree of relationships called a phylogeny. And that’s when they saw it: deeply nested inside a large group of parasites were our everyday, non-parasitic, allergy-causing dust mites. “This result was so surprising that we decided to contact our colleagues to obtain their feedback prior to sending these data for publication,” said lead author Pavel Klimov. “Parasites can quickly evolve highly sophisticated mechanisms for host exploitation and can lose their ability to function away from the host body,” he explained. “Many researchers in the field perceive such specialization as evolutionarily irreversible.” But, their data were clear. “All our analyses conclusively demonstrated that house dust mites have abandoned a parasitic lifestyle, secondarily becoming free-living.”
In hot springs of Yellowstone National Park, lives an "extremophile" red alga, Galdieria sulphuraria. Galdieria uses energy from the sun to produce sugars through photosynthesis. In the darkness of old mineshafts in drainage as caustic as battery acid, it feeds on bacteria and survives high concentrations of arsenic and heavy metals. How has a one-celled alga acquired such flexibility and resilience? To answer this question, an international research team led by Gerald Schoenknecht of Oklahoma State University and Andreas Weber and Martin Lercher of Heinrich-Heine-Universitat (Heinrich-Heine University) in Dusseldorf, Germany, decoded genetic information in Galdieria. The scientists made an unexpected discovery: Galdieria's genome shows clear signs of borrowing genes from its neighbors. Many genes that contribute to Galdieria's adaptations were not inherited from its ancestor red algae, but were acquired from bacteria or archaebacteria. This "horizontal gene transfer" is typical for the evolution of bacteria, researchers say. However, Galdieria is the first known organism with a nucleus (called a eukaryote) that has adapted to extreme environments based on horizontal gene transfer. "The age of comparative genome sequencing began only slightly more than a decade ago, and revealed a new mechanism of evolution--horizontal gene transfer--that would not have been discovered any other way," says Matt Kane, program director in the National Science Foundation's (NSF) Division of Environmental Biology, which funded the research.
"This finding extends our understanding of the role that this mechanism plays in evolution to eukaryotic microorganisms." The alga owes its ability to survive the toxic effects of such elements as mercury and arsenic to transport proteins and enzymes that originated in genes it swiped from bacteria. It also copied genes offering tolerance to high salt concentrations, and an ability to make use of a wide variety of food sources. The genes were copied from bacteria that live in the same extreme environment as Galdieria. "Why reinvent the wheel if you can copy it from your neighbor?" asks Lercher. "It's usually assumed that organisms with a nucleus cannot copy genes from different species--that's why eukaryotes depend on sex to recombine their genomes. "How has Galdieria managed to overcome this limitation? It's an exciting question." What Galdieria did is "a dream come true for biotechnology," says Weber. "Galdieria has acquired genes with interesting properties from different organisms, integrated them into a functional network and developed unique properties and adaptations." In the future, genetic engineering may allow other algae to make use of the proteins that offer stress tolerance to Galdieria. Such a development would be relevant to biofuel production, says Schoenknecht, as oil-producing algae don't yet have the ability to withstand the same extreme conditions as Galdieria.
In 1853 Edward Frederick Kelaart, a physician and naturalist, collected a strange frog on the island of Sri Lanka then a British colony known as Ceylon. The specimen was a large shrub frog (about 2 inches or 5.5 centimeters long) with black-outlined white specks on lime-green skin. He dubbed it "starry" after its pale specks, but that was last anyone heard of it. Even the holotype—the body of the amphibian collected by Kelaart—went missing. Fast forward nearly 160 years—two world wars, Sri Lanka's independence, and a man on the moon—when a recent expedition into Sri Lanka's Peak Wilderness rediscovered a beguiling frog with pinkish specks.
"These quite stunning frogs were observed perched on leaves in the canopy. They were slow moving, we collected samples which we thought were new species. But after reviewing past work, especially extinct species, it was evident that this was Pseudophilautus stellatus," L.J. Mendis Wickramasinghe told mongabay. Kelaart's starry shrub frog, or Pseudophilautus stellatus, had been re-discovered!
“When fed a diet that induces obesity these mice don’t get fat. It may be possible to duplicate this in humans using existing technology that targets this specific gene,” Prof. McManaman said. The team created a strain of mice without the Plin2 gene which produces a protein that regulates fat storage and metabolism. They immediately found that the mice were resistant to obesity. Usually, mice fed a high fat diet will eat voraciously, yet these showed an unusual restraint. Not only did they eat less, they were more active. Their fat cells were also 20 percent smaller than typical mice and did not show the kind of inflammation usually associated with obesity, the study said. Obesity-associated fatty liver disease, common in obese humans and rodents, was absent in the mice without the Plin2 gene. “The mice were healthier,” Prof. McManaman said. “They had lower triglyceride levels, they were more insulin-sensitive, they had no incidents of fatty liver disease and there was less inflammation in the fat cells.” “The absence of the gene may cause fat to be metabolized faster.” “Now we want to know why this works physiologically,” the scientist said. “We want to better understand how this affects food consumption.” According to the study, understanding how Plin2 is involved in the control of energy balance will provide new insights into the mechanisms by which nutrition overload is detected, and how individuals adapt to, or fail to adapt to, dietary challenges. The consequences for people are highly significant since they also possess the Plin2 gene. “It could mean that we have finally discovered a way to disrupt obesity in humans,” Prof. McManaman said. “That would be a major breakthrough.”
