But it turns out that remarkable ability isn’t so mysterious after all — suggesting that researchers could learn how to replicate it in people.

Scientists had long credited the diminutive amphibious creature’s outsized capabilities to “pluripotent” cells that, like human embryonic stem cells, have the uncanny ability to morph into whatever appendage, organ or tissue happens to be needed or due for a replacement.

But in a paper set to appear Thursday in the journal Nature, a team of seven researchers, including a University of Florida zoologist, debunks that notion. Based on experiments on genetically modified axolotl salamanders, the researchers show that cells from the salamander’s different tissues retain the “memory” of those tissues when they regenerate, contributing with few exceptions only to the same type of tissue from whence they came.

Standard mammal stem cells operate the same way, albeit with far less dramatic results — they can heal wounds or knit bone together, but not regenerate a limb or rebuild a spinal cord. What’s exciting about the new findings is they suggest that harnessing the salamander’s regenerative wonders is at least within the realm of possibility for human medical science.

“I think it’s more mammal-like than was ever expected,” said Malcolm Maden, a professor of biology, member of the UF Genetics Institute, and author of the paper. “It gives you more hope for being able to someday regenerate individual tissues in people.”

Also, the salamanders heal perfectly, without any scars whatsoever, another ability people would like to learn how to mimic, Maden said.

Axolotl salamanders, originally native to only one lake in central Mexico, are evolutionary oddities that become sexually reproducing adults while still in their larval stage. They are useful scientific models for studying regeneration because, unlike other salamanders, they can be bred in captivity and have large embryos that are easy to work on.

When an axolotl loses, for example, a leg, a small bump forms over the injury called a blastema. It takes only about three weeks for this blastema to transform into a new, fully functioning replacement leg — not long considering the animals can live 12 or more years.

The cells within the blastema appear embryonic-like and originate from all tissues around the injury, including the cartilage, skin and muscle. As a result, scientists had long believed these cells were pluripotential — meaning they came from a variety of sites and could make a variety of things once functioning in their regenerative mode.

Maden and his colleagues at two German institutions tested that assumption using a tool from the transgenic kit: the GFP protein. When produced by genetically modified cells, GFP proteins have the useful quality of glowing livid green under ultraviolet light. This allows researchers to follow the origin, movement and destination of the genetically modified cells.

The researchers experimented on both adult and embryonic salamanders.

With the embryos, the scientists grafted transgenic tissue onto sites already known to develop into certain body parts, then observed how and where the cells organized themselves as the embryo developed. This approach allowed them to see, literally, what tissues the transgenic tissue made. In perhaps the most vivid result, the researchers grafted GFP-modified nerve cells onto the part of the embryo known to develop into the nervous system. Once the creatures developed, ultraviolet light exams of the adults revealed the GFP cells stretched only along nerve pathways — like glowing green strings throughout the body

With the adults, they took tissue from specific parts or organs from transgenic GFP-producing axolotls, grafted it onto normal axolotls, then cut away a chunk of the grafted tissue to allow regeneration. They could then determine the fate of the grafted green cells in the emerging blastema and replacement tissue.

The researchers’ main conclusion: Only ‘old’ muscle cells make ‘new’ muscle cells, only old skin cells make new skin cells, only old nerve cells make new nerve cells, and so on. The only hint that the axolotl cells could revamp their function came with skin and cartilage cells, which in some circumstances seemed to swap roles, Maden said.

Maden said the findings will help researchers zero in on why salamander cells are capable of such remarkable regeneration. “If you can understand how they regenerate, then you ought to be able to understand why mammals don’t regenerate,” he said.

Maden said UF researchers will soon begin raising and experimenting on transgenic axolotls at UF as part of the The Regeneration Project, an effort to treat human brain and other diseases by examining regeneration in salamanders, newts, starfish and flatworms.

The analysis of a well-preserved skull from 54 million years ago contradicts some common assumptions about brain structure and evolution in the first primates. The study also narrows the possibilities for what caused primates to evolve larger brain sizes. The study is scheduled to appear online the week of June 22 in the Proceedings of the National Academy of Sciences.

The skull belongs to a group of primitive primates known as Plesiadapiforms, which evolved in the 10 million years between the extinction of the dinosaurs and the first traceable ancestors of modern primates. The 1.5-inch-long skull was found fully intact, allowing researchers to make the first virtual mold of a primitive primate brain.

“Most explanations on the evolution of primate brains are based on data from living primates,” said lead author Mary Silcox, an anthropologist at the University of Winnipeg and research associate at UF’s Florida Museum of Natural History. “There have been all these inferences about what the brains of the earliest primates would look like, and it turns out that most of those inferences are wrong.”

Researchers used CT scans to take more than 1,200 cross-sectional X-ray images of the skull, which were combined into a 3-D model of the brain.

“A large and complex brain has long been regarded as one of the major steps that sets primates apart from the rest of mammals,” said Florida Museum vertebrate paleontologist and study co-author Jonathan Bloch. “At our very humble beginnings, we weren’t so special. That happened over tens of millions of years.”

The animal, Ignacius graybullianus, represents a side branch on the primate tree of life, Bloch
said. “You can think of it as a cousin of the main line lineage that would have given rise ultimately to us.”

In previous research, Bloch and Silcox established that Plesiadapiforms were transitional species. Ignacius was similar to modern primates in terms of its diet and tree-dwelling but did not leap from tree to tree like modern fast-moving primates.

In many ways, the early primate behaved like living primates but with a brain that was one-half to two-thirds the size of the smallest modern primates. This means that factors such as tree-dwelling and fruit-eating can be eliminated as potential causes for primates evolving larger brain sizes, Silcox said, because “the smaller brained Ignacius was already doing those things.”

