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A new toad from the ”warm valleys” of Peruvian Andes

A new species of toad was discovered hiding in the leaf litter of the Peruvian Yungas. The word is used widely by the locals to describe ecoregion of montane rainforests, and translates as “warm valley” in English. The new species Rhinella yunga was baptized after its habitat preference. The study was published in the open access journal ZooKeys. Like many other toads of the family Bufonidae the new species Rhinella yunga has a cryptic body coloration resembling the decaying leaves in the forest floor (“dead-leaf pattern”), which is in combination with expanded cranial crests and bony protrusions cleverly securing perfect camouflage. The different colors and shapes within the same species group however make the traditional morphological methods of taxonomic research hard to use to identify the real species diversity within the family. Nevertheless, Rhinella yunga is distinct from all related species in absence of a tympanic membrane, a round membranous part of hearing organ being normally visible on both sides of a toad’s head. “It appears that large number of still unnamed cryptic species remains hidden under some nominal species of the Rhinella margaritifera species group,” explains Dr Jiří Moravec, National Museum Prague, Czech Republic.

Among the other interesting characteristics of the true toads from the family Bufonidae are a typical warty, robust body and a pair of large poison excreting parotid glands on the back of their heads. The poison is excreted by the toads when stressed as a protective mechanism. Some toads, like the cane toad Rhinella marina, are more toxic than others. Male toads also possess a special organ, which after removing of testes becomes an active ovary and the toad, in effect, becomes female.

http://www.sciencedaily.com/  Science Daily February 4, 2014

http://www.sciencedaily.com/releases/2014/01/140117104033.htm  Original web page at Science Daily

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Early-life exposure of frogs to herbicide increases mortality from fungal disease

The combination of the herbicide atrazine and a fungal disease is particularly deadly to frogs, shows new research from a University of South Florida laboratory, which has been investigating the global demise of amphibian populations. USF Biologist Jason Rohr said the new findings show that early-life exposure to atrazine increases frog mortality but only when the frogs were challenged with a chytrid fungus, a pathogen implicated in worldwide amphibian declines. The research is published in the new edition of Proceedings of the Royal Society B. “Understanding how stressors cause enduring health effects is important because these stressors might then be avoided or mitigated during formative developmental stages to prevent lasting increases in disease susceptibility,” Rohr said. The study was conducted by Rohr and Lynn Martin, Associate Professors of USF’s Department of Integrative Biology; USF researchers Taegan McMahon and Neal Halstead; and colleagues at the University of Florida, Oakland University, and Archbold Biological Station. Their experiments showed that a six-day exposure to environmentally relevant concentrations of atrazine, one of the most common herbicides in the world, increased frog mortality 46 days after the atrazine exposure, but only when frogs were challenged with the chytrid fungus. This increase in mortality was driven by a reduction in the frogs’ tolerance of the infection.

Moreover, the researchers found no evidence of recovery from the atrazine exposure and the atrazine-induced increase in disease susceptibility was independent of when the atrazine exposure occurred during tadpole development. “These findings are important because they suggest that amphibians might need to be exposed only to atrazine briefly as larvae for atrazine to cause persistent increases in their risk of chytri-induced mortality,” Rohr said. “Our findings suggest that reducing early-life exposure of amphibians to atrazine could reduce lasting increases in the risk of mortality from a disease associated with worldwide amphibian declines.” Until this study, scientists knew little about how early-life exposure to stressors affected the risk of infectious diseases for amphibians later in life. “Identifying which, when, and how stressors cause enduring effects on disease risk could facilitate disease prevention in wildlife and humans, an approach that is often more cost-effective and efficient than reactive medicine,” Rohr said. The findings are also the latest chapter in research Rohr and his lab has conducted on the impact of atrazine on amphibians. These findings are consistent with earlier studies that concluded that, while the chemical typically does not directly kill amphibians and fish, there is consistent scientific evidence that it negatively impacts their biology by affecting their growth and immune and endocrine systems.

Science Daily
November 12, 2013

Original web page at Science Daily

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Frogs that hear with their mouth: X-rays reveal a new hearing mechanism for animals without an ear

Gardiner’s frogs from the Seychelles islands, one of the smallest frogs in the world, do not possess a middle ear with an eardrum yet can croak themselves, and hear other frogs. An international team of scientists using X-rays has now solved this mystery and established that these frogs are using their mouth cavity and tissue to transmit sound to their inner ears The results are published in the Proceedings of the National Academy of Sciences on September 2, 2013. The team led by Renaud Boistel from CNRS and University of Poitiers, comprised also scientists from Institut Langevin of ESPCI ParisTech, the Laboratoire de Mécanique et d’Acoustique in Marseilles, the Institute of Systems and Synthetic Biology at the University of Evry (France), the Nature Protection Trust of Seychelles, and the European Synchrotron ESRF in Grenoble. The way sound is heard is common to many lineages of animals and appeared during the Triassic age (200-250 million years ago). Although the auditory systems of the four-legged animals have undergone many changes since, they have in common the middle ear with eardrum and ossicles, which emerged independently in the major lineages. On the other hand, some animals notably most frogs, do not possess an outer ear like humans, but a middle ear with an eardrum located directly on the surface of the head. Incoming sound waves make the eardrum vibrate, and the eardrum delivers these vibrations using the ossicles to the inner ear where hair cells translate them into electric signals sent to the brain. Is it possible to detect sound in the brain without a middle ear? The answer is no because 99.9% of a sound wave reaching an animal is reflected at the surface of its skin.

“However, we know of frog species that croak like other frogs but do no have tympanic middle ears to listen to each other. This seems to be a contradiction,” says Renaud Boistel from the IPHEP of the University of Poitiers and CNRS. “These small animals, Gardiner’s frogs, have been living isolated in the rainforest of the Seychelles for 47 to 65 million years, since these islands split away from the main continent. If they can hear, their auditory system must be a survivor of life forms on the ancient supercontinent Gondwana.” To establish whether these frogs actually use sound for communicate with each other, the scientists set up loudspeakers in their natural habitat and broadcast pre-recorded frog songs. This caused males present in the rainforest to answer, proving that they were able to hear the sound from the loudspeakers. The next step was to identify the mechanism by which these seemingly deaf frogs were able to hear sound. Various mechanisms have been proposed: an extra-tympanic pathway through the lungs, muscles which in frogs connect the pectoral girdle to the region of the inner ear, or bone conduction. “Whether body tissue will transport sound or not depends on its biomechanical properties. With X-ray imaging techniques here at the ESRF, we could establish that neither the pulmonary system nor the muscles of these frogs contribute significantly to the transmission of sound to the inner ears,” says Peter Cloetens, a scientist at the ESRF who took part in the study. “As these animals are tiny, just one centimetre long, we needed X-ray images of the soft tissue and the bony parts with micrometric resolution to determine which body parts contribute to sound propagation.”

Numerical simulations helped to investigate the third hypothesis, that the sound was received through the frog’s heads. These simulations confirmed that the mouth acts as a resonator, or amplifier, for the frequencies emitted by this species. Synchrotron X-ray imaging on different species showed that the transmission of the sound from the oral cavity to the inner ear has been optimized by two evolutionary adaptations: a reduced thickness of the tissue between the mouth and the inner ear and a smaller number of tissue layers between the mouth and the inner ear. “The combination of a mouth cavity and bone conduction allows Gardiner’s frogs to perceive sound effectively without use of a tympanic middle ear,” concludes Renaud Boistel.

Science Daily
September 17, 2013

Original web page at Science Daily

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Salamanders under threat from deadly skin-eating fungus

A new species of fungus that eats amphibians’ skin has ravaged the fire salamander population in the Netherlands, bringing it close to regional extinction. Fire salamanders, recognisable by their distinctive yellow and black skin patterns, have been found dead in the country’s forests since 2010. The population has fallen to around 10 individuals, less than four per cent of its original level, but what has been killing them has been a mystery until now. Scientists from Ghent University, Imperial College London, Vrije Universiteit Brussel and the Dutch conservation group Ravon have isolated a new species of fungus from the dead animals and found that it can rapidly kill fire salamanders. They have named the fungus Batrachochytrium salamandrivorans, the second part meaning “salamander-eating,” and report their findings today in the Proceedings of the National Academy of Sciences. Fungi are increasingly recognised as important threats to biodiversity. A species related to the new fungus, Batrachochytrium dendrobatidis (Bd), has plagued amphibian populations across the globe and is thought to have wiped out more than 200 species worldwide. It causes the disease chytridiomycosis, which the International Union for the Conservation of Nature has called the single most devastating infectious disease in vertebrate animals.

The study’s lead author, Professor An Martel from the University of Ghent, said: “In several regions, including northern Europe, amphibians appeared to be able to co-exist with Bd. It is therefore extremely worrying that a new fungus has emerged that causes mass mortalities in regions where amphibian populations were previously healthy.” Co-author Professor Matthew Fisher, from Imperial College London, said: “It is a complete mystery why we are seeing this outbreak now, and one explanation is that the new salamander-killing fungus has invaded the Netherlands from elsewhere in the world. We need to know if this is the case, why it is so virulent, and what its impact on amphibian communities will be on a local and global scale. Our experience with Bd has shown that fungal diseases can spread between amphibian populations across the world very quickly. We need to act urgently to determine what populations are in danger and how best to protect them.” The fungus can be passed between salamanders by direct contact, and possibly by indirect contact although this hasn’t been proven. It invades the animal’s skin, eventually destroying it completely. In tests, the fungus was not able to infect midwife toads, which have been threatened by chytridiomycosis, but whether other species might be vulnerable is unknown. The scientists have brought surviving salamanders into captivity to protect the remaining population in the Netherlands. To aid further studies, they have also developed a diagnostic tool that enables the new fungus to be quickly identified. They tested 100 salamanders from Belgium, where the population has remained healthy, but so far there is no sign that the fungus has spread beyond the Netherlands.