Biological samples are fragile, if they’re not kept at cold temperatures, they quickly degrade. And refrigeration in labs and on trucks, planes, and ships is costly and requires a huge amount of energy. The company Biomatrica has developed a solution that allows these fragile materials to be stored at room temperature. The technology mimics the microscopic water bear’s survival strategy. The water bear, an arthropod also known as a tardigrade, lumbers across moist surfaces of mosses and lichens. But when those dry up, the water bear goes into a suspended state that could last anywhere from a few months to a century. Other organisms, such as brine shrimp and the resurrection fern, employ similar strategies to survive extreme conditions. Judy Müller-Cohn and Rolf Müller, founders of Biomatrica, were inspired by a visit to a toy store, where they saw sea monkeys (brine shrimp in their dried state) for sale. Müller-Cohn, a molecular biologist who has lost thousands of samples due to freezer breakdowns, and her business partner, Müller, looked into extremophile biology for an alternative storage method. The key is the sugar trehalose. As water becomes scarce, trehalose inside the water bear loses water. Instead of forming sharp-edged crystals that can damage DNA, membranes, and cells, the sugar transforms into a glassy state. This sugar-glass surrounds the water bear’s molecules, protecting them from high temperatures and also preventing chemical reactions and denaturation. All it takes to revive the water bear is water, which dilutes the trehalose and gently releases the molecules from their suspended state. Biomatrica created a molecule that performs the same function as trehalose—to stabilize biological samples for transport without refrigeration. The potential environmental benefits are huge. In a 2009 study, Stanford University researchers estimated that replacing 2,000 laboratory freezers with room-temperature storage technology could, over a ten-year period, reduce the university’s carbon footprint by 18,000 metric tons—the equivalent of consuming 1.83 million gallons of gasoline. Considering that in the U.S. alone, there are more than 40,000 biological and biomedical research laboratories located on university campuses, the potential savings thanks to the tiny water bear are tremendous.
Infrared imaging has revealed that much of a penguin’s outer surface is cooler than the surrounding air -- except, of course, for their unfeathered eyes, beaks, and feet -- suggesting that extreme radiative cooling draws heat from a penguin’s surroundings. Emperor Penguins with blue bellies, green beaks, and red eyes huddle over a patch of black snow — a multicolored Antarctic landscape, as seen through the eye of an infrared thermal imager. The psychedelic colors, which correspond to different temperatures, reveal that much of a penguin’s outer surface is cooler than the surrounding air — except, of course, for their unfeathered eyes, beaks, and feet. “Most of the body that is covered by thick plumage was found to be, on average, 4 to 6 degrees C colder than surrounding air temperature,” said biophysical ecologist Dominic McCafferty of the University of Glasgow. Only the birds’ eyes measured above freezing. “At first, we were very surprised by this discovery,” he said. The observations, reported today in Biology Letters, suggest that extreme radiative cooling draws heat from a penguin’s feathery surface. On a clear, cold night, you can see the effects of radiative cooling in the frost that forms on windows, roofs, and grasses. But because they’re insulated beneath layers of feathers and fat, the birds can still maintain a body temperature of about 39 degrees C (102 degrees F), even when shuffling through the -40 C Antarctic night. The team studied a breeding colony in Terre Adélie, Antarctica, during June 2008. After scanning through hundreds of pictures, scientists selected and analyzed 40 birds separated from their peers by more than one body length. Then, they developed a model describing how heat is transferred between different penguin parts and the freezing air. Next, McCafferty hopes to use thermal imaging to study how huddling together helps penguins save energy. “The emperor penguin could not stay warm throughout the Antarctic winter without huddling for shelter and to share body heat,” McCafferty said. The reported temperature differences are certainly plausible, says biophysical ecologist George Bakken of Indiana State University, who studies thermal regulation in a number of animal species. But Bakken notes that radiative cooling occurs most efficiently when the air is still, which it wasn’t when McCafferty’s team was photographing the Antarctic penguins. “It is conceivable that those temperatures might be off a little bit, and the surface is not quite as cold as they say it is,” Bakken said.
Climate change could see dozens of lizard species becoming extinct within the next 50 years, according to new research published today. The often one-directional evolutionary adaptation of certain lizard species' reproductive modes could see multiple extinctions as the global temperature increases.