The mold suggests a “startling combination” of features in the early primate that requires a rethinking of primate brain evolution, said Florida State University anthropologist Dean Falk, who was not involved in the study.

“Hypotheses about early primate brain evolution often link keen smell with nocturnal insect-eating, and a more recently evolved increase in visual processing with fruit-eating in arboreal habitats,” Falk said.

The move to larger brain size occurred during an evolutionary burst that happened 10 million years after the extinction of the dinosaurs. At that point, visual features in the brain became much more prominent while the olfactory bulbs became proportionately smaller.

More than likely, Bloch said, this change in brain structure and size was related to primates living in closed canopy forests that brought trees closer together and allowed for more leaping. But answering that will require the discovery and analysis of new fossils.

Changes in brain size and brain structure in the early stages of primate evolution have generated enormous debates for decades. But until now, fossil evidence has been lacking.

Many models of the ancestral primate brain are based on tree shrews, which come from southeast Asia and are distantly related to humans. But with some 70 million years of evolution between them and humans, “it turns out tree shrew brains are not a good model,” Silcox said.

The team headed by Eric Ford, an assistant professor of astronomy, used the Canary Islands-based GTC to observe a known star and its Jupiter-sized orbiting planet as part of an effort aimed in part at learning how planets contract in size as their stars age. With analysis of the data from the observations now under way, the team also hoped to glean insights about how to tune the GTC’s capabilities to study not only huge, gaseous Jupiter-size planets but also Neptune-sized or “super-Earth”-sized planets that could be closer in composition to Earth.

“The excellent site and large size of the GTC plus the unique filtering capabilities of its detectors will allow astronomers to minimize the effects of Earth’s atmosphere,” Ford said. “By repeatedly measuring the color of exoplanets’ host stars, astronomers can study the atmospheres of exoplanets — and distinguish small planets from other phenomena such as large star spots or binary stars.”

The UF team’s late-May observations were among several announced earlier this week by the Instituto de Astrofisica de Canarias that marked the long-awaited scientific debut of the GTC, first launched in 2000 on the island of La Palma, and only recently completed. UF contributed $5 million to the roughly $180 million telescope and owns a 5 percent share – the only U.S. institution with an ownership stake in the telescope. The Spanish government owns 90 percent, with Mexico owning the remaining 5 percent.

The GTC’s unique 34.1-foot primary mirror, composed of 36 hexagonal segments, gives it unparalleled abilities to see deep into the universe and examine distant objects in great detail. The telescope is equally notable for the ultra-precise computer control of its mirror segments — control that makes possible more finely detailed images than achievable with other telescopes. Its size and controllability makes the GTC powerful enough to detect an ordinary candle from 20,000 miles away — and resolve the width of its flame from six miles away.

UF astronomers say they will use the telescope to learn more about what occurred in the earliest years of the universe, how stars, planets and galaxies come into being, and to discover and learn more about planets outside our solar system.

“We made this investment because we want our excellent faculty and students to have as much opportunity as possible for top-class research,” said Stan Dermott, chairman of the astronomy department. “In astronomy, that requires access to the best facilities.”

Ford, graduate student Knicole Colón, and postdoctoral associates Brian Lee and Suvrath Mahadven, tapped a Spanish-built astronomical instrument, OSIRIS, to gather the data on the extrasolar star, HAT-P-3, and its planet, HAT-P-3b.

However, A UF-designed and built instrument, CanariCam, is anticipated to be the second instrument installed on the GTC. Among other goals, CanariCam will explore origins and early evolution of planetary systems by imaging the protoplanetary disks where planets are born. UF astronomers also made significant contributions to a third instrument expected to be installed on the GTC known as FRIDA.

“The University of Florida is a partner not just in the observing sense,” Dermott said. “We are also a partner in the sense of being the major builder of instruments for the telescope.”

The GTC’s first, ceremonial observations occurred in 2007, before the telescope’s mirror was complete. A formal inauguration is planned for July 24 on the island of La Palma. King Juan Carlos I and Queen Sofia of Spain will preside over the ceremony.

Now, a team of University of Florida chemists is the latest to report a new mechanism to transform light straight into motion – albeit at a very, very, very tiny scale.

In a paper expected to appear soon in the online edition of the journal Nano Letters, the UF team reports building a new type of “molecular nanomotor” driven only by photons, or particles of light. While it is not the first photon-driven nanomotor, the almost infinitesimal device is the first built entirely with a single molecule of DNA — giving it a simplicity that increases its potential for development, manufacture and real-world applications in areas ranging from medicine to manufacturing, the scientists say.

“It is easy to assemble, has fewer parts and theoretically should be more efficient,” said Huaizhi Kang, a doctoral student in chemistry at UF and the first author of the paper.

The scale of the nanomotor is almost vanishingly small.

In its clasped, or closed, form, the nanomotor measures 2 to 5 nanometers — 2 to 5 billionths of a meter. In its unclasped form, it extends as long as 10 to 12 nanometers. Although the scientists say their calculations show it uses considerably more of the energy in light than traditional solar cells, the amount of force it exerts is proportional to its small size.

But that won’t necessarily limit its potential.

In coming years, the nanomotor could become a component of microscopic devices that repair individual cells or fight viruses or bacteria. Although in the conceptual stage, those devices, like much larger ones, will require a power source to function. Because it is made of DNA, the nanomotor is biocompatible. Unlike traditional energy systems, the nanomotor also produces no waste when it converts light energy into motion.

“Preparation of DNA molecules is relatively easy and reproducible, and the material is very safe,” said Yan Chen, a UF chemistry doctoral student and one of the authors of the paper.

Applications in the larger world are more distant. Powering a vehicle, running an assembly line or otherwise replacing traditional electricity or fossil fuels would require untold trillions of nanomotors, all working together in tandem — a difficult challenge by any measure.