Science Daily
September 17, 2013

Original web page at Science Daily

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How ‘teamwork’ between egg and sperm works: Little-known protein identified in vertebrate fertilization process

Researchers from Heidelberg have decoded a previously unknown molecular mechanism in the fertilisation process of vertebrates. The team of scientists at the Center for Molecular Biology of Heidelberg University identified a specific protein in frog egg extracts that the male basal bodies need, but that is produced only by the reproductive cells of the female. This “teamwork” between the egg and sperm is what makes embryo development possible. The results of the research were published in The Journal of Cell Biology. Several years ago Prof. Dr. Oliver Gruß and his colleagues used sensitive mass spectrometry to begin looking for protein materials that were newly synthesised during meiosis, as new egg cells were formed, thus making cell division efficient. In the process, they identified a previously little-known protein. The so-called synovial sarcoma X breakpoint protein (SSX2IP) is indeed formed during meiosis, but not required for it. “At first we were at a loss to explain the function of SSX2IP,” says Dr. Felix Bärenz, a member of Oliver Gruß’ working group. The breakthrough came when the researchers went one step further, simulating fertilisation of the frog’s egg in the test tube.

It was then they discovered that the SSX2IP produced after fertilisation and penetration of the egg by the sperm reanimated the basal bodies of the sperm. Because the egg loses its basal bodies as it matures, the reactivation of the male’s basal bodies is vital for the embryo’s development. They, in turn, build the embryo’s division apparatus — the mitotic spindles — without whose precise function continued cell division and successful embryo development would be impossible. “In a cell culture, we were also able to prove that SSX2IP plays a similar role in human cells,” explains Prof. Gruß. Without the human SSX2IP protein, obvious errors occurred in the function of division apparatus. “It’s therefore quite conceivable that defects in SSX2IP synthesis during human egg maturation could lead to infertility or embryonic deformities,” surmises the Heidelberg biochemist.

Science Daily
September 3, 2013

Original web page at Science Daily

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Bullfrogs may help spread deadly amphibian fungus, but also die from it

Amphibian populations are declining worldwide and a major cause is a deadly fungus thought to be spread by bullfrogs, but a two-year study shows they can also die from this pathogen, contrary to suggestions that bullfrogs are a tolerant carrier host that just spreads the disease. When researchers raised the frogs from eggs in controlled experimental conditions, they found at least one strain of this pathogen, Batrachochytrium dendrobatidis, also called Bd or a chytrid fungus, can be fatal to year-old juveniles. However, bullfrogs were resistant to one other strain that was tested. The findings, made by researchers at Oregon State University and the University of Pittsburgh, show that bullfrogs are not the sole culprit in the spread of this deadly fungus, and add further complexity to the question of why amphibians are in such serious jeopardy. About 40 percent of all amphibian species are declining or are already extinct, researchers say. Various causes are suspected, including this fungus, habitat destruction, climate change, pollution, invasive species, increased UV-B light exposure, and other forces. “At least so far as the chytrid fungus is involved, bullfrogs may not be the villains they are currently made out to be,” said Stephanie Gervasi, a zoology researcher in the OSU College of Science. “The conventional wisdom is that bullfrogs, as a tolerant host, are what helped spread this fungus all over the world. But we’ve now shown they can die from it just like other amphibians.”

The research suggests that bullfrogs actually are not a very good host for the fungus, which first was identified as a novel disease of amphibians in 1998. So why the fungus has spread so fast, so far, and is causing such mortality rates is still not clear. “One possibility for the fungal increase is climate change, which can also compromise the immune systems of amphibians,” said Andrew Blaustein, a distinguished professor of zoology at OSU and international leader in the study of amphibian declines. “There are a lot of possible ways the fungus can spread. People can even carry it on their shoes.” The average infection load of the chytrid fungus in bullfrogs, regardless of the strain, is considerably lower than that of many other amphibian species, researchers have found. Some bullfrogs can reduce and even get rid of infection in their skin over time. While adult bullfrogs may be carriers of some strains of Bd in some areas, the researchers concluded, different hosts may be as or more important in other locations. International trade of both amphibian and non-amphibian animal species may also drive global pathogen distribution, they said. The findings of this study were published in EcoHealth, a professional journal.

Science Daily
July 9, 2013

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An ‘extinct’ frog makes a comeback in Israel

The first amphibian to have been officially declared extinct by the International Union for Conservation of Nature (IUCN) has been rediscovered in the north of Israel after some 60 years and turns out to be a unique “living fossil,” without close relatives among other living frogs. The Hula painted frog was catalogued within the Discoglossus group when it was first discovered in the Hula Valley of Israel in the early 1940s. The frog was thought to have disappeared following the drying up of the Hula Lake at the end of the 1950s, and was declared extinct by the IUCN in 1996. As a result, the opportunity to discover more about this species’ history, biology and ecology was thought to have disappeared. However, a team of Israeli, German and French researchers now report in the scientific journal Nature Communications on an in-depth scientific analysis of this enigmatic amphibian. Based on new genetic analyses of rediscovered individuals and the morphologic analyses of extant and fossil bones, the conclusion is that the Hula frog differs strongly from its other living relatives, the painted frogs from northern and western Africa. Instead, the Hula frog is related to a genus of fossil frogs, Latonia, which were found over much of Europe dating back to prehistoric periods and has been considered extinct for about a million years, The results imply that the Hula painted frog is not merely another rare species of frog, but is actually the sole representative of an ancient clade of frogs (a group with a single common ancestor). Plans to reflood parts of the Hula Valley and restore the original swamp habitat are in place, which may allow expansion in population size and a secure future for the Hula painted frog.

Science Daily
June 25, 2013

Original web page at Science Daily

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Do salamanders’ immune systems hold the key to regeneration?

Salamanders’ immune systems are key to their remarkable ability to regrow limbs, and could also underpin their ability to regenerate spinal cords, brain tissue and even parts of their hearts, scientists have found. In research published today in the Proceedings of the National Academy of Sciences researchers from the Australian Regenerative Medicine Institute (ARMI) at Monash University found that when immune cells known as macrophages were systemically removed, salamanders lost their ability to regenerate a limb and instead formed scar tissue. Lead researcher, Dr James Godwin, a Fellow in the laboratory of ARMI Director Professor Nadia Rosenthal, said the findings brought researchers a step closer to understanding what conditions were needed for regeneration. “Previously, we thought that macrophages were negative for regeneration, and this research shows that that’s not the case — if the macrophages are not present in the early phases of healing, regeneration does not occur,” Dr Godwin said. “Now, we need to find out exactly how these macrophages are contributing to regeneration. Down the road, this could lead to therapies that tweak the human immune system down a more regenerative pathway.”

Salamanders deal with injury in a remarkable way. The end result is the complete functional restoration of any tissue, on any part of the body including organs. The regenerated tissue is scar free and almost perfectly replicates the injury site before damage occurred. “We can look to salamanders as a template of what perfect regeneration looks like,” Dr Godwin said. Aside from “holy grail” applications, such as healing spinal cord and brain injuries, Dr Godwin believes that studying the healing processes of salamanders could lead to new treatments for a number of common conditions, such as heart and liver diseases, which are linked to fibrosis or scarring. Promotion of scar-free healing would also dramatically improve patients’ recovery following surgery. There are indications that there is the capacity for regeneration in a range of animal species, but it has, in most cases been turned off by evolution. “Some of these regenerative pathways may still be open to us. We may be able to turn up the volume on some of these processes,” Dr Godwin said. “We need to know exactly what salamanders do and how they do it well, so we can reverse-engineer that into human therapies.”

Science Daily
June 11, 2013

Original web page at Science Daily

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Cannibal tadpoles key to understanding digestive evolution

A carnivorous, cannibalistic tadpole may play a role in understanding the evolution and development of digestive organs, according to research from North Carolina State University. These findings may also shed light on universal rules of organ development that could lead to better diagnosis and prevention of intestinal birth defects. NC State developmental biologist Nanette Nascone-Yoder, graduate student Stephanie Bloom and postdoc Cris Ledon-Rettig looked at Xenopus laevis (African clawed frog) and Lepidobatrachus laevis (Budgett’s frog) tadpoles. These frog species differ in diet and last shared a common ancestor about 110 million years ago. Like most tadpoles, Xenopus exist primarily on a diet of algae, and their long, simple digestive tracts are not able to process insects or proteins until they become adult frogs. Budgett’s is an aggressive species of frog which is carnivorous — and cannibalistic — in the tadpole stage. Nascone-Yoder knew that Budgett’s tadpoles had evolved shorter, more complex guts to digest protein much earlier in their development. She and her team exposed Xenopus embryos to molecules that inactivated a variety of genes to see if any might coax Xenopus to develop a more carnivore-like digestive tract. Remarkably, five molecules caused Xenopus tadpoles to develop guts that were closer in appearance to those of the Budgett’s tadpoles. Taking it one step further, Nascone-Yoder exposed Budgett’s frog embryos to molecules with opposite effects, and got tadpole guts that were closer to those of Xenopus.

“Essentially, these molecules are allowing us to tease apart the processes that play a key role in gut development,” Nascone-Yoder says. “Understanding how and why the gut develops different shapes and lengths to adapt to different diets and environments during evolution gives us insight into what types of processes can be altered in the context of human birth defects, another scenario in which the gut also changes its shape and function.” The researchers’ next steps include finding out whether the changes in these gut tubes were merely cosmetic, or if they also function (digest) differently. The findings appear in Evolution and Development.