Via Maria Nunzia
University of Arizona geneticists have discovered the oldest known genetic branch of the human Y chromosome – the hereditary factor determining male sex. The new divergent lineage, which was found in an individual who submitted his DNA to Family Tree DNA, a company specializing in DNA analysis to trace family roots, branched from the Y chromosome tree before the first appearance of anatomically modern humans in the fossil record.
"Our analysis indicates this lineage diverged from previously known Y chromosomes about 300,000 ago, a time when anatomically modern humans had not yet evolved," said Michael Hammer, an associate professor in the University of Arizona's department of ecology and evolutionary biology and a research scientist at the UA's Arizona Research Labs. "This pushes back the time the last common Y chromosome ancestor lived by almost 70 percent."
Unlike the other human chromosomes, the majority of the Y chromosome does not exchange genetic material with other chromosomes, which makes it simpler to trace ancestral relationships among contemporary lineages. If two Y chromosomes carry the same mutation, it is because they share a common paternal ancestor at some point in the past. The more mutations that differ between two Y chromosomes the farther back in time the common ancestor lived. Originally, a DNA sample obtained from an African American living in South Carolina was submitted to the National Geographic Genographic Project. When none of the genetic markers used to assign lineages to known Y chromosome groupings were found, the DNA sample was sent to Family Tree DNA for sequencing. Fernando Mendez, a postdoctoral researcher in Hammer's lab, led the effort to analyze the DNA sequence, which included more than 240,000 base pairs of the Y chromosome.
Antibacterial 'nanopillars' on cicada wings pull bacterial membranes apart. The veined wing of the clanger cicada kills bacteria solely through its physical structure — one of the first natural surfaces found to do so. An international team of biophysicists has now come up with a detailed model of how this defence works on the nanoscale. The results are published in the latest issue of the Biophysical Journal. The clanger cicada (Psaltoda claripennis) is a locust-like insect whose wings are covered by a vast hexagonal array of 'nanopillars' — blunted spikes on a similar size scale to bacteria (see video, bottom). When a bacterium settles on the wing surface, its cellular membrane sticks to the surface of the nanopillars and stretches into the crevices between them, where it experiences the most strain. Lead study author Elena Ivanova of Australia's Swinburne University of Technology in Hawthorne, Victoria, says that she was surprised that the bacterial cells are not actually punctured by the nanopillars. The rupturing effect is more like “the stretching of an elastic sheet of some kind, such as a latex glove. If you take hold of a piece of latex in both hands and slowly stretch it, it will become thinner at the centre, [and] will begin to tear,” she explains. To test their model, Ivanova and her team irradiated bacteria with microwaves to generate cells that had different levels of membrane rigidity. Their hypothesis was that the more rigid bacteria would be less likely to rupture between the nanopillars. The results validated the model, but also demonstrated that the cicada’s nanopillar defence is limited to bacteria that have sufficiently soft membranes. Further study of the cicada’s wing is needed before its physical-defence properties can be mimicked in man-made materials. Anne-Marie Kietzig, a chemical engineer at McGill University in Montreal, Canada, who was not involved in the study, suggests that materials based on this model could one day be applied to public surfaces that commonly harbour disease, such as bus railings. “This would provide a passive bacteria-killing surface,” she says, adding that it “does not require active agents like detergents, which are often environmentally harmful”.
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Vall d’Hebron Institute of Oncology (VHIO) scientists eradicate lung tumours in a pre-clinical mouse model. Previous studies had already shown that Myc was a key protein in tumour development and had established how to inhibit Myc through gene therapy. The protein Myc is involved in the development of diverse tumours and so Myc-targeted therapy could make a positive contribution to the therapeutic options for different types of cancer. The study has managed to eliminate mouse lung tumours by inhibiting Myc, a protein that plays a key role in the development of many different tumours. The results, published in the journal Genes & Development, confirm that repeated, long-term treatment does not cause side effects. Even more importantly, no resistance to treatment has been encountered, which is one of the biggest concerns with anticancer therapies. These results show that anticancer therapies based on Myc inhibition are a safe, effective therapeutic option in new drug development. Myc is a protein that plays a big role in regulating gene transcription and it is involved in cell processes such as proliferation, differentiation and apoptosis (programmed cell death - an essential part of regenerating tissues and eliminating damaged cells). It acts as a regulator gene that controls the expression of some 15% of human genes. However, imbalances in this protein bring about uncontrolled cell growth which in turn can lead to the onset of cancer in different tissues. In fact, deregulated Myc is found in most tumours, including cervical, breast, colon, lung and stomach cancer. The work conducted by the Mouse Models of Cancer Therapy group at the VHIO, led by Dr Laura Soucek, shows that Myc can be controlled and inhibited through a mutant called Omomyc that hijacks Myc and prevents it from acting. “Even if we clearly identify a mechanism behind tumour development, it is still extremely complex to pinpoint how to intervene in cells' internal machinery or modify genetic processes,” explained Dr Soucek. “We have found a way to inhibit Myc through Omomyc,” she continued. “We induced Omomyc expression in mice through gene therapy and managed to activate and deactivate it by administering an antibiotic to the mice in their drinking water.”