“The major difficulty lies ahead,” said Weihong Tan, a UF professor of chemistry and physiology, author of the paper and the leader of the research group reporting the findings. “That is how to collect the molecular level force into a coherent accumulated force that can do real work when the motor absorbs sunlight.”

Tan added that the group has already begun working on the problem.

“Some prototype DNA nanostructures incorporating single photo-switchable motors are in the making which will synchronize molecular motions to accumulate forces,” he said.

To make the nanomotor, the researchers combined a DNA molecule they created in the lab with azobenzene, a chemical compound that responds to light. A high-energy photon prompts one response; lower energy another.

To demonstrate the movement, the researchers attached a fluorophore, or light-emitter, to one end of the nanomotor and a quencher, which can quench the emitting light, to the other end. Their instruments recorded emitted light intensity that corresponded to the motor movement.

“Radiation does cause things to move from the spinning of radiometer wheels to the turning of sunflowers and other plants toward the sun,” said Richard Zare, distinguished professor and chairman of chemistry at Stanford University. “What Professor Tan and co-workers have done is to create a clever light-actuated nanomotor involving a single DNA molecule. I believe it is the first of its type.”

The National Institutes of Health and the National Science Foundation funded the research. The other coauthors of this paper are Haipeng Liu, Joseph A. Phillips, Zehui Cao, Youngmi Kim, Zunyi Yang and Jianwei Li.

Led by Florida Museum of Natural History vertebrate paleontologist Larisa DeSantis, researchers examined fossil teeth from mammals at two sites representing different climates in Florida: a glacial period about 1.9 million years ago and a warmer, interglacial period about 1.3 million years ago. The researchers found that interglacial warming resulted in dramatic changes to the diets of animal groups at both sites. The study appears in the June 3 issue of PLoS ONE.

“When people are modeling future mammal distributions, they’re assuming that the niches of mammals today are going to be the same in the future,” DeSantis said. “That’s a huge assumption.”

Co-author Robert Feranec, curator of vertebrate paleontology at the New York State Museum, said scientists cannot predict what species will do based on their current ecology.

“The study definitively shows that climate change has an effect on ecosystems and mammals, and that the responses are much more complex than we might think,” Feranec said.

The two sites in the study, both on Florida’s Gulf Coast, have been excavated quite extensively, DeSantis said. During glacial periods, lower sea levels nearly doubled Florida’s width, compared with interglacial periods. But because of Florida’s low latitude, no ice sheets were present during the glacial period. Despite the lack of glaciers in Florida, the two sites show dramatic ecological changes occurred between the two periods.

Both sites include some of the same animal groups, allowing DeSantis, Feranec and Bruce MacFadden, Florida Museum curator of vertebrate paleontology, to clarify how mammals and their environments responded to interglacial warming.

The research examined carbon and oxygen isotopes within tooth enamel to understand the diets of medium to large mammals, including pronghorn, deer, llamas, peccaries, tapirs, horses, mastodons, mammoths and gomphotheres, a group of extinct elephant-like animals.

Differences in how plants photosynthesize give them distinct carbon isotope ratios. For example, trees and shrubs process carbon dioxide differently than warm-season grasses, resulting in different carbon isotope ratios. These differences are incorporated in mammalian tooth enamel, allowing scientists to determine the diets of fossil mammals. Lower ratio values suggest a browsing diet (trees and shrubs) while a higher ratio suggests a grazing diet (grasses).

Animals at the glacial site were predominantly browsing on trees and shrubs, while some of those same animals at the warmer interglacial site became mixed feeders that also grazed on grasses. Increased consumption of grasses by mixed feeders and elephant-like mammals indicates Florida’s grasslands likely expanded during interglacial periods.

Tooth enamel locks in the chemical signatures of the plants and water an animal consumes, allowing paleontologists to understand the diets and associated climate of fossil specimens that are millions of years old. To find these signatures, researchers run samples of tooth enamel through a mass spectrometer.

DeSantis and her collaborators analyzed enamel samples from 115 fossil teeth. For two of the specimens she took serial samples, small samples that run perpendicular to the growth axis and give insight into how the diet and climate changed over a specific period of time.

“That’s one of the cool things about using mammal teeth,” she said. “We can actually look at how variable the climate was within a year, millions of years ago.”

The study highlights the importance of the fossil record in understanding long-term ecological responses to changes over time, DeSantis said. While ecological studies of modern impacts can cover only limited spans of time, “this study emphasizes the importance of using the fossil record to look at how mammals and other animals responded to climate change in the past, also helping us gain a better understanding of how they might respond in the future.”

At the same time, plants will proliferate, nurtured by balmier temperatures, more nutrients from decomposing soil and the increasing abundance of the greenhouse gas they depend on for growth.

These connected but contrasting changes have raised a question for scientists who study the causes and consequences of global climate change: Will the shrubs and incipient forests spreading across the Arctic compensate for the permafrost’s rising release of carbon, blunting its impact on a warming planet? Or, with twice as much carbon locked up in the permafrost as now present in the atmosphere, will the lush growth become overwhelmed — like a kitchen sponge put down to stem a water main break?

Researchers led by a University of Florida ecologist may have an answer. In a paper set to appear May 28 in the journal Nature, the team reports experimental results suggesting tundra plant growth may keep up with rising carbon dioxide initially.

But if thawing continues in a warmer world, the permafrost will spew carbon for decades, and the plants will become overwhelmed — unable to sop up the excess carbon despite even the most vigorous growth.

“At first, with the plants offsetting the carbon dioxide, it will appear that everything is fine, but actually this conceals the initial destabilization of permafrost carbon,” said Ted Schuur, a UF associate professor of ecology and lead author of the paper. “But it doesn’t last, because there is so much carbon in the permafrost that eventually the plants can’t keep up.”