Science Daily
May 28, 2013

Original web page at Science Daily

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The underground adventures of the Mediterranean frog Rana iberica

Do frogs live underground? The answer is yes, some amphibians, such as salamanders and frogs have been often reported to dwell in subterranean habitats, some of them completely adjusted to the life in darkness, and others just spending a phase of their lifecycle in an underground shelter. Up until 2010, however, no one suspected that the Mediterranean anuran frog Rana iberica — commonly known as Iberian brown frog and usually found in streams — also participates in underground adventures. A new study published in the open access journal Subterranean Biology confirms the first report of Rana iberica reproduction in a cave-like habitat, with all life stages observed in the galleries. Serra da Estrela Natural Park is located in north-central Portugal and is the largest protected area and one of the most biodiverse regions in Portugal and the Iberian Peninsula. Several drainage galleries were created for water capture in the 1950s, even before the establishment of the boundaries of the Natural Park. It is namely in these artificial subterranean habitats that the Iberian brown frog was discovered dwelling underground by biologists.

“The unusual sighting of R. iberica motivated a series of subsequent visits that started in 2011 up until December 2012 to understand the use of this artificial subterranean habitat by this species.,” explains the lead author of the study Dr. Gonçalo M. Rosa. “All life stages were observed in the gallery during the study period, particularly adults, which were observed every month of the year.” The Iberian brown frog does not only seek refuge in the drainage galleries as a sporadic visitor. During long observations, adults from the species have been noted in the galleries, often standing on the ground or in crevices, swimming underwater or even climbing up the walls. There is evidence of mating activity, and batches of eggs have been found stuck to submerged rocks in the subterranean stream. Recently hatched tadpoles were also observed, initially remaining stationary above the egg mass for about two weeks, then swimming in the streams and feeding on the dead egg mass. The galleries are used by other amphibians as well, and larvae of the fire salamander Salamandra salamandra gallaica have been recorded twice while preying on brown frog tadpoles.

The choice of the artificial drainage gallery for a habitat of the Iberian brown frog may appear odd initially. However, it seems that the animals find a refuge in the cool and humid tunnels, often containing a small stream. These artificial subterranean habitats are in fact often used as a refuge for many species. They are, for example, particularly important for the salamander Chioglossa lusitanica, an Iberian endemic of conservation concern. Scientists express their fear that such preferences for underground habitats might in fact be a sign for the ecological dangers of the dramatic climate changes experienced by the Iberian region. Monitoring the subterranean activity of various species might provide important cues for future conservation efforts.

Science Daily
May 14, 2013

Original web page at Science Daily

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Scientists produce cloned embryos of extinct frog

The genome of an extinct Australian frog has been revived and reactivated by a team of scientists using sophisticated cloning technology to implant a “dead” cell nucleus into a fresh egg from another frog species. The bizarre gastric-brooding frog, Rheobatrachus silus — which uniquely swallowed its eggs, brooded its young in its stomach and gave birth through its mouth — became extinct in 1983. But the Lazarus Project team has been able to recover cell nuclei from tissues collected in the 1970s and kept for 40 years in a conventional deep freezer. The “de-extinction” project aims to bring the frog back to life. In repeated experiments over five years, the researchers used a laboratory technique known as somatic cell nuclear transfer. They took fresh donor eggs from the distantly related Great Barred Frog, Mixophyes fasciolatus, inactivated the egg nuclei and replaced them with dead nuclei from the extinct frog. Some of the eggs spontaneously began to divide and grow to early embryo stage — a tiny ball of many living cells. Although none of the embryos survived beyond a few days, genetic tests confirmed that the dividing cells contain the genetic material from the extinct frog.

“We are watching Lazarus arise from the dead, step by exciting step,” says the leader of the Lazarus Project team, Professor Mike Archer, of the University of New South Wales, in Sydney. “We’ve reactivated dead cells into living ones and revived the extinct frog’s genome in the process. Now we have fresh cryo-preserved cells of the extinct frog to use in future cloning experiments. “We’re increasingly confident that the hurdles ahead are technological and not biological and that we will succeed. Importantly, we’ve demonstrated already the great promise this technology has as a conservation tool when hundreds of the world’s amphibian species are in catastrophic decline.” UNSW’s Professor Archer spoke publicly for the first time today about the Lazarus Project and also about his ongoing interest in cloning the extinct Australian thylacine, or Tasmanian tiger, at the TEDx DeExtinction event in Washington DC, hosted by Revive and Restore and the National Geographic Society. Researchers from around the world are gathered there to discuss progress and plans to ‘de-extinct’ other extinct animals and plants. Possible candidate species include the woolly mammoth, dodo, Cuban red macaw and New Zealand’s giant moa.

Science Daily
April 2, 2013

Original web page at Science Daily

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What do American bullfrogs eat when they’re away from home? Practically everything

American bullfrogs are native to eastern North America but have been transported by people to many other parts of the globe, and other parts of North America, where they have readily established populations and become an invasive alien menace to native ecosystems. In the largest study of its kind to date, the stomach contents of over 5,000 invasive alien American bullfrogs from 60 lakes and ponds on southern Vancouver Island were examined to identify the native and exotic animals that they had preyed upon. The study was published in the open access journal NeoBiota. Over 15 classes of animals were reported from a total of 18,814 identifiable prey remains, including terrestrial and aquatic insects, spiders, crayfish, fish, frogs, salamanders, newts, snakes, lizards, turtles, birds, and small mammals. The study examined the stomach contents of adults and juveniles of all size-classes, but excluded tadpoles. These results show that bullfrogs will attack and consume virtually any organism that is within reach and can be swallowed, including their own species.

Previous studies on bullfrog diet have examined relatively small numbers of stomachs from a comparatively small number of lakes and ponds. Our results reinforce the general consensus that there is good reason for concern about the ecological harm that uncontrolled populations of American bullfrogs might have, or are having, on populations of native species. For decades, bullfrogs have been transported and released around the world by prospective frog-farmers, pet owners, game managers, recreational fishermen, biological supply houses; and even by entrants in frog jumping contests. They adapt readily to a variety of habitats from the tropics to temperate zones and once established, their numbers grow fast with each adult female producing about 20,000 or more eggs per year. For these reasons, American bullfrogs are internationally recognized as one of the 100 worst invasive alien species in the world.

Science Daily
April 2, 2013

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Parallels in amphibian and bat declines from pathogenic fungi

Pathogenic fungi have substantial effects on global biodiversity, and 2 emerging pathogenic species—the chytridiomycete Batrachochytrium dendrobatidis, which causes chytridiomycosis in amphibians, and the ascomycete Geomyces destructans, which causes white-nose syndrome in hibernating bats—are implicated in the widespread decline of their vertebrate hosts. We synthesized current knowledge for chytridiomycosis and white-nose syndrome regarding disease emergence, environmental reservoirs, life history characteristics of the host, and host–pathogen interactions. We found striking similarities between these aspects of chytridiomycosis and white-nose syndrome, and the research that we review and propose should help guide management of future emerging fungal diseases.

Fungi and fungus-like organisms have been recognized historically as prominent plant pathogens that can have detrimental effects on agricultural crops and wild flora. Fisher et al. recently reviewed the increasing role and recognition of pathogenic fungi that affect global biodiversity. Their analyses showed that most (91%) recent extinctions and extirpations caused by fungal disease have affected animals rather than plants. In particular, 2 emerging pathogenic fungi—the chytridiomycete Batrachochytrium dendrobatidis, which causes chytridiomycosis in amphibians, and the ascomycete Geomyces destructans, which causes white-nose syndrome (WNS) in hibernating bats—are implicated in the widespread decline of their vertebrate hosts. In general, increased global biosecurity and monitoring are recommended to prevent and manage emerging fungal diseases, but there are also pressing research needs that can help specifically address these 2 devastating pathogenic fungi. We call attention to parallels between chytridiomycosis and WNS and highlight areas where urgent research is required. Comparison of these diseases also illustrates broader themes and questions that can be used to direct research on future emerging fungal diseases.

Emerging Infectious Diseases
March 19, 2013

Original web page at Emerging Infectious Diseases

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Eyes work without connection to brain: Ectopic eyes function without natural connection to brain

For the first time, scientists have shown that transplanted eyes located far outside the head in a vertebrate animal model can confer vision without a direct neural connection to the brain. Biologists at Tufts University School of Arts and Sciences used a frog model to shed new light — literally — on one of the major questions in regenerative medicine, bioengineering, and sensory augmentation research. “One of the big challenges is to understand how the brain and body adapt to large changes in organization,” says Douglas J. Blackiston, Ph.D., first author of the paper “Ectopic Eyes Outside the Head in Xenopus Tadpoles Provide Sensory Data For Light-Mediated Learning,” in the February 27 issue of the Journal of Experimental Biology. “Here, our research reveals the brain’s remarkable ability, or plasticity, to process visual data coming from misplaced eyes, even when they are located far from the head.” Blackiston is a post-doctoral associate in the laboratory of co-author Michael Levin, Ph.D., professor of biology and director of the Center for Regenerative and Developmental Biology at Tufts University.

Levin notes, “A primary goal in medicine is to one day be able to restore the function of damaged or missing sensory structures through the use of biological or artificial replacement components. There are many implications of this study, but the primary one from a medical standpoint is that we may not need to make specific connections to the brain when treating sensory disorders such as blindness.” In this experiment, the team surgically removed donor embryo eye primordia, marked with fluorescent proteins, and grafted them into the posterior region of recipient embryos. This induced the growth of ectopic eyes. The recipients’ natural eyes were removed, leaving only the ectopic eyes. Fluorescence microscopy revealed various innervation patterns but none of the animals developed nerves that connected the ectopic eyes to the brain or cranial region. To determine if the ectopic eyes conveyed visual information, the team developed a computer-controlled visual training system in which quadrants of water were illuminated by either red or blue LED lights. The system could administer a mild electric shock to tadpoles swimming in a particular quadrant. A motion tracking system outfitted with a camera and a computer program allowed the scientists to monitor and record the tadpoles’ motion and speed.