In the study, multiple lung tumours were induced in the mouse (up to 200 tumours in each individual) and Myc inhibition episodes were achieved by activating Omomyc expression for 4-weeks, followed by 4-week rest periods. This therapy - known as metronomic therapy - was maintained for more than a year, regularly checking tumour progress in each mouse. All mice became tumour free after the first inhibition period, but 63% of cases then relapsed. After the second Myc inhibition period, only 11% of the initial tumours reappeared. According to Dr Soucek, “the most important finding was that there were no signs of resistance to treatment. This is one of the biggest disadvantages of many anticancer therapies: the disease develops resistance and can return even more aggressively.” Finally, only two remaining tumours were found after more than one year of treatment among the mice that received eight inhibition and rest cycles. Dr Soucek found that Omomyc expression had been suppressed in these tumours, and this was the only adaptive mechanism that mice developed to treatment. “These results are hugely positive for us, because one year of life in a mouse is equivalent to almost 40 human years. The fact that the results are maintained over time, that there is no tumour relapse and no resistance, suggests that Myc-targeted therapy may offer an unprecedented way forward."
These encouraging results provide sufficient scientific evidence to consider taking the next step: inhibiting Myc in patients. “Now our challenge for the future is to make Myc inhibition feasible from a pharmacological point of view, so that it can be administered, and done so safely. This will be the last step before designing clinical trials with Myc inhibitors,” explained Dr Soucek. “We're so excited about reaching this turning point and I am quite certain that it will change the course of cancer therapy, despite there being a long road ahead.”
After cloning 25 generations from a single mouse, the next step for a Japanese lab is to attempt to make clones from mouse fur, stuffed bodies and mouse cells in excrement. Teruhiko Wakayama at the RIKEN Center for Developmental Biology in Kobe, Japan, who carried out the work, says the technique could help in producing high-quality animals for farms and conservation purposes. "If a 'super cow' that could produce a lot of milk or Kobe beef could be cloned at low cost, then not only consumers but also farmers would be happy," he says. Twenty-five generations of clones have come from the mouse, and all 580 of them were healthy, lived normal lifespans and could have healthy pups through normal mating. In 2008, Wakayama's team produced clones from dead mice that had been frozen for 16 years. "My lab is now trying to make cloned mice from fur, stuffed bodies, and excrement," says Wakayama. Enthusiasm for therapeutic cloning, as the technique that led to Dolly the sheep is known, waned in the mid-2000s following scientific fraud scandals in South Korea and the difficulty of producing animals without abnormalities. Researchers struggled to produce cloned cattle, pigs, cats and dogs beyond two or three generations. Now Wakayama's team has emphatically broken through this barrier thanks to a chemical which more faithfully resets the cell nucleus to be cloned back to an embryonic state. First, the team emptied a mouse egg cell of its nucleus. Then they inserted a nucleus from the adult mouse to be cloned before putting this cell into a bath of an enzyme blocker called trichostatin. The resulting embryos – all females – had fewer abnormalities in their histones, the packing materials for chromosomes. Previous studies had identified faulty histones in cloned embryos as a possible reason for the poor success rate of cloning, as well as clone abnormalities. A possible explanation for the previous limit on the number of "reclones" is a build up of such abnormalities over successive generations. "So far, nobody has been able to explain the reason for this," says Wakayama. "We thought that this limitation was caused by the accumulation of genetic or epigenetic abnormalities." "This is very impressive work. If this translates to other mammalian species – including humans – it could be a major game changer," says Robert Lanza, chief medical officer at Advanced Cell Technology, a company based in Marlborough, Massachusetts, that is developing treatments based on stem cells. Wakayama says he doesn't know if his technique will make it easier to clone primates, let alone humans, and has no plans to try. "I am a mouse researcher and have no experience with other species. I will not even attempt to use rats, because male rats are extremely difficult to clone." One application of cloning is to preserve endangered species, as advocated late last year by Brazil. The ability to make clones from fur, specimens preserved in museums and excrement would potentially allow the "resurrection" of extinct animals.
Researchers discover how transmissible facial cancer hides from the immune system. Tasmanian devils are dying of a contagious cancer called devil facial tumor disease, which spreads between animals when they tussle over food. Now, a team of scientists has discovered how the disease infects new hosts by sneaking past the devil's immune system. The work could help in developing a vaccine that might prevent healthy devils from catching the cancer. “It’s probably the most promising lead we’ve had for a vaccine since the initial characterization of the disease,” says immunogeneticist Hannah Siddle of the University of Cambridge, UK. Devil facial tumor disease emerged in 1996 and has slashed the Tasmanian devil population by 60%. If left unchecked, it could drive the species to extinction in 20–30 years.