Schuur noted most of the 13 million square kilometers, or roughly 5 million square miles, of permafrost in Alaska, Canada, Siberia and parts of Europe remain frozen. However, thawing already occurring around its southern edges is expected to expand this century.

Should that occur, this study suggests the permafrost could lose in the range of 1 gigaton of carbon, or 1 billion tons, per year – about the same order of magnitude as being added by current deforestation of the tropics, another large biospheric source, Schuur said.

While burning fossil fuels contributes considerably more carbon, about 8.5 gigatons annually, that process can at least in theory be controlled – whereas once the permafrost thaw begins, it sets up a self-reinforcing loop far from human activity and potentially difficult to stop.

That highlights the urgent need to address human-caused emissions now, Schuur said.

“It is not an option to be putting insulation on top of the tundra,” he said. “If we address our own emissions, either by reducing deforestation or controlling emissions from fossil fuels, that’s the key to minimizing the changes in the permafrost carbon pool.”

Researchers from UF used hand-built, automated chambers to trap and measure carbon dioxide losses in Alaska year-round from 2004 through 2006. Thawing at the research sites near Denali National Park, in central Alaska, varies considerably, with some plots much more extensively thawed than others.

The researchers determined how long each spot had been thawing using long-term data from permafrost-monitoring instruments combined with historical aerial photographs. With a total of 18 of the automated chambers, they measured the release and uptake of carbon between the tundra and the atmosphere. This resulted in a measurement of net ecosystem carbon exchange – the total carbon each spot lost, or gained, due to thawing permafrost.

The results were clear.

Tundra sites that had thawed for the past 15 years gained net carbon, as increasingly verdant plant growth was greater than the permafrost’s carbon losses. However, radiocarbon dating of carbon dioxide showed that old carbon from the permafrost was already being released in higher amounts due to thaw – signifying that all was not well with the permafrost carbon even in that time period. The site that began thawing decades before gained net carbon emission to the atmosphere, revealing that more thaw caused significantly more old carbon loss — despite greening of the vegetation, including more shrubs.

Said Jason Vogel, a UF postdoctoral associate and author of the paper: “The plants are still growing faster in the extensively thawed area, but that’s not enough to keep up with the greater microbial activity releasing old carbon from deeper in the soil.”

As a result, even as the Arctic greens, its escalating old carbon loss “could make permafrost a large biospheric carbon source in a warmer world,” according to the paper.

The other authors are Kathryn Crummer, a UF lab technician; Hanna Lee, a UF doctoral student; James Sickman, of the University of California, Riverside; and T.E. Osterkamp of the University of Alaska, Fairbanks. The research was funded by the National Science Foundation, NASA and a cooperative agreement with the National Park Service.

Researchers at the Powell Gene Therapy Center at the University of Florida have discovered that signals from the brain to the diaphragm — the muscle that controls breathing — are too weak to initiate healthy respiration in mouse models of the disease.

The discovery for the first time shifts responsibility to the nervous system for the severe breathing problems experienced by infants with Pompe disease, a rare genetic disorder that causes extreme muscle weakness. Children born with the disorder usually die before age 2.

“For years what we have thought is principally a muscle disease may actually be caused by problems with signaling between the spinal cord and the muscle,” said Dr. Barry Byrne, a UF pediatric cardiologist, a member of the UF Genetics Institute and the director of the Powell Gene Therapy Center. “As we’ve treated children with this disease, we found many of them have become ventilator-dependent, so we went back to the laboratory and found that a significant part of the respiratory deficit is in the spinal cord and not in the diaphragm alone.”

The findings, which will be published the week of May 25 in the online early edition of the Proceedings of the National Academy of Sciences, also have a bearing on motor neuron diseases, a group of incurable brain disorders that destroy cells that influence essential muscle activity such as speaking, walking, breathing and swallowing. Notable among these is ALS, technically known as amyotrophic lateral sclerosis or, more commonly, Lou Gehrig’s disease.

Although many laboratory discoveries never advance to the point where they can be confirmed in patients, scientists will be able to evaluate whether there is indeed a neural aspect to Pompe disease in a clinical safety study of a gene therapy in six infants with the disorder.

The clinical trial, which will begin this summer at UF, had previously advanced on its merits as a therapy for breathing problems in a group of patients who have very few treatment alternatives.

Children with Pompe disease cannot produce the enzyme acid alpha-glucosidase, or GAA. Without the enzyme, sugars and starches that are stored in the body as glycogen accumulate and destroy muscle cells, particularly those of the heart and respiratory muscles.

In this first-in-humans gene therapy for neuromuscular disease, scientists will incorporate the correct gene to produce GAA into an adeno-associated virus, which already exists in most people, and inject it into each patient’s diaphragm. The intent is to “infect” cells of Pompe patients with the genetic machinery they have been missing since birth.

Now, in addition to testing the safety of the dosage and watching closely for signs of therapeutic effects, researchers will fortuitously be able to study the response of the phrenic nerve, which shuttles impulses from the brain to the diaphragm via the spinal cord.

In the PNAS study, UF researchers examined breathing in mice with a form of Pompe disease and in a line of mice genetically engineered to produce GAA only in muscle, not in the central nervous system. In both models, phrenic nerve bursts to stimulate breathing were substantially weaker than in normal mice. As a backdrop, they considered a detailed analysis of a Pompe disease patient’s nervous system, finding similar unhealthy glycogen buildup in the spinal cord and deficient neural output to the diaphragm.

“Treatments that target muscle alone may be ineffective,” Byrne said. “Fortunately the gene transfer we are attempting also affects the phrenic nerve, and we know in mice we can restore phrenic nerve stimulation of the diaphragm. Ultimately we hope that by restoring the function of this gene in both muscle and nerve the patients may have improved respiratory function and possibly breathe independently.”