The team made exciting discoveries: Just over 19 percent of the animals with optic nerves that connected to the spine demonstrated learned responses to the lights. They swam away from the red light while the blue light stimulated natural movement. Their response to the lights elicited during the experiments was no different from that of a control group of tadpoles with natural eyes intact. Furthermore, this response was not demonstrated by eyeless tadpoles or tadpoles that did not receive any electrical shock. “This has never been shown before,” says Levin. “No one would have guessed that eyes on the flank of a tadpole could see, especially when wired only to the spinal cord and not the brain.” The findings suggest a remarkable plasticity in the brain’s ability to incorporate signals from various body regions into behavioral programs that had evolved with a specific and different body plan. “Ectopic eyes performed visual function,” says Blackiston. “The brain recognized visual data from eyes that impinged on the spinal cord. We still need to determine if this plasticity in vertebrate brains extends to different ectopic organs or organs appropriate in different species.” One of the most fascinating areas for future investigation, according to Blackiston and Levin, is the question of exactly how the brain recognizes that the electrical signals coming from tissue near the gut is to be interpreted as visual data.

Science Daily
March 19, 2013

Original web page at Science Daily

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Amphibian study shows how biodiversity can protect against disease

The richer the assortment of amphibian species living in a pond, the more protection that community of frogs, toads and salamanders has against a parasitic infection that can cause severe deformities, including the growth of extra legs, according to a new study by the University of Colorado Boulder. The findings, published Feb. 14 in the journal Nature, support the idea that greater biodiversity in larger-scale ecosystems, such as forests or grasslands, may also provide greater protection against diseases, including those that attack humans. For example, a larger number of mammal species in an area may curb cases of Lyme disease, while a larger number of bird species may slow the spread of West Nile virus. “How biodiversity affects the risk of infectious diseases, including those of humans and wildlife, has become an increasingly important question,” said Pieter Johnson, an assistant professor in the Department of Ecology and Evolutionary Biology and lead author of the study. “But as it turns out, solidly testing these linkages with realistic experiments has proven very challenging in most systems.”

Researchers have struggled to design comprehensive studies that could illuminate the possible connection between disease transmission and the number of species living in complex ecosystems. Part of the problem is simply the enormous number of organisms that may need to be sampled and the vast areas over which those organisms may roam. The new CU-Boulder study overcomes that problem by studying smaller, easier-to-sample ecosystems. Johnson and his team visited hundreds of ponds in California, recording the types of amphibians living there as well as the number of snails infected by the pathogen Ribeiroia ondatrae. Snails are an intermediate host used by the parasite during part of its life cycle. “One of the great challenges in studying the diversity-disease link has been collecting data from enough replicate systems to differentiate the influence of diversity from background ‘noise,’ ” Johnson said. “By collecting data from hundreds of ponds and thousands of amphibian hosts, our group was able to provide a rigorous test of this hypothesis, which has relevance to a wide range of disease systems.” Johnson’s team buttressed its field observations both with laboratory tests designed to measure how prone to infection each amphibian species is and by creating pond replicas outside using large plastic tubs stocked with tadpoles that were exposed to a known number of parasites. All of the experiments told the same story, Johnson said. Greater biodiversity reduced the number of successful amphibian infections and the number of deformed frogs.

In all, the CU-Boulder researchers spent three years sampling 345 wetlands and recording malformations — which include missing, misshapen or extra sets of hind legs — caused by parasitic infections in 24,215 amphibians. They also catalogued 17,516 snails. The results showed that ponds with half a dozen amphibian species had a 78 percent reduction in parasite transmission compared to ponds with just one amphibian species. The research team also set up experiments in the lab and outdoors using 40 artificial ponds, each stocked with 60 amphibians and 5,000 parasites. The reason for the decline in parasitic infections as biodiversity increases is likely related to the fact that ponds add amphibian species in a predictable pattern, with the first species to appear being the most prone to infection and the later species to appear being the least prone. For example, the research team found that in a pond with just one type of amphibian, that amphibian was almost always the Pacific chorus frog, a creature that is able to rapidly reproduce and quickly colonize wetland habitats, but which is also especially vulnerable to infection and parasite-induced deformities.

On the other hand, the California tiger salamander was typically one of the last species to be added to a pond community and also one of the most resistant to parasitic infection. Therefore, in a pond with greater biodiversity, parasites have a higher chance of encountering an amphibian that is resistant to infection, lowering the overall success rate of transmission between infected snails and amphibians. This same pattern — of less diverse communities being made up of species that are more susceptible to disease infection — may well play out in more complex ecosystems as well, Johnson said. That’s because species that disperse quickly across ecosystems appear to trade off the ability to quickly reproduce with the ability to develop disease resistance. This research reaches the surprising conclusion that the entire set of species in a community affects the susceptibility to disease,” said Doug Levey, program director in the National Science Foundation’s Division of Environmental Biology, which helped fund the research. “Biodiversity matters.” The sheer magnitude of the recent study also reinforces the connection between deformed frogs and parasitic infection, Johnson said. Beginning in the mid-1990s reports of frogs with extra, missing or misshapen legs skyrocketed, attracting widespread attention in the media and motivating scientists to try to figure out the cause. Johnson was among the researchers who found evidence of a link between infection with Ribeiroia and frog deformities, though the apparent rise in reports of deformations, and its underlying cause, remains controversial.

While the new study has implications beyond parasitic infections in amphibians, it does not mean that an increase in biodiversity always results in a decrease in disease, Johnson cautioned. Other factors also affect rates of disease transmission. For example, a large number of mosquitoes hatching in a particular year will increase the risk of contracting West Nile virus, even if there has been an increase in the biodiversity of the bird population. Birds act as “reservoir hosts” for West Nile virus, harboring the pathogen indefinitely with no ill effects and passing the pathogen onto mosquitoes. “Our results indicate that higher diversity reduces the success of pathogens in moving between hosts,” Johnson said. “Nonetheless, if infection pressure is high, for instance in a year with high abundance of vectors, there will still be a significant risk of disease; biodiversity will simply function to dampen transmission success.”

Science Daily
March 5, 2013

Original web page at Science Daily

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How tadpoles re-grow their tails: Implications for human healing

Scientists at The University of Manchester have made a surprising finding after studying how tadpoles re-grow their tails which could have big implications for research into human healing and regeneration. It is generally appreciated that frogs and salamanders have remarkable regenerative capacities, in contrast to mammals, including humans. For example, if a tadpole loses its tail a new one will regenerate within a week. For several years Professor Enrique Amaya and his team at The Healing Foundation Centre in the Faculty of Life Sciences have been trying to better understand the regeneration process, in the hope of eventually using this information to find new therapies that will improve the ability of humans to heal and regenerate better. In an earlier study, Professor Amaya’s group identified which genes were activated during tail regeneration. Unexpectedly, that study showed that several genes that are involved in metabolism are activated, in particular those that are linked to the production of reactive oxygen species (ROS) — chemically reactive molecules containing oxygen. What was unusually about those findings is that ROS are commonly believed to be harmful to cells.

Professor Amaya and his group decided to follow up on this unexpected result and their new findings will be published in the next issue of Nature Cell Biology. To examine ROS during tail regeneration, they measured the level of H2O2 (hydrogen peroxide, a common reactive oxygen species in cells) using a fluorescent molecule that changes light emission properties in the presence of H2O2. Using this advanced form of imaging, Professor Amaya and his group were able to show that a marked increase in H2O2 occurs following tail amputation and interestingly, they showed that the H2O2 levels remained elevated during the entire tail regeneration process, which lasts several days. Talking about the research Professor Amaya says: “We were very surprised to find these high levels of ROS during tail regeneration. Traditionally, ROS have been thought to have a negative impact on cells. But in this case they seemed to be having a positive impact on tail re-growth.” To assess how vital the presence of ROS are in the regeneration process, Professor Amaya’s team limited ROS production using two methods. The first was by using chemicals, including an antioxidant, and the second was by removing a gene responsible for ROS production. In both cases the regeneration process was inhibited and the tadpole tail did not grow back.

Professor Amaya says: “When we decreased ROS levels, tissue growth and regeneration failed to occur. Our research suggests that ROS are essential to initiate and sustain the regeneration response. We also found that ROS production is essential to activate Wnt signalling, which has been implicated in essentially every studied regeneration system, including those found in humans. It was also striking that our study showed that antioxidants had such a negative impact on tissue regrowth, as we are often told that antioxidants should be beneficial to health.” The publication of Professor Amaya’s study comes just days after a paper from the Nobel Prize winner and co-discoverer of the structure of DNA, James Watson, who has suggested antioxidants could be harmful to people in the later stages of cancer. Professor Amaya comments: “It’s very interesting that two papers suggesting that antioxidants may not always be beneficial have been published recently. Our findings and those of others are leading to a reversal in our thinking about the relative beneficial versus harmful effects that oxidants and antioxidants may have on human health, and indeed that oxidants, such as ROS, may play some important beneficial roles in healing and regeneration.”

Science Daily
February 5, 2013

Original web page at Science Daily

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Trade rules must be tightened to halt frog-killing fungus

Frogs are in trouble. In the 1990s researchers in Spain, Australia and Central America discovered that amphibians in rainforests and mountain lakes were dying in large numbers. The killer, it turned out, was chytridiomycosis, a disease caused by the fungus Batrachochytrium dendrobatidis (Bd), which has since been found around the world. Scientists have rushed to understand the disease, and have attempted different ways to mitigate its spread. But science alone is not sufficient. Mark Auliya, a herpetologist and trade-policy expert at the Helmholtz Centre for Environmental Research in Leipzig, Germany, says that policies have to change on an international level. Auliya is part of the European Union (EU) project Risk Assessment of Chytridiomycosis to European Amphibian Biodiversity (RACE), in which teams of scientists are each looking at different aspects of the disease: genetics, physiological and behavioural effects, and geography. RACE will end in 2013 and Auliya is preparing to make a raft of policy recommendations based on the project. He spoke to Nature about the compelling need for new animal-trade legislation.