Researchers had assumed that the disease spread easily between animals because of the devil's low genetic diversity, particularly in the genes of the major histocompatibility complex (MHC), which produce proteins that sit on the surface of cells and help the immune system to detect threats such as viruses or tumors. Once the disease emerged in one devil, presumably dodging its immune system by producing these proteins, it was thought that it would be able to fool the immune defences of the whole population.
But rather than producing the same MHC molecules found across all devils, Siddle and her colleagues found that the cancerous cells do not produce MHC molecules at all. “That was a big surprise,” she says. More surprising still was that the MHC genes in tumor cells had not been disabled by mutations. Instead, the genes responsible for the production of three proteins — β2-microglobulin, TAP1 and TAP2 — had been largely switched off. These proteins are necessary for transporting MHC to a cell’s membrane. Siddle even managed to reverse this problem using interferon-γ — a molecule that is known to encourage the production of MHC proteins. “The fact that it worked was wonderful and made perfect sense,” says Jim Kaufman, who was lead investigator on the study.
It is unclear if devil facial tumor disease will also evolve to be less aggressive with time, but with the Tasmanian devil facing extinction, Kaufman is not waiting to find out. He and his team are now working with Australian colleagues to develop a vaccine. Their plan is to prime healthy devils by giving them cancerous cells that already bear MHC proteins. Their immune systems should then recognize either tiny amounts of MHC on the surface of a cancer cell, or other proteins released as the tumors grow. “We’d start enough of an immune response to tip the balance in favour of the devil,” says Kaufman. “We’ve got some way to go, but we feel quite hopeful that we’ll come up with something.”
Although the priority is to save the Tasmanian devil from extinction, Kaufman also thinks that such research is important should a contagious cancer ever evolve to spread between humans. “Every once in a while, a new disease comes out of nowhere,” he says. “It’s useful to know what might hit people or other animals in the future.”
Mice that received transplants of human glial progenitor cells learned much more quickly than normal mice, according to a study published today (March 7) in Cell Stem Cell. The findings support the theory that glial cells made a significant contribution to the evolution of our own enhanced cognitive abilities. “This work is very exciting and surprising because it demonstrates that there may be something special about human glial progenitor cells that contribute to the amazing complexity and computational abilities of the human brain,” said Robert Malenka, a neuroscientist at Stanford University who was not involved in the study, in an email to The Scientist. For many years, glia cells, non-neuronal cells present in the same numbers as neurons in the brain, were thought to play only a supporting role, providing structure, insulation, and nutrients for neurons. But in the past 20 years it has become clear that glia also participate in the transmission of electrical signals. Specifically, astrocytes—a type of glial cell with thousands of tendrils that reach and encase synapses—can modulate signals passing between neurons and affect the strength of those connections over time. Recent studies have also demonstrated that human astrocytes are very different from those found in mouse and rat brains, on which most previous studies of astrocyte physiology were based. Human astrocytes are more numerous, larger, and more complex, and they are capable of far more rapid signaling responses than rodent astrocytes. Together, these results suggest that astrocytes may have been critical to the evolution of enhanced neural processing in humans. Having already transplanted human glial progenitor cells (GPCs) to restore myelination in myelin-deficient mice, Steven Goldman of University of Rochester Medical Center in New York and colleagues realized that they could repeat the trick in normal mice to assess the contribution of human-specific astrocytes to synaptic plasticity and learning. Goldman’s team grafted human GPCs into the brain of baby mice and waited until they became adults, by which time a large proportion of their forebrain glia were replaced by human cells differentiated from the GPCs, including astrocytes with the same structure and functional capabilities as in humans. The researchers then looked at long-term potentiation (LTP)—the strengthening of synaptic connections and a key mechanism underlying learning—in the hippocampus, and found that it was significantly enhanced in mice with human GPCs compared with normal mice and mice engrafted with mouse GPCs. Goldman and colleagues also assessed the performance of the mice on several behavioral tasks that measure leaning and memory—including auditory fear conditioning, a maze test, and object-location memory—and found across the board that mice with human GPCs learned significantly more quickly than normal mice.
Via Luisa Meira
Coffee and citrus plants use caffeine to manipulate the memory of honeybees, a new study says. A cup of coffee doesn't just provide a jolt for people in the morning. Bees may crave a buzz too. Scientists have found that some plants, like the coffee plant (Coffea), use caffeine to manipulate the memory of bees. The nectar in their flowers holds low levels of caffeine that pollinators find highly rewarding.
Bitter-tasting caffeine primarily arose in plants as a toxic defense against herbivores like garden slugs. At high doses, caffeine can be toxic and repellent to pollinators. However, at low concentrations, caffeine appears to have a secondary advantage, attracting honeybees and enhancing their long-term memory, said lead author Geraldine Wright, a neuroscientist at Newcastle University in England, whose study was published online March 7 in the journal Science.