In addition to Pompe disease, this finding has relevance for congenital and other forms of muscular dystrophy, according to Xiao Xiao, a distinguished professor of gene therapy at the University of North Carolina Eshelman School of Pharmacy at Chapel Hill who was not involved in the research.

“People did not realize there was nerve involvement in these diseases until this study,” Xiao said. “It provides us with a new target for therapy, but it also gives us a new challenge. Not only do we have to deliver to therapy to the muscle and heart, we now have to deliver it to the nerve. Fortunately Dr. Byrne is very well-qualified and positioned to take this therapy from the bench to the bedside.”

The general therapy for children with Pompe disease involves intravenous infusions to replace the missing GAA enzyme, according to Dr. Robert D. Steiner, a professor of pediatrics and molecular and medical genetics and vice chair for pediatric research at Oregon Health & Science University and OHSU Doernbecher Children’s Hospital. In a subset of patients, the enzyme replacement therapy helps initially, but becomes ineffective over time.

“I think this study begins to explain some of the difficulties we’ve had in treating patients,” said Steiner, who did not participate in the research. “The findings are clear that central nervous system involvement is likely to be important in Pompe disease, and that treatments that do not take this into account will not be 100 percent effective in the long-term. It is very reasonable to pursue gene therapy for treatment of this disease, because gene therapy makes it possible to target the central nervous system.”

Other members of the UF research team include Cathryn Mah, an assistant professor of pediatrics, and Paul Reier, a professor of neuroscience, both in the College of Medicine; and David Fuller, an assistant professor of physical therapy in the College of Public Health and Health Professions. The research was funded by the National Institutes of Health.

GAINESVILLE, Fla. — The birds are watching. They know who you are. And they will attack.

Nope, not Hitchcock.

It’s science.

University of Florida biologists are reporting that mockingbirds recognize and remember people whom the birds perceive as threatening their nests. If the white-and-grey songbirds common in cities and towns throughout the Southeast spot their unwelcome guests, they screech, dive bomb and even sometimes graze the visitors’ heads — while ignoring other passers-by or nearby strangers.

“We tend to view all mockingbirds as equal, but the feeling is not mutual,” said Doug Levey, a UF professor of biology. “Mockingbirds certainly do not view all humans as equal.”

The research is described in a paper set to appear this week in the online edition of the Proceedings of the National Academy of Sciences.

The paper describes the first published research showing that wild animals living in their natural settings recognize individuals of other species, Levey said. It may provide clues as to why mockingbirds and selected other bird and animal species flourish in heavily populated cities and suburbs — while other species either grow rare or disappear entirely.

“The real puzzle in the field of urban ecology is to figure out why certain species thrive around humans,” Levey said. “One of the hypotheses is that they have some innate ability to adapt and innovate in ways that other species don’t.”

Mockingbirds are among the most common birds on the University of Florida campus in Gainesville, where they nest in trees and shrubs close to the ground. For the research, student volunteers walked up to the nests, reached through the foliage and gently touched the nests’ edges, then walked away. The same volunteers repeated the same visits again the next day, and again for two more days. On the fifth day, however, different volunteers approached the
nests. All told, 10 volunteers tested 24 nests at least five times last spring and summer, during the mockingbird nesting season.

It didn’t take a bird’s eye view to spot the resulting pattern, Levey said.

On the third and fourth days, the birds flushed from their nests more rapidly each time the increasingly familiar students appeared — even though the students took different paths toward the nests on successive days and wore different clothes. The birds also gave more alarm calls and flew more and aggressively each succeeding day, with some especially defensive birds even grazing intruders’ heads — not exactly deadly, but annoying, because the birds tend to hit the same spot repeatedly, Levey said.

And yet when different students approached the nests on the fifth day, the birds hardly ruffled their feathers, waiting to flush until last moment. They also gave fewer alarm calls and attacked much less than on the previous day with the familiar intruder.

On a campus of 51,000-plus students, paths are filled with students walking back and forth from class all day every weekday — so it’s no stretch to say that thousands of different people come within a few feet of mockingbird nests during the breeding season.

And yet, the mockingbirds in the study were clearly able to recognize and remember a single individual, based on just two brief negative encounters at their nest. Levey said that sharply contrasts with laboratory studies, in which pigeons recognized people only after extensive training. “Sixty seconds of exposure was all it took for mockingbirds to learn to identify different individuals and pick them out of all other students on campus,” Levey said.

For most wild animals, urban development brings less habitat and more predators. Many species flee or die off, but a few persist, and some thrive. It seems obvious that these species do better around people, but why?

Few people bother mockingbird nests, so that is hardly an answer. Rather, Levey said, the birds’ ability to recognize people suggests perceptual powers that give them an edge in dealing with the complexities of urban environments — such as being able to judge which cats may be aware of nests and which are simply passing blithely nearby.

“We don’t believe mockingbirds evolved an ability to distinguish between humans. Mockingbirds and humans haven’t been living in close association long enough for that to occur.” Levey said. “We think instead that our experiments reveal an underlying ability to be incredibly perceptive of everything around them, and to respond appropriately when the stakes are high.”

In findings to be published this week in the online early edition of the Proceedings of the National Academy of Sciences, scientists describe how they looked at all of the proteins produced by the smallpox virus in concert with human proteins, and discovered one particular interaction that disables one of the body’s first responders to injury — inflammation.

“This virus that has killed more humans than any other contains secrets about how the human immune system works,” said Grant McFadden, a professor of molecular genetics and microbiology at the College of Medicine and a member of the UF Genetics Institute. “I’m always amazed at how sophisticated these pathogens are, and every time we look, they have something new to teach us about the human immune system.”

With researchers from the University of Alberta, the Centers for Disease Control and Prevention and a private company called Myriad Genetics, UF researchers for the first time systematically screened the smallpox proteome — the entire complement of new proteins produced by the virus — during interactions with proteins from human DNA.