Two or three years ago we had about 200 Bd-infected amphibian species and now we have more than 500. Bd is now distributed in more than 50 countries, on all continents that harbour amphibians. There are almost 7,000 amphibian species, but less than 3% are covered by the Convention on International Trade in Endangered Species of Wild Fauna and Flora (CITES). To control Bd in Europe there has to be a completely new EU-imposed comprehensive disease-control directive, which includes the regulation of all amphibian-trade activities across all entities that house or deal with amphibians. At this stage we cannot focus on specific species — we have to consider them all because potentially every amphibian species can have and spread the disease. There is nothing legislating against Bd in particular. CITES came into effect in the mid 1970s, intended to ensure that species as a whole are not harmed by trade activities. But that didn’t mean by spreading disease. CITES has now officially recognized the spread of diseases through trade activities or through the movement of wildlife. However, it also recognizes that the convention is not the major player in this.

We have hundreds of pet shops across Europe; we have hundreds of exotic-wildlife and reptile fairs; the frog-leg trade is another problem. But we have a lack of enforcement of existing trade regulations, and there are loopholes freely used by the consumers. We need standardized hygiene control. There must be something like an EU veterinary council imposing a single EU-wide hygiene and quarantine strategy to prevent spread of these diseases. We’re not looking at an improved law system, we’re looking at a completely revised law, which encompasses all these issues: trade, conservation of amphibian species and disease control. We also need harder sanctions on wildlife crime, which is still a trivial offence in most countries. What can scientists, such as those involved in RACE, add to the debate? The most striking result accomplished by the scientific community in the past year has been showing very clearly that global trade patterns have contributed to the spread of chytridiomycosis. We know that the global panzootic lineage of Bd has spread through trade activities. We also know that there are species that carry the disease but don’t necessarily die from it, such as the North American bullfrog (Rana catesbeiana), an invasive species that can adapt well to different habitats. There is an upcoming opportunity: the EU’s animal-health strategy is set to be renewed in 2013. Emerging infectious diseases have been put on the agenda, and RACE scientists have a chance to inform how the strategy deals with that. This will probably include wild species, disease control and trade issues. This revised law should ideally impose amphibian-trade regulations among the different stakeholders: the pet industry, biomedical research, zoos and aquaria.

Nature
June 26, 2012

Original web page at Nature

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Richer parasite diversity helps protect frogs from viruses that cause malformed limbs

Increases in the diversity of parasites that attack amphibians cause a decrease in the infection success rate of virulent parasites, including one that causes malformed limbs and premature death, says a new University of Colorado Boulder study. According to CU-Boulder Assistant Professor Pieter Johnson, scientists are concerned about how changes in biodiversity affect the risk of infectious diseases in humans and wildlife. Charting the relationships between parasites and amphibians is important since few studies have examined the influence of parasite diversity on disease, and the fact that amphibians are declining faster than any group of animals on the planet due to human activities like habitat loss, pollution and emerging diseases, Johnson said. In the new study, the team sampled 134 California ponds for the parasites, known as trematodes, comparing their abundance and distribution with the health of more than 2,000 Pacific chorus frogs. The CU team combined the field studies with extensive lab experiments that charted the health of the frogs in the presence of different combinations of the six most common amphibian parasites, including the Ribeiroia group whose larvae burrow into tadpole limb regions and form cysts that disrupt normal frog and toad leg development, causing extra or missing limbs.

The new study showed when the chorus frogs were exposed to all six trematode types simultaneously, the infection success rate was 42 percent lower than for frogs exposed to only a single species of parasite. “Our results show increases in parasite diversity consistently cause a decrease in infection success by the most virulent parasite,” said Johnson of the ecology and evolutionary biology department. A paper by Johnson and co-author Jason Hoverman, a CU-Boulder postdoctoral researcher, appears in this week’s issue of the Proceedings of the National Academy of Sciences. The project was funded by grants from the National Science Foundation and a David and Lucile Packard Foundation fellowship awarded to Johnson in 2008.While the six parasites used in the study are responsible for about 95 percent of trematode infections in the wild, most of the world’s parasites cause limited damage to host individuals, said Johnson. In the PNAS study, only two parasites, Ribeiroia and a parasite group called Echinostoma — which can trigger amphibian mortality — were known to be particularly dangerous to their host species. The primary study results support the idea that higher biodiversity can help protect against certain diseases, but few previous studies had considered the diversity of the parasites themselves. Because many parasites compete with each other, ecological systems richer in parasites can act as a buffer against virulent pathogens. Johnson said the combination of extensive field and lab work helped strengthen the study results.

One surprising study finding was that under certain conditions, increases in parasite diversity could increase or decrease host disease. In that aspect of the study, the infection rates were dependent on the order in which the six parasite species were added to the habitats of the frogs, and whether newly added parasite species replaced other parasites or were added alongside them, he said. If a dangerous parasite is first on the scene, it tends to be replaced when less dangerous species are added, decreasing the odds of host disease. But if a dangerous parasite species is added to an environment already harboring parasites, the study showed either a neutral effect or an increase in disease, Johnson said. “Collectively, our findings illustrate the importance of considering the hidden role of parasite diversity in affecting disease risk,” said Johnson. “While our study was on amphibian diseases, there is ample evidence to suggest similar processes can be occurring in humans and other groups of animals.” Recent studies also have shown similar relationships between host diversity and the risk of disease in some plants, mammals, birds and coral. A decrease in vertebrate host species for ticks carrying Lyme disease, for example, can increase the risk of Lyme disease in humans, said Johnson. “It could be that the most dangerous parasites occur in greater numbers in disturbed environments,” said Hoverman, who recently accepted a position as assistant professor at Purdue University’s forestry and natural resources department. “If we are trying to minimize disease risk in humans or in threatened groups of animals like amphibians, studies like this will be able to tell us which scenarios are most likely to occur.”

The new study has implications for declining biodiversity being seen across the planet as a result of human activities, including amphibians, said Johnson. Roughly 40 percent of amphibian species around the world are in decline, and more than 200 have gone extinct since the 1970s, some as a result of the often-fatal chytrid fungus that infects amphibian skin. Some scientists argue that rapid global amphibian decline seen today is driving the next great mass extinction event, he said. Trematodes have a complex life cycle that involve snails, amphibians and predators. Host snails release parasite larvae in the water, infecting amphibians and causing deformities that include extra or missing legs. Deformed frogs and toads rarely survive long because of their susceptibility to predators like wading birds, which ingest them and later release trematodes that infect other snails, completing the life cycle. Deformed frogs first gained attention in the mid-1990s when a group of Minnesota schoolchildren discovered a pond where more than half of the leopard frogs had missing or extra limbs, said Johnson. Since then reports of deformed amphibians have been widespread in the United States, leading to speculation they were being caused by factors like pollution, increased ultraviolet radiation or parasitic infection.

A 2008 study by Johnson showed American toads who pal around with gray tree frogs reduce their chances of parasitic infections known to cause limb malformations because trematode larva that infect tree frog tadpoles are killed by the tadpoles’ immune systems. In 2007, Johnson led a study showing high levels of nutrients like nitrogen and phosphorus used in North American farming and ranching activities fuel trematode infections by elevating the abundance and reproduction of snail species that host the parasites.

Science Daily
June 12, 2012

Original web page at Science Daily 2012

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Deadly frog fungus at work in the wild

The fungal infection that has killed a record number of amphibians worldwide leads to deadly dehydration in frogs in the wild, according to a new study by University of California, Berkeley and San Francisco State University researchers. High levels of an aquatic fungus called Batrachochytrium dendrobatidis (Bd) disrupt fluid and electrolyte balance in wild frogs, the scientists say, severely depleting the frogs’ sodium and potassium levels and causing cardiac arrest and death. Their findings confirm what researchers have seen in carefully controlled lab experiments with the fungus, but SF State biologist Vance Vredenburg said the data from wild frogs provide a much better idea of how the disease progresses. “The mode of death discovered in the lab seems to be what’s actually happening in the field,” he said, “and it’s that understanding that is key to doing something about it in the future.” The study is published online by peer-reviewed journal PLoS ONE. At the heart of the new study are blood samples drawn from mountain yellow-legged frogs by Vredenburg, who is an assistant professor of biology at SF State, and colleagues in 2004, as the chytrid epidemic swept through the basins of the Sierra Nevada range. “It’s really rare to be able to study physiology in the wild like this, at the exact moment of a disease outbreak,” said UC Berkeley ecologist Jamie Voyles, the lead author of the study. Unfortunately, it is a study that can’t be duplicated, at least not in the Sierra Nevada. Frog populations there have been devastated by chytrid, declining by 95 percent after the fungus was first detected in 2004. “It’s been really sad to walk around the basins and think, ‘Wow, they’re really all gone,'” Vredenburg said. The chytrid fungus attacks an amphibian’s skin, causing it to become up to 40 times thicker in some instances. Since frogs depend on their skin to absorb water and essential electrolytes like sodium from their environment, Voyles and her colleagues knew that chytrid would disrupt fluid balance in the infected amphibians, but were surprised to find that electrolyte levels were much lower than anticipated for the Sierra Nevada sample. “It’s clear that this fungus has a profound effect in the wild,” Voyles said.