"We show that caffeine—a compound whose ecological role is mainly to deter and poison herbivores—actually acts like a drug in an ecologically relevant context," Wright said. "The plant is secretly drugging the pollinator. It may help the bee, but the plant cares more about having a pollinator with high fidelity!"
An international team of scientists has found that levels of a peptide called hypocretin increase when humans are happy but decrease when they are sad. The neurochemical changes underlying human emotions and social behaviour are largely unknown. A team of scientists now reports on the changes in the levels of two hypothalamic neuropeptides,hypocretin-1 and melanin-concentrating hormone (MCH), measured in the human amygdala. The team shows that hypocretin-1 levels are maximal during positive emotion, social interaction and anger, behaviors that induce cataplexy in human narcoleptics.
In contrast, MCH levels are minimal during social interaction, but are increased after eating. Both peptides are at minimal levels during periods of postoperative pain despite high levels of arousal. Melanin-concentrating hormone levels increase at sleep onset, consistent with a role in sleep induction, whereas hypocretin-1 levels increase at wake onset, consistent with a role in wake induction. Levels of these two peptides in humans are not simply linked to arousal, but rather to specific emotions and state transitions. Other arousal systems may be similarly emotionally specialized.
“The current findings explain the sleepiness of narcolepsy, as well as the depression that frequently accompanies this disorder,” said senior author Prof Jerome Siegel of the University of California Los Angeles’ Semel Institute for Neuroscience and Human Behavior. “The findings also suggest that hypocretin deficiency may underlie depression from other causes.” “Depression is the leading cause of psychiatric disability in the U.S,” Prof Siegel said. “More than 6 percent of the population is affected each year, with lifetime prevalence exceeding 15 percent. Yet the use of antidepressants, such as selective serotonin reuptake inhibitors (SSRIs), has not been based on evidence of a deficiency, or excess, of any neurotransmitter. Several recent studies have questioned whether SSRIs, as well as other depression-fighting drugs, are any more effective than placebos.”
Researchers in Japan successfully cloned 581 healthy mice from the same furry source. Remember Dolly the Sheep? Having started her life in a test tube in 1996, she was the first animal cloned by scientists using a somatic cell (as distinct, say from a germline cell, or “gamete,” like sperm and eggs). Dolly was beautiful. She was Scottish. Her mere existence was profound. It was also unusually short, at just six years. But scientists in Japan have now succeeded in cloning mice using the same technique that created Dolly with more or less perfect results: The mice are healthy, they live just as long as regular mice, and they’ve been flawlessly cloned and recloned from the same source to the 25th generation. Researchers claim it's the first example of seamless, repeat cloning using the Dolly method—known as “somatic cell nuclear transfer” (SCNT)—in which the nucleus from an adult source animal is transferred to an egg with its nucleus removed. Until recently, the process was fraught with failures and mutations. But the team led by Teruhiko Wakayama, whose results were published today in the journal Cell Stem Cell, was able to create 581 clones from the same original mouse. Scientists, including Dolly’s creator, have long felt the process was still too unstable—and too wasteful of precious eggs, given the failure rate—to be used on humans any time soon. But perhaps it's not so far off, after all. Cue the Clone Wars fantasies. Cloning of this kind has been fraught with trouble since the beginning, though to be fair Dolly was an unequivocal success story, whose early demise was relatively inconclusive. To be sure, Dolly developed arthritis at the young age of four and died of a kind of lung cancer when she was not yet six. Most sheep like her live to about 11 or 12. But the cancer that killed her was caused by a common, contagious virus that is deadly to any sheep, her creators concluded. In other words, they claimed, Dolly’s death wasn’t specifically linked to her having been cloned. But Dolly had certain abnormalities that were indicative of the sorts of problems researchers would face using the SCNT method. With Dolly, the telomeres in her cells—which act a bit like “molecular clocks” for the length of time cells can effectively renew—were abnormally short. They were identical in length to the telomeres of the source sheep from which Dolly was cloned, which was six years-old. In other words, there’s a good chance she was never long for this world, with or without the cancer. The early-onset arthritis hinted as much, though according to the scientists who created her, the arthritis was never explained. Cloning experiments since then have produced varying results. In experiments with cattle, for example, some scientists found their clones’ telomeres had been restored to their original lengths. What seemed consistent, however, was that cloning successive generations from the same source—creating a clone of a clone, and so on—always led to some kind genetic degradation, worsening from one copy to the next. It’s thought that the genetic abnormalities we all possess simply worsened with each repeat. Cloning clones was like dubbing copies of copies of cassettes. Eventually, the copies were useless. In the case of animals, they always failed after just a few replications. Beginning in 2005, however, Wakayama and his team began adding trichostatin, a histone deacetylase inhibitor, to the medium used to facilitate the cell-cloning process. Doing so seems to have inhibited what the study’s authors describe as “accumulations of epigenetic or genetic abnormalities in the mice, even after repeated cloning.” We don’t know yet if the process holds up indefinitely, but the 25 generations the Japanese researchers have created so far is a pretty good start.