These protein-on-protein interactions resulted in a particularly devastating pairing between a viral protein called G1R and a human protein called human nuclear factor kappa-B1, which is believed to play a role in the growth and survival of both healthy cells and cancer cells by activating genes involved in immune responses and inflammation.

“One of the strategies of the virus is to inhibit inflammation pathways, and this interaction is an inhibitor of human inflammation such that we have never seen before,” McFadden said. “This helps explain some of the mechanisms that contribute to smallpox pathogenesis. But another side of this is that inflammation can sometimes be harmful or deadly to people, and we may learn a way to inhibit more dangerous inflammation from this virus.”

Smallpox is blamed for an estimated 300 million deaths in the 20th century alone, and outbreaks have occurred almost continuously for thousands of years. The disease was eradicated by a worldwide vaccination campaign, and the last case of smallpox in the United States was in 1949, according to the CDC. The last naturally occurring case in the world was in Somalia in 1977.

With the exception of stores of the virus held in high-containment facilities in the United States and Russia, smallpox no longer exists on the planet. Since it was no longer necessary for prevention, and because the vaccines themselves were risky, routine vaccination against smallpox was stopped. However, public health concerns regarding the possible re-emergence of the virus through bioterrorism have led to renewed interest in the development of treatments for the disease and safer vaccines.

A team of scientists and engineers from Stanford University, the University of Florida and Lawrence Livermore National Laboratory is the first to create one of two basic types of semiconductors using an exotic, new, one-atom-thick material called graphene. The findings could help open the door to computer chips that are not only smaller and hold more memory — but are also more adept at uploading large files, downloading movies, and other data- and communication-intensive tasks.

A paper about the findings, co-authored by eight researchers, is set to be published Friday in the journal Science.

“There are still enormous challenges to really put it into products, but I think this really could play an important role,” said Jing Guo, a UF assistant professor of electrical and computer engineering and one of two UF authors who contributed.

The team made, modeled and tested what is known in the industry as an “n-type” transistor out of graphene nanoribbon. Graphene is a form of carbon that has been called “atomic chicken wire,” thanks to its honeycomb-like structure of interconnected hexagons. A graphene nanoribbon is a nanometer-wide strip cut from a graphene layer.

The team’s feat is significant because basic transistors come in only two forms — “p-type” and “n-type” — referring to the presence of holes and electrons, respectively. “P-type” graphene semiconductors had already been achieved, so the manufacture of an “n-type” graphene semiconductor completes the fundamental building blocks.

“This work is essentially finding a new way to modify a graphene nanoribbon to make it able to conduct electrons,” Guo said. “This addresses a very fundamental requirement for graphene to be useful in the production of electronics.”

First isolated in 2004, graphene has spurred a great excitement in the chip research community because of its promising electrical properties and bare-minimum atomic size.

Scientists and engineers believe that after decades of development, silicon is fast reaching the upper limits of its physical performance. If the rapid evolution of ever-shrinking, ever-more-powerful, ever-cheaper semiconductors is to continue, they say, new materials must be found to complement or even replace silicon. Graphene is among the leading candidates for these nanoelectronics of the future.

Researchers at a number of institutions have reported using graphene to create a variety of simple transistor devices recently, with the Massachusetts Institute of Technology reporting in March the successful test of a graphene chip that can multiply electrical signals.

Guo said the team built and modeled the first-ever graphene nanoribbon n-type “field-effect transistor” using a new and novel method that involves affixing nitrogen atoms to the edge of the nanoribbon. The method also has the potential to make the edges of the nanometer-wide ribbon smoother, which is a key factor to make the transistor faster.

“This uses chemistry to really address the major challenges of electrical engineering when you get into such these small nanoscale dimensionalities,” he said. “It is very unusual for electrical engineers, who are used to dealing with bulk structures of at least millions of atoms.”

As exciting as the findings are, researchers must overcome many challenges before graphene semiconductors could be manufactured in bulk for use in consumer products, Guo said. For one thing, graphene is extremely expensive, so its cost would have to be reduced substantially. Also, to mimic or exceed silicon, engineers would have to figure out how to build not just one, but billions of transistors, on a tiny graphene fleck.

Five Stanford researchers led by Hongjie Dai, J.G. Jackson-C.J. Wood Professor of Chemistry, did the experimental work behind the findings. Guo and fellow author Youngki Yoon, who earned his doctoral degree from UF last December and is now at the University of California, Berkeley, did the computer modeling and simulation. The team also included Peter Webber of Lawrence Livermore National Laboratory.

Said Dai, “This work is just a beginning. It suggests that graphene chemistry and chemistry at the edges are rich areas to explore for both fundamental and practical reasons for this material.”

The UF portion of the research was funded by the National Science Foundation and the Office of Naval Research. The Stanford portion was funded by MARCO MSD, Intel and the Office of Naval Research.

The work, by researchers at UF’s Institute of Food and Agricultural Sciences, hinges on some organisms’ ability to produce folate despite lacking one of the essential enzymes typically used to produce the compound.

As they report in the online edition of the Journal of Bacteriology, microbiologist Valérie de Crécy-Lagard and biochemist Andrew Hanson discovered that many bacteria use the same substitute for the enzyme as the parasite that causes malaria.

Folate, a vitamin best known for its importance to healthy pregnancies, is also essential to fueling the cell division that enables bacteria to spread.

Humans don’t have the biological process that produces folate, so drugs that disrupt the process are ideal candidates for disease treatments. Two widely used antibiotics, trimethoprim and sulfamethoxazole, use this approach.