“Wildlife diseases can be just as devastating to our health and economy as agricultural and human diseases,” says Sam Scheiner, NSF program officer for EEID. “Bd has been decimating frog and salamander species worldwide, which may fundamentally disrupt natural systems. This study is an important advance in our understanding of the disease, a first step in finding a way to reduce its effects.” Scientists want to learn as much as they can about how chytrid affects wild amphibians, with the hope that these findings will lead to better treatments for the infection. For instance, Voyles said, the new study suggests that individual frogs being treated for the infection might benefit from having electrolyte supplementation in the advanced stages of the disease. Researchers like Vredenburg already are experimenting with different ways of treating individual frogs, such as applying antifungal therapies or inoculating the frogs with “probiotic” bacteria that produce a compound that kills the fungus. “The disease is not very hard to treat in the lab with antifungals. We know we can treat animals there,” Vredenburg said. “But in nature, the disease is still a moving target.”

It is still unclear exactly how chytrid spreads across a region, and which frogs might be susceptible to re-infection after treatment. Earlier this year, Vredenburg and colleagues published a paper showing that a common North American frog might be an important carrier of the infection. Chytrid has killed off more than 200 amphibian species across the globe, but Voyles said the new studies offer “sort of a glimmer of hope that it might be possible to do something to mitigate the loss of frogs in the field.”

Science Daily
May 15, 2012

Original web page at Science Daily

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Facial defects shown to self-repair

Developmental biologists at Tufts University have identified a “self-correcting” mechanism by which developing organisms recognize and repair head and facial abnormalities. This is the first time that such a mechanism has been reported for the face and the first time that this kind of flexible, corrective process has been rigorously analyzed through mathematical modeling. The research, reported in the May 2012 issue of the journal Developmental Dynamics, used a tadpole model to show that developing organisms are not genetically “hard-wired” with a set of pre-determined cell movements that result in normal facial features. Instead, the process of development is more adaptive and robust. Cell groups are able to measure their shape and position relative to other organs and perform the movements and remodeling needed to compensate for significant patterning abnormalities, the study shows. “A big question has always been, how do complex shapes like the face or the whole embryo put themselves together? We have found that when we created defects in the face experimentally, facial structures move around in various ways and mostly end up in their correct positions,” said Michael Levin, Ph.D., senior author on the paper and director of the Center for Regenerative and Developmental Biology in Tufts University’s School of Arts and Sciences. “This suggests that what the genome encodes ultimately is a set of dynamic, flexible behaviors by which the cells are able to make adjustments to build specific complex structures. If we could learn how to bioengineer systems that reliably self-assembled and repaired deviations from the desired target shape, regenerative medicine, robotics, and even space exploration would be transformed.”

Previous research had found self-correcting mechanisms in other embryonic processes — though never in the face — but such mechanisms had not been mathematically analyzed to understand the precise dynamics of the corrective process. “What was missing from previous studies — and to our knowledge had never been done in an animal model — was to precisely track those changes over time and quantitatively compare them,” said first author Laura Vandenberg, Ph.D., post-doctoral associate at the Center for Regenerative and Developmental Biology. Such an analysis is crucial in order to begin to understand what information is being generated and manipulated in order for a complex structure to rearrange and repair itself. Co-author with Levin and Vandenberg was Dany S. Adams, Ph.D. Adams is a research associate professor in the Department of Biology and a member of the center. The Tufts biologists induced craniofacial defects in Xenopus frog embryos by injecting specific mRNA into one cell at the two-cell stage of development; this resulted in abnormal structures on one side of the embryos. They then characterized changes in the shape and position of the craniofacial structures, such as jaws, branchial arches, eyes, otic capsules and olfactory pits, through “geometric morphometric analysis,” which measured positioning of a total of 32 landmarks on the top and bottom sides of the tadpoles.

Images of tadpoles taken at precise intervals showed that as they aged, the craniofacial abnormalities, or perturbations, became less apparent. This was particularly true for the jaws and branchial arches. Eye and nose tissue became more normal over time but varied in ability to achieve a completely expected shape and position. Changes in the shape and position of facial features are a normal part of development, as any baby animal shows. With age, faces elongate and eyes, nose and jaws move relative to each other. But the movement is normally slight. In contrast, the Tufts research team found that in tadpoles with severe malformations, the facial structures shifted dramatically in order to repair those malformations. It was, the researchers said, as if the system were able to recognize departures from the normal state and undertake corrective action that would not typically take place. “We were quite astounded to see that, long before they underwent metamorphosis and became frogs, these tadpoles had normal looking faces. Imagine the implications of an animal with a severe ‘birth defect’ that, with time alone, can correct that defect,” said Vandenberg.

These results, say the Tufts biologists, are consistent with an information exchange process in which a structure triangulates its distance and angle from a stable reference point. While further study is needed, the researchers propose that “pings” (information-containing signals) are exchanged between an “organizing center” — such as the brain and neural network — and individual craniofacial structures. The article points out that congenital malformations of craniofacial structures comprise a significant class of birth defects such as cleft lip, cleft palate and microphthalmia, affecting more than 1 in every 600 births. Demystifying the “face-fixing” mechanism by further research at the molecular level could inspire new approaches to correcting birth defects in humans. “Such understanding would have huge implications not only for repairing birth defects, but also for other areas of systems biology and complexity science. It could help us build hybrid bioengineered systems, for synthetic or regenerative biology, or entirely artificial robotic systems that can repair themselves after damage or reconfigure their own structure to match changing needs in a complex environment,” said Levin.

Science Daily
May 15, 2012

Original web page at Science Daily

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Athletic frogs have faster-changing genomes

Physically fit frogs have faster-changing genomes, says a new study of poison frogs from Central and South America. Stretches of DNA accumulate changes over time, but the rate at which those changes build up varies considerably between species, said author Juan C. Santos of the National Evolutionary Synthesis Center in Durham, North Carolina. In the past, biologists trying to explain why some species have faster-changing genomes than others have focused on features such as body size, generation time, fecundity and lifespan. According to one theory, first proposed in the 1990s, species with higher resting metabolic rates are likely to accumulate DNA changes at a faster rate, especially among cold-blooded animals such as frogs, snakes, lizards and fishes. But subsequent studies failed to find support for the idea. The problem with previous tests is that they based their measurements of metabolism on animals at rest, rather than during normal physical activity, Santos said. “Animals rarely just sit there,” Santos said. “If you go to the wild, you’ll see animals hunting, reproducing, and running to avoid being eaten. The energetic cost of these activities is far beyond the minimum amount of energy an animal needs to function.”

To test the idea, Santos scoured forests in Colombia, Ecuador, Venezuela, and Panama in search of poison frogs, subjecting nearly 500 frogs — representing more than 50 species — to a frog fitness test. He had the frogs run in a rotating plastic tube resembling a hamster wheel, and measured their oxygen uptake after four minutes of exercise. The friskiest frogs had aerobic capacities that were five times higher than the most sluggish species, and were able to run longer before they got tired. “Physically fit species are more efficient at extracting oxygen from each breath and delivering it to working muscles,” Santos said. To estimate the rate at which each species’ genome changed over time, he also reconstructed the poison frog family tree, using DNA sequences from fifteen frog genes. When he estimated the number of mutations, or changes in the DNA, for each species over time, a clear pattern emerged — athletic frogs tended to have faster-changing genomes. Santos tested for other factors as well, such as body and clutch sizes, but athletic prowess was the only factor that was consistently correlated with the pace of evolution.

Why fit frogs have faster-changing genomes remains a mystery. One possibility has to do with harmful molecules called free radicals, which increase in the body as a byproduct of exercise. During exercise, the circulatory system provides blood and oxygen to the tissues that are needed most — the muscles — at the expense of less active tissues, Santos explained. When physical activity has stopped, the rush of blood and oxygen when circulation is restored to those tissues produces a burst of free radicals that can cause wear and tear on DNA, eventually causing genetic changes that — if they affect the DNA of cells that make eggs or sperm — can be passed to future generations. Before you ditch your exercise routine, Santos offers some words of caution. The results don’t debunk the benefits of regular physical exercise, which is known to reduce the risk of cancer, heart disease, and diabetes. “What applies to cold-blooded animals such as poison frogs doesn’t necessarily apply to warm-blooded animals such as humans,” Santos said. The findings appeared in the April 10th issue of Molecular Biology and Evolution.

Science Daily
May 1, 2012

Original web page at Science Daily

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Deadly frog disease spreads through tolerant species

There is no point sending healthy animals out into the world if they’re just going to catch a deadly disease. Pacific tree frogs that can survive a normally lethal fungus infection are spreading it to species that cannot. Such “reservoir” species could threaten frogs released from captive breeding programmes. Between 2003 and 2010, the deadly chytrid fungus slashed the populations of two frog species in the Sierra Nevada, while populations of a third species – the Pacific tree frog (Pseudacris regilla) – held steady. That isn’t because the Pacific tree frogs avoided infection: two-thirds of the Sierra Nevada population carry the fungus, Vance Vredenburg of San Francisco State University has now found. That suggests they can tolerate infection and so could spread the pathogen to new areas. Conservationists are breeding threatened amphibians in captivity in the hope of eventually re-establishing them in the wild. But reintroductions will fail if there is a reservoir species nearby, Vredenburg warns. The solution may be to breed from frog populations already decimated by the chytrid fungus, says Matthew Fisher of Imperial College London. There is evidence that some frogs are evolving tolerance, and survivors from an affected population are more likely to have the vital genes. These frogs could be cross-bred with susceptible individuals, accelerating the spread of tolerance – although Fisher admits the approach will be expensive. Journal reference: PLoS One.

New Scientist
April 3, 2012

Original web page at New Scientist

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Why are there so many colors of poisonous frogs?