When it comes to harboring viruses deadly to humans, bats are grand champions. The flying mammals are the reservoir for everything from rabies (100% deadly) to Ebola. Now, scientists have found a new virus hosted by bats, one that doesn't seem to be able to cause disease in other animals. The discovery may provide clues to what enables some viruses to cause severe disease. The new Cedar virus is named after the little town of Cedar Grove in Queensland, Australia, where it was found in 2009. Australian scientists discovered it in the urine from bat colonies while screening for the Hendra virus. Hendra and its close viral cousin Nipah are henipaviruses that kill between 40% and 100% of all the animals and humans they infect, making them among the most deadly viruses known. In the laboratory, the team found that Cedar virus could infect ferrets and guinea pigs—the animals produced infection-fighting antibodies to the virus. However, mysteriously they did not become clinically ill at all. What's more, there are no recorded cases in humans. A genetic analysis revealed that the Cedar virus is also a henipavirus—but with one major key difference: Unlike other henipaviruses, the Cedar virus does not produce what is called a "V protein". The V protein gives the Hendra and Nipah viruses the ability to evade the human immune system, making them deadly to most hosts. By comparing the lethal and benign henipaviruses, "We may gain insights into what makes Hendra so dangerous," says molecular virologist Glenn Marsh of the Australian Animal Health Laboratory in Geelong. The team's focus on the V protein is "intriguing, and deserves to be followed up," says Benhur Lee, a microbiologist at the University of California, Los Angeles, David Geffen School of Medicine. Marsh says his team plans to conduct follow up experiments. "Using genetic engineering it may be possible to modify the virus so it does produce the V protein or alternatively put the gene from Hendra virus into Cedar virus and see if that makes the virus pathogenic." Lee warns, however, that even if the V gene does help make henipaviruses so dangerous, it's probably not the only gene responsible.
Deep in water-filled underground caves beneath Australia's Nullarbor Plain, cave divers have discovered unusual 'curtains' of biological material – known as Nullarbor cave slimes. An unusual combination of microbes thrive in the Weebubbie caves. "Earlier studies on the community suggested that there was an unusual chemistry going on in the caves, but we didn't know how the microbes were making a living in the cave environment," says the lead scientist Professor Ian Paulsen, Macquarie University. In order to find this 'missing link', the team of researchers made use of a range of new technologies, such next-generation sequencing of environmental DNA and scanning electron microscopy to take an in-depth look at the composition of the Weebubbie cave slime community. This approach detected a dominant group of organisms in the cave slimes, known as the Thaumarchaeota. This community of microbes thrives in the total dark, independent of photosynthesis. It is thought that the periodic inundations of the Nullarbor caves by the sea occurred a number of times in the geological past and so researchers suggest that the Weebubbie Thaumarchaeota may have a marine origin. "We know that the Nullarbor Plain's karst system arose from the sea in the Middle Miocene period and so this may be a clue as to where the Weebubbie Thaumarchaeota came from," says Professor Paulsen The research team says this analysis shows that the organisms make up the Weebubbie cave slime community make their living in a very unusual way – by oxidizing ammonia in the salty cave water – and are completely independent of sunlight and ecosystems on the surface. "It just goes to show that life in the dark recesses of the planet comes in many strange forms, many of which are still unknown," says Professor Paulsen.
The flip of a single molecular switch helps create the mature neuronal connections that allow the brain to bridge the gap between adolescent impressionability and adult stability. Scientists have long known that the young and old brains are very different. Adolescent brains are more malleable or plastic, which allows them to learn languages more quickly than adults and speeds recovery from brain injuries. The comparative rigidity of the adult brain results in part from the function of a single gene that slows the rapid change in synaptic connections between neurons. The Nogo Receptor 1 gene is required to suppress high levels of plasticity in the adolescent brain and create the relatively quiescent levels of plasticity in adulthood. In mice without this gene, juvenile levels of brain plasticity persist throughout adulthood. When researchers blocked the function of this gene in old mice, they reset the old brain to adolescent levels of plasticity. "These are the molecules the brain needs for the transition from adolescence to adulthood," said Stephen Strittmatter. Vincent Coates Professor of Neurology, Professor of Neurobiology and senior author of the paper. "It suggests we can turn back the clock in the adult brain and recover from trauma the way kids recover." Rehabilitation after brain injuries like strokes requires that patients re-learn tasks such as moving a hand. Researchers found that adult mice lacking Nogo Receptor recovered from injury as quickly as adolescent mice and mastered new, complex motor tasks more quickly than adults with the receptor. "This raises the potential that manipulating Nogo Receptor in humans might accelerate and magnify rehabilitation after brain injuries like strokes," said Feras Akbik, Yale doctoral student who is first author of the study. Researchers also showed that Nogo Receptor slows loss of memories. Mice without Nogo receptor lost stressful memories more quickly, suggesting that manipulating the receptor could help treat post-traumatic stress disorder. "We know a lot about the early development of the brain," Strittmatter said, "But we know amazingly little about what happens in the brain during late adolescence."