“It had been a big mystery ever since we started decoding bacterial genomes—what are we not seeing that allows certain bacteria to produce folate even though they are missing an essential step in the process?” Crécy-Lagard said. “The answer had already been found in the parasite that causes malaria.”
In 2008, a team led by John Hyde at the University of Manchester discovered that the malaria parasite may bypass the need for the folate enzyme FolB, instead using another enzyme, called PTPS.

As one of their first steps, the UF researchers verified that the malaria parasite’s enzyme substitution would work in bacteria by replacing the regular gene for FolB in E. coli (the lab mouse of the bacteriology world) with the PTPS gene from the malaria parasite.

This was the first time that this substitution had been shown to work in a living creature. The previous malaria parasite experiments had only offered biochemical, “test-tube” evidence.

As a side note, de Crécy-Lagard said the PTPS gene-bearing E. coli will make the gene easier to study for antimalarial drug development than such work would be in the malaria parasite. While single-celled, the parasite is significantly more complex and harder to handle than bacteria.

The researchers then went on to discover which bacteria this substitution may apply to by conducting a genomic and biochemical analysis of many types of bacteria known to lack FolB. The exact number of bacterial species that lack FolB is not known because of the sheer number of bacteria species that exist.

While this leaves more room for exploration, there is also work to be done to uncover how many more complex organisms also use the PTPS substitution.

Diatoms, single-celled organisms that are a vital part of ocean ecosystems, are likely candidates, Hanson said.

“Folate is an essential ingredient to virtually all life,” Hanson said. “And we have a long road to travel before we fully understand it.”

Rather than rush to publication with their individual findings on the current flu outbreak, the computational biologists have opened their work in progress to each other and the public through a Web site: http://tree.bio.ed.ac.uk/groups/influenza.

Researchers in Britain came up with the idea to rapidly release data analysis results. The site allows a broad collaborative yet independent effort by allowing registered users to post their results and comment on the work of others. Contributors hail from institutions around the world, including the University of Oxford, the University of Edinburgh, the University of Florida, the University of Arizona, the University of California-Los Angeles, the University of Hong Kong and Belgium’s Rega Institute.

“It’s a really new concept, because basically there is a worldwide emergency, so this is a very fast way to have data circulating very quickly in the scientific community,” said Marco Salemi, a UF assistant professor of pathology immunology and laboratory medicine, who has contributed results to the Web site.

Site creators caution that analyses are preliminary and corrections likely will be needed.

Still, there is great value and a certain sense of community in displaying the information, the researchers say. Their analyses are based on viral DNA sequences generated and published by the National Center for Biotechnology Information, and the nonprofit Global Initiative on Sharing Avian Influenza data.

“My opinion was, since they’re publishing the sequence data openly, it makes sense for us to publish our analysis of that data openly,” said the University of Oxford’s Oliver Pybus, who with the University of Edinburgh’s Andrew Rambaut developed the site.

Analyses done so far point to the virus’ immediate origins in swine flu variants with links to avian and human strains through a process called reassortment, in which gene segments from different viruses shuffle and reassemble into new viruses.

“One important result is that the new virus derived its genes from both swine and human lineage, some of which, in turn, originated from an avian influenza pool,” said Becca Gray, a UF postdoctoral fellow working with Salemi.

Several analyses suggest that some segments of the 2009 H1N1 genome might have originated two to five years ago, and others as recently as September 2008.

“In retrospect, maybe it’s not that surprising if the strain was lost among the normal flu season in Mexico,” Pybus said. “This is suggesting that there are more people affected than those who became severely ill or died — we don’t hear about the mildly ill.”

Gray, Salemi and others are characterizing amino acid changes in the viral genome associated with the current outbreak, and investigating how those changes might affect the new H1N1 virus’ transmission rate and ability to cause disease.

While the current effort of quickly assembling and presenting data means there isn’t yet traditional peer review, the site has a self-correcting mechanism.

“If someone puts up a mistake or a silly error, they’re immediately pounced on by everyone else,” Pybus joked.

Salemi called it a sort of “worldwide peer review” because everyone can chip in with disagreements or suggestions for improvement.

“We’re not trying to pretend that what we’re putting there is what we would put in a finalized paper,” Pybus said. “We’re not explaining the results very fully, the site is very much for the cognoscenti — there’s jargon in there. Still, we’ve attempted to distill some of the most important points.”

The site employs a “wiki” — a simple program that allows contributors to upload and edit their own results. The application also lends itself to the graphics- and data-heavy computational analyses involved.

The collaborators aren’t quite sure yet how this open effort will affect their ability to publish their work in scientific journals.

“I guess it’s a bit of an experiment at the moment,” Pybus said. “It shouldn’t preclude publication later, but it’s up to the editors of the journals to make that decision. As an experiment, I hope it works out.”

In a study published in the April issue of Nature Genetics, researchers describe how a protein typically associated with good joint health could help counter one of the body’s defenses gone awry.

Iron is essential to the biomolecular mechanics of cell division, and bacterial infections need it in copious amounts to spread. As a natural antibiotic control system, the human body restricts iron distribution when tissues are inflamed or irritated.

Iron is also needed to produce hemoglobin with which the blood carries oxygen. During long illnesses that trigger this defense mechanism, hemoglobin production drops — choking off oxygen and further weakening already damaged bodies.

This leads to a condition known as anemia of chronic disease. Unlike anemia brought on by a lack of dietary iron, genetic conditions or bleeding, this type of anemia can only be treated by alleviating its root cause.

In cases involving intractable conditions such as AIDS, that’s often impossible.

However, with the analytical help of UF researcher Mitch Knutson, scientists at Harvard Medical School found that a compound called bone morphogenetic protein 6 (BMP6) interferes with the regulatory hormone hepcidin to release pent-up iron.

“As modern medicine improves and we continue to live longer, it means that the number of people living with long-term illnesses that are difficult to cure is skyrocketing,” said Knutson, an iron metabolism expert at the Institute of Food and Agricultural Sciences. “Right now, the only way to get rid of the anemia that makes these conditions worse is to get rid of the disease that’s the problem in the first place. If you can sidestep that, you could make a lot of people better in a significant way.”

Research has thus far been confined to mice and test-tube samples. But the researchers predict that treatment for humans could ultimately take the easy-to-administer form of an injection.

The work also lends insight to a condition known as juvenile hemochromatosis, a genetic disease sometimes called “iron overload,” in which iron accumulates in the liver, heart, joints and brain. The damage often leads to diabetes and arthritis.

“Iron is essential for life, but too much or too little of this element is deadly,” said Billy Andriopoulos Jr., a researcher at Harvard Medical School. “Understanding how our body maintains a safe balance is complicated, which is why it’s a good thing that researchers like Mitch contribute to the effort.”

Scientists from the University Hospital of Modena and Reggio Emilia in Modena, Italy, and the University of Zagreb in Croatia also contributed.

A lock-like molecule designed by University of Florida chemistry researchers clasps or unclasps based on exposure to light. In laboratory tests, the chemists put the lock on an enzyme involved in blood clotting. They then exposed the enzyme to visible and ultraviolet light. The clasp opened and closed, clotting the blood or letting it flow.

The results suggest that the biological hardware could one day be used to prevent the formation of tiny blood vessels that feed tumors. The little lock could also be placed in drugs, giving doctors the ability to release them only on diseased cells, tissues or organs — maximizing their efficacy while preventing side effects from damage to healthy tissue.

Endoscopic lights inserted into the patient could unlock the drugs when desired — or, the drugs could be activated by simply exposing the skin nearest the targets to near-infrared light, which penetrates the skin.
“The major idea is to use photons to manipulate a molecule’s function,” said Weihong Tan, the V.T. and Lois Jackson chaired professor of chemistry and a member of the UF Shands Cancer Center. “The next step would be to deliver therapeutic re-agents at the site, for example, of a cancer tumor.”

A paper about the research is set to appear next week in the online edition of the Proceedings of the National Academy of Sciences.

Youngmi Kim, who earned her doctorate in chemistry from UF in December and is the paper’s first author, said the lock has two interconnected parts: a molecule that responds to light, and a short, single strand of active DNA known to scientists as an aptamer. In its natural state, the aptamer binds with an enzyme called thrombin, which regulates blood clotting. The aptamer inactivates the enzyme, which allows the blood to flow freely.

Kim’s locking version, however, folds itself into a curved, closed shape when exposed to visible light. That prevents it from binding, or clasping, which means the enzyme remains active and the blood clots. But with ultraviolet light, the curving shape dissolves, freeing the aptamer to clasp, inactivating the enzyme, and allowing the blood to flow freely.

Tan said further research could point to ways to use the lock in combination with thrombin or other substances, natural or artificial, to inhibit the growth of blood vessels around tumors or the delivery of nutrients through those vessels.

The locking molecule could also be affixed to a wide range of other drugs to remain inactive until they reached their targets and light is applied, he said.

Not only that, but Tan said he has made progress on related research using similar mechanisms to make “hydrogels” that liquefy or gel around a target in response to light.

The research was funded by the National Science Foundation, the National Institutes of Health, and the UF Center for Nano-Bio Sensors, a state-supported Center of Excellence. The latest findings are part of a larger effort that has produced several new applications for both aptamers and nanomaterials.

The other authors of the PNAS paper are Joe Phillips, Haipeng Liu and Huaizhi Kang. Kim did the research for her doctoral dissertation in Tan’s lab.

A UF study, published online this week in the journal Plant, Cell and Environment, showed that when mouse-ear cress plants with the added gene were grown in arsenic-laden soil, their leaves contained as little as one-seventh the arsenic of control plants.

The study raises hopes that UF researchers can get similar results by putting the gene into rice plants, said Bala Rathinasabapathi, an associate professor with UF’s Institute of Food and Agricultural Sciences and co-author of the paper. If so, it could lead to new varieties for countries such as China and Bangladesh, where rice is a staple and the grain often absorbs arsenic from soil and water.

“In rice, it’s a very important problem,” he said.

Rice is the only crop plant that accumulates arsenic to a notable degree, said Rathinasabapathi, of the horticultural sciences department. When consumed even in small amounts over time, the toxic heavy metal increases cancer risk.

Arsenic has been used in pesticides, herbicides and wood preservatives. In some areas, residual arsenic from these products contaminates soil. In others, naturally occurring arsenic contaminates drinking and irrigation water used by millions.

The brake fern probably has many genes that allow it to absorb arsenic and survive, Rathinasabapathi said. So far, UF researchers have pinpointed one, a gene involved in production of glutaredoxin, a protein that helps plants deal with environmental stress.

This study was the first attempt to put that gene into another plant, he said. It was partly funded by an IFAS Research Innovation Award Rathinasabapathi received, amounting to about $12,500.

Other authors of the paper were Sabarinath Sundaram, a former UF postdoctoral associate now with Texas A&M University; Shan Wu, a UF biological scientist; and Lena Ma, a professor with UF’s soil and water science department.

Rathinasabapathi isn’t sure why the gene prevented cress plants from accumulating arsenic.

“Ferns are generally not very well investigated, genetically,” he said. “There may be many genes in the brake fern that will help with stress tolerance and may be helpful in improving crops, that is the overarching theme to my research program.”

The UF study is an interesting step, but there are challenges in producing viable low-arsenic rice varieties, said Andrew Meharg, biogeochemistry chair with the University of Aberdeen’s School of Biological Sciences in Scotland.

The mechanisms that control the arsenic content of rice grain are poorly understood, he said. If transgenic varieties were developed, they would need to outperform existing varieties in arsenic