Hopping around in the Peruvian jungle, near the border with Brazil, is a menagerie of tiny poison dart frogs. Their wealth of colors and patterns—some have golden heads atop white-swirled bodies, others wear full-torso tattoos of black and neon-yellow stripes—act as the world’s worst advertisement to predators: Don’t eat me, I’m toxic. But why have so many designs evolved when a single one might do? Evolutionary biologist Mathieu Chouteau of the University of Montreal in Canada ventured into the rainforest to find out. He was on the trail of Ranitomeya imitator, a single species of poison dart frog that comes in about 10 different patterns. That variability should be confusing for predators, he says, because the warnings are supposed to be a message to them, and it would make more sense to give them only one design to keep track of.

To figure out what was going on, Chouteau enlisted his girlfriend’s help to make 3600 models of frogs, each 18 millimeters long. “It was, like, at least a month of working full-time,” he says. They pressed black clay into frog-shaped molds and painted each one in one of two patterns: yellow striped or reticulated, like a giraffe, with green lines. They also made brown frogs as a nontoxic-looking control. Then Chouteau packed the frogs in his carryon baggage and flew to Peru. The models represent the frogs that live in two different sites: one in the Amazonian lowland and one in a valley at about 500 meters above sea level. The two sites are separated by a high ridge. In one very long day at each site, Chouteau set out 900 of the frogs on leaves along narrow trails used by locals to hunt in the forest. For the next 3 days, he went back and checked them to see whether the soft clay recorded evidence of attacks by birds.

Birds mostly avoided the model that looked like the local frog, but they attacked the model that looked like the frog from the other site, Chouteau reports in the December issue of The American Naturalist. In the high valley, the land of the reticulated frogs, only 7.2% of the model frogs with the reticulated pattern were attacked, whereas 14.2% of the brown models and 26.6% of the yellow-striped models were attacked. The pattern was roughly reversed at the other site. And that helps explain the diversity of frogs in the rainforest, Chouteau says. Different frog patterns rule at different sites, and birds keep these designs going by weeding out any frogs that deviate from the norm. “This study shows quite nicely how, once you’ve got the diversity, it’s stabilized,” says Chris Jiggins, an evolutionary biologist at the University of Cambridge in the United Kingdom. But where the diversity comes from, he says, is “a bit of an outstanding question.” It’s possible that frogs with a particular pattern are somehow better suited to the environment where they live, but he thinks the differences more likely arise because of drift. Random changes in pattern get established and then keep evolving, making the frogs distinctive. “What’s actually kind of surprising is the birds are really going for these frogs,” he says. “You’d think, these frogs are so nasty, you wouldn’t go anywhere near a poison dart frog.” Maybe the rainforest is so diverse that it’s always worth trying something, even something brightly colored.

ScienceNow
November 15, 2011

Original web page at ScienceNow

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Researchers find genes that help frogs resist fungus

For several decades, the fungal pathogen Batrachochytrium dendrobatidis (Bd) has been decimating frogs, yet some populations and species have been able to resist the fatal disease, called chytridiomycosis. Now, for the first time, researchers have identified a genetic mechanism in lowland leopard frogs that makes some frogs resistant to Bd. Although many researchers have explored environmental and pathogenic factors that contribute to chytridiomycosis, this study complements those by specifically looking at host genetic factors that might play a role in resistance. The researchers discovered that variation in a gene associated with a frog’s ability to identify pathogens and initiate an immune response determined whether a frog resisted the disease. They also found evidence that one form of the gene that gives frogs immunity to chytridiomycosis has been positively selected in recent generations.

The findings offer hope that frogs may adapt to the disease, as long as their habitats are protected and their populations expand enough to diversify their gene pools. “This is the first demonstration that host genetics determine susceptibility to Bd,” said Anna Savage, the lead author of a paper published Sept. 26 in the Proceedings of the National Academy of Sciences, and a graduate student working in the lab of Kelly Zamudio, Cornell professor of ecology and evolutionary biology and the paper’s senior author. In this study, Savage reared lowland leopard frogs from five distinct populations in Arizona to a disease-free adulthood in the lab. She then infected them with a Bd strain that was new to all five populations. All frogs from three populations died. In the two remaining populations, seven frogs from each survived. Savage then analyzed immune system major histocompatibility complex (MHC) genes, which code for a molecule that binds to foreign pathogens and initiates an immune response in the host. Specifically, Savage sequenced MHC genes that control the regions of these molecules that bind, like a lock and key, to pathogens; if the molecule and Bd bind, the frog survives.

She found 33 distinct alleles (or forms of this MHC gene), showing large variability. Almost all of the frogs that had two forms of the gene (called heterozygotes) survived, while almost all of the frogs with only one form (homozygotes) died. Since Bd has many proteins that could be recognized by different MHC molecules, having more than one form of the MHC gene may have increased the survivors’ chances for binding to the pathogen. The researchers also found that one of the 33 gene variants, called allele Q, was only found among survivors. “The study shows that allele Q is a candidate resistance allele, and more broadly, heterozygous frogs had a higher chance of survival,” Savage said. She also found evidence for positive selection along the evolutionary lineage leading to allele Q, which provides hope that frogs will evolve and adapt to Bd if habitats are maintained. “This is one case where we have shown selection and adaptation for resistance to this particular disease. The hope is that we can detect this signal of evolved resistance to other species as well,” said Zamudio.

eBioNews
October 18, 2011

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Cellular laser microsurgery illuminates research in vertebrate biology

Using an ultrafast femtosecond laser, researchers at Tufts University in Medford, Mass., were able to label, draw patterns on, and remove individual melanocytes cells from a species of frog tadpole (Xenopus) without damaging surrounding cells and tissues. Melanocytes are the cells responsible for skin pigment; they also are descendants of a specific type of stem cell that has regenerative potential and other characteristics similar to some cancer cells. By precisely marking and ablating these cells, the researchers were able to track how melanocytes migrated and regenerated within a live organism. The researchers hope this technique will enable new avenues of research in wound repair, regenerative medicine, and cancer studies. The new method could also be used to study how certain organisms respond to spinal cord damage and how they are able to regenerate portions of their spinal cords.

According to the researchers, femtosecond lasers have already become important tools in biological studies because of the ability to affect highly localized tissues. The laser in their research, described in the August issue of the Optical Society’s (OSA) open access journal Biomedical Optics Express, operated at a wavelength of 800 nm, which more readily affected melanocytes while protecting surrounding tissues. This highly selective characteristic enabled the study of cells both on the surface of the skin and in deeper tissue.

Science Daily
September 6, 2011

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Deadly amphibian disease found in the last disease-free region of central America

Smithsonian scientists have confirmed that chytridiomycosis, a rapidly spreading amphibian disease, has reached a site near Panama’s Darien region. This was the last area in the entire mountainous neotropics to be free of the disease. This is troubling news for the Panama Amphibian Rescue and Conservation Project, a consortium of nine U.S. and Panamanian institutions that aims to rescue 20 species of frogs in imminent danger of extinction. Chytridiomycosis has been linked to dramatic population declines or even extinctions of amphibian species worldwide. Within five months of arriving at El Cope in western Panama, chytridiomychosis extirpated 50 percent of the frog species and 80 percent of individuals. “We would like to save all of the species in the Darien, but there isn’t time to do that now,” said Brian Gratwicke, biologist at the Smithsonian Conservation Biology Institute and international coordinator for the Panama Amphibian Rescue and Conservation Project. “Our project is one of a few to take an active stance against the probable extinction of these species. We have already succeeded in breeding three species in captivity. Time may be running out, but we are looking for more resources to take advantage of the time that remains.”

The Darien National Park is a World Heritage site and represents one of Central America’s largest remaining wilderness areas. In 2007, Doug Woodhams, a research associate at the Smithsonian Tropical Research Institute, tested 49 frogs at a site bordering the Darien. At that time, none tested positive for the disease. In January 2010, however, Woodhams found that 2 percent of the 93 frogs he tested were infected. “Finding chytridiomycosis on frogs at a site bordering the Darien happened much sooner than anyone predicted,” Woodhams said. “The unrelenting and extremely fast-paced spread of this fungus is alarming.” The Panama Amphibian Rescue and Conservation Project has already established captive assurance colonies in Panama of two priority species endemic to the Darien — the Pirre harlequin frog (Atelopus glyphus) and the Toad Mountain harlequin frog (A. certus). In addition, the Smithsonian’s National Zoo maintains an active breeding program for the Panamanian golden frog, which is Panama’s national animal. The Panamanian golden frog is critically endangered, according to the International Union for Conservation of Nature, and researchers have not seen them in the wild since 2008.

“We would like to be moving faster to build capacity,” Gratwicke said. “One of our major hurdles is fundraising to build a facility to house these frogs. Until we jump that hurdle, we’re limited in our capacity to take in additional species.” Nearly one-third of the world’s amphibian species are at risk of extinction. While the global amphibian crisis is the result of habitat loss, climate change and pollution, chytridiomycosis is at least partly responsible for the disappearances of 94 of the 120 frog species thought to have gone extinct since 1980. “These animals that we are breeding in captivity will buy us some time as we find a way to control this disease in the wild and mitigate the threat directly,” said Woodhams, who was the lead author of a whitepaper Mitigating Amphibian Disease: strategies to maintain wild populations and control chytridiomycosis. This paper, published in Frontiers in Zoology, systematically reviews disease-control tools from other fields and examines how they might be deployed to fight chytrid in the wild. One particularly exciting lead in the effort to find a cure is that anti-chytrid bacteria living on frog skin may have probiotics properties that protect their amphibian host from chytrid by secreting anti-fungal chemicals. Woodhams recently discovered that some Panamanian species with anti-chytrid skin bacteria transmit beneficial skin chemicals and bacteria to their offspring. The paper, Social Immunity in Amphibians: Evidence for Vertical Transmission of Innate Defenses, was published in Biotropica in May. “We are all working around the clock to find a cure,” Gratwicke said. “Woodhams’ discovery that defenses can indeed be transferred from parent to offspring gives us hope that if we are successful at developing a cure in the lab, we may find a way to use it to save wild amphibians.”

Science Daily
June 28, 2011

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Global catastrophic amphibian declines have multiple causes, no simple solution

Amphibian declines around the world have forced many species to the brink of extinction, are much more complex than realized and have multiple causes that are still not fully understood, researchers conclude in a new report. The search for a single causative factor is often missing the larger picture, they said, and approaches to address the crisis may fail if they don’t consider the totality of causes — or could even make things worse. No one issue can explain all of the population declines that are occurring at an unprecedented rate, and much faster in amphibians than most other animals, the scientists conclude in a study just published in the Annals of the New York Academy of Sciences. The amphibian declines are linked to natural forces such as competition, predation, reproduction and disease, as well as human-induced stresses such as habitat destruction, environmental contamination, invasive species and climate change, researchers said.

“An enormous rate of change has occurred in the last 100 years, and amphibians are not evolving fast enough to keep up with it,” said Andrew Blaustein, a professor of zoology at Oregon State University and an international leader in the study of amphibian declines. “We’re now realizing that it’s not just one thing, it’s a whole range of things,” Blaustein said. “With a permeable skin and exposure to both aquatic and terrestrial problems, amphibians face a double whammy,” he said. “Because of this, mammals, fish and birds have not experienced population impacts as severely as amphibians — at least, not yet.” The totality of these changes leads these researchers to believe that Earth is now in a major extinction episode similar to five other mass extinction events in the planet’s history. And amphibians are leading the field — one estimate indicates they are disappearing at more than 200 times that of the average extinction rate. Efforts to understand these events, especially in the study of amphibians, have often focused on one cause or another, such as fungal diseases, invasive species, an increase in ultraviolet radiation due to ozone depletion, pollution, global warming, and others. All of these and more play a role in the amphibian declines, but the scope of the crisis can only be understood from the perspective of many causes, often overlapping. And efforts that address only one cause risk failure or even compounding the problems, the researchers said.

“Given that many stressors are acting simultaneously on amphibians, we suggest that single-factor explanations for amphibian population declines are likely the exception rather than the rule,” the researchers wrote in their report. “Studies focused on single causes may miss complex interrelationships involving multiple factors and indirect effects.” One example is the fungus B. dendrobatidis, which has been implicated in the collapse of many frog populations around the world. However, in some populations the fungus causes no problems for years until a lethal threshold is reached, studies have shown. And while this fungus disrupts electrolyte balance, other pathogens can have different effects such as a parasitic trematode that can cause severe limb malformations, and a nematode that can cause kidney damage. The combination and severity of these pathogens together in a single host, rather than any one individually, are all playing a role in dwindling frog populations. Past studies at OSU have found a synergistic impact from ultraviolet radiation, which by itself can harm amphibians, and a pathogenic water mold that infects amphibian embryos. And they linked the whole process to water depths at egg-laying sites, which in turn are affected by winter precipitation in the Oregon Cascade Range that is related to climate change.

The problems facing amphibians are a particular concern, scientists say, because they have been one of Earth’s great survivors — evolving about 400 million years ago before the dinosaurs, persisting through ice ages, asteroid impacts, and myriad other ecological and climatic changes. Their rapid disappearance now suggests that the variety and rate of change exceeds anything they have faced before, the researchers said. “Modern selection pressures, especially those associated with human activity, may be too severe and may have arisen too rapidly for amphibians to evolve adaptations to overcome them,” the researchers concluded.

Science Daily
May 17, 2011

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Giant fire-bellied toad’s brain brims with powerful germ-fighters

Frog and toad skins already are renowned as cornucopias of hundreds of germ-fighting substances. Now a new report in ACS’s Journal of Proteome Research reveals that the toad brains also may contain an abundance of antibacterial and antiviral substances that could inspire a new generation of medicines. Ren Lai and colleagues point out that scientists know little about the germ-fighting proteins in amphibian brains, despite many studies showing that amphibians synthesize and secrete a remarkably diverse array of antimicrobial substances in their skin. So they decided to begin filling that knowledge gap by analyzing brains from the Giant Fire-Bellied Toad and the Small-webbed Bell Toad. They discovered 79 different antimicrobial peptides, the components of proteins, including 59 that were totally new to science. The diversity of the peptides “is, to our knowledge, the most extreme yet described for any animal brains,” they noted. Some of the peptides showed strong antimicrobial activity, crippling or killing strains of staph bacteria, E. coli, and the fungus that causes yeast infections in humans. These promising findings suggest that the toad brains might be a valuable source for developing new antibacterial and antiviral drugs.

Science Daily
May 3, 2011

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Treadmill tests for poison frogs show toxic species are more physically fit

The most toxic, brightly colored members of the poison frog family may also be the best athletes, says a new study. So-named because some native peoples use their skin secretions to poison their darts, the poison dart frogs of the Amazon jungle are well known for their bitter taste and beautiful colors. The spectacular hues of these forest frogs serve to broadcast their built-in chemical weapons: skin secretions containing nasty toxins called alkaloids. Like the red, yellow and black bands on a coral snake or the yellow stripes on a wasp, their contrasting color patterns warn would-be predators to stay away, said lead author Juan Santos of the National Evolutionary Synthesis Center in Durham, NC. As it turns out, the most boldly-colored and bad-tasting species are also the most physically fit, the authors report this week in the journal Proceedings of the National Academy of Sciences.

In forests in Colombia, Ecuador, Venezuela, and Panamá, Santos subjected nearly 500 poison frogs — representing more than 50 species — to a frog fitness test. He measured their oxygen uptake during exercise using a rotating plastic tube, turning the tube like a hamster wheel to make the frogs walk. Santos estimated the frogs’ metabolic rates while at rest, and again after four minutes of exercise. The result? The most dazzling and deadly species had higher aerobic capacity than their drab, nontoxic cousins. “They’re better able to extract oxygen from each breath and transport it to their muscles, just like well-trained athletes,” Santos said. Poisonous species owe their athletic prowess to their unusual foraging habits, explained co-author David Cannatella of the University of Texas at Austin. Unlike snakes and other poisonous animals which make their own venom, poison frogs get their toxins from their food.

“They acquire their alkaloid chemicals by eating ants and mites,” Cannatella said. Because of their picky diet, poisonous frogs have to forage far and wide for food. “Nontoxic species basically stay in one place and don’t move very much and eat any insect that comes close to them,” Santos said. “But the bright, poisonous frogs are very picky about what they eat.” “It’s not like a buffet where they can get everything they need to eat in one place,” Cannatella added. “Ants and mites are patchy, so the frogs have to move around more to find enough food.” This combination of toxic skin and bold colors — a syndrome known as aposematism — evolved in tandem with specialized diet and physical fitness multiple times across the poison frog family tree, the authors explained. In some cases the frogs’ physical fitness may have evolved before their unusual diet, making it possible to forage for harder-to-find food. But the specific sequence of events was likely different for different branches of the tree, Santos said.
The findings appeared in the March 28 issue of Proceedings of the National Academy of Sciences.

eBioNews.com
April 19, 2011

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Dopamine controls formation of new brain cells

A study of the salamander brain has led researchers at Karolinska Institutet to discover a hitherto unknown function of the neurotransmitter dopamine. In an article published in the scientific journal Cell Stem Cell they show how in acting as a kind of switch for stem cells, dopamine controls the formation of new neurons in the adult brain. Their findings may one day contribute to new treatments for neurodegenerative diseases, such as Parkinson’s. The study was conducted using salamanders which unlike mammals recover fully from a Parkinson’s-like condition within a four-week period. Parkinson’s disease is a neurodegenerative disease characterised by the death of dopamine-producing cells in the mid-brain. As the salamander re-builds all lost dopamine-producing neurons, the researchers examined how the salamander brain detects the absence of these cells. This question is a fundamental one since it has not been known what causes the new formation of nerve cells and why the process ceases when the correct number have been made.

What they found out was that the salamander’s stem cells are automatically activated when the dopamine concentration drops as a result of the death of dopamine-producing neurons, meaning that the neurotransmitter acts as a constant handbrake on stem cell activity. “The medicine often given to Parkinson’s patients is L-dopa, which is converted into dopamine in the brain,” says Dr Andras Simon, who led the study at the Department of Cell and Molecular Biology. “When the salamanders were treated with L-dopa, the production of new dopamine-producing neurons was almost completely inhibited and the animals were unable to recover. However, the converse also applies. If dopamine signalling is blocked, new neurons are born unnecessarily.” As in mammals, the formation of neurons in the salamander mid-brain is virtually non-existent under normal circumstances. Therefore by studying the salamander, scientists can understand how the production of new nerve cells can be resumed once it has stopped, and how it can be stopped when no more neurons are needed. It is precisely in this regulation that dopamine seems to play a vital part. Many observations also suggest that similar mechanisms are active in other animal species too. Further comparative studies can shed light on how neurotransmitters control stem cells in the brain, knowledge that is of potential use in the development of therapies for neurodegenerative diseases.

“One way of trying to repair the brain in the future is to stimulate the stem cells that exist there,” says Dr Simon. “This is one of the perspectives from which our study is interesting and further work ought to be done on whether L-dopa, which is currently used in the treatment of Parkinson’s, could prevent such a process in other species, including humans. Another perspective is how medicines that block dopamine signalling and that are used for other diseases, such as psychoses, affect stem cell dynamics in the brain.” The salamander is a tailed member of the frog family most known for its ability to regenerate lost body parts, such entire limbs.

Science Daily
April 19, 2011

Original web page at Science Daily