Building on earlier pioneering work by researchers at the University of California, San Diego, an international consortium of university researchers has produced the most comprehensive virtual reconstruction of human metabolism to date. Scientists could use the model, known as Recon 2, to identify causes of and new treatments for diseases like cancer, diabetes and even psychiatric and neurodegenerative disorders. Each person’s metabolism, which represents the conversion of food sources into energy and the assembly of molecules, is determined by genetics, environment and nutrition. Doctors have long recognized the importance of metabolic imbalances as an underlying cause of disease, but scientists have been ramping up their research on the connection as a result of compelling evidence enabled by the Human Genome Project and advances in systems biology, which leverages the power of high-powered computing to build vast interactive databases of biological information. “Recon 2 allows biomedical researchers to study the human metabolic network with more precision than was ever previously possible. This is essential to understanding where and how specific metabolic pathways go off track to create disease,” said Bernhard Palsson, Galletti Professor of Bioengineering at UC San Diego Jacobs School of Engineering. “It’s like having the coordinates of all the cars in town, but no street map. Without this tool, we don’t know why people are moving the way they are,” said Palsson. He likened Recon 2 to Google mapping for its ability to merge complex details into a single, interactive map. For example, researchers looking at how metabolism sets the stage for cancerous tumor growth could zoom in on the “map” for finely detailed images of individual metabolic reactions or zoom out to look at patterns and relationships among pathways or different sectors of metabolism. This is not unlike how you can get a street view of a single house or zoom out to see how the house fits into the whole neighborhood, city, state, country and globe. And just as Google maps brings together a broad set of data – such as images, addresses, streets and traffic flow – into an easily navigated tool, Recon 2 pulls together a vast compendium of data from published literature and existing models of metabolic processes. Recon 2 is already proving its utility, according to Ines Thiele, a professor at the University of Iceland and UC San Diego alumna, who led the Recon 2 effort. Thiele earned her Ph.D. in bioinformatics as a student of Palsson’s and was part of the original Recon 1 team. Thiele said Recon 2 has successfully predicted alterations in metabolism that are currently used to diagnose certain inherited metabolic diseases. “The use of this foundational resource will undoubtedly lead to a myriad of exciting predictions that will accelerate the translation of basic experimental results into clinical applications,” said Thiele. “Ultimately, I envision it being used to personalize diagnosis and treatment to meet the needs of individual patients. In the future, this capability could enable doctors to develop virtual models of their patients’ individual metabolic networks and identify the most efficacious treatment for various diseases including diabetes, cancer and neurodegenerative diseases.” As much as Recon 2 marks a significant improvement over Recon 1, there is still much work to be done, according to the research team. Thiele said Recon 2 accounts for almost 1,800 genes of an estimated 20,000 protein-coding genes in the human genome. “Clearly, further community effort t will be required to capture chemical interactions with and between the rest of the genome,” she said.
A new experiment simulating conditions in deep space reveals that the complex building blocks of life could have been created on icy interplanetary dust and then carried to Earth, jump-starting life. Chemists from the University of California, Berkeley, and the University of Hawaii, Manoa, showed that conditions in space are capable of creating complex dipeptides – linked pairs of amino acids – that are essential building blocks shared by all living things. The discovery opens the door to the possibility that these molecules were brought to Earth aboard a comet or possibly meteorites, catalyzing the formation of proteins (polypeptides), enzymes and even more complex molecules, such as sugars, that are necessary for life. “It is fascinating to consider that the most basic biochemical building blocks that led to life on Earth may well have had an extraterrestrial origin,” said UC Berkeley chemist Richard Mathies, coauthor of a paper published online last week and scheduled for the March 10, 2013 print issue of The Astrophysical Journal. While scientists have discovered basic organic molecules, such as amino acids, in numerous meteorites that have fallen to Earth, they have been unable to find the more complex molecular structures that are prerequisites for our planet’s biology. As a result, scientists have always assumed that the really complicated chemistry of life must have originated in Earth’s early oceans. In an ultra-high vacuum chamber chilled to 10 degrees above absolute zero (10 Kelvin), Seol Kim and Ralf Kaiser of the Hawaiian team simulated an icy snowball in space including carbon dioxide, ammonia and various hydrocarbons such as methane, ethane and propane. When zapped with high-energy electrons to simulate the cosmic rays in space, the chemicals reacted to form complex, organic compounds, specifically dipeptides, essential to life. At UC Berkeley, Mathies and Amanda Stockton then analyzed the organic residues through the Mars Organic Analyzer, an instrument that Mathies designed for ultrasensitive detection and identification of small organic molecules in the solar system. The analysis revealed the presence of complex molecules – nine different amino acids and at least two dipeptides – capable of catalyzing biological evolution on earth.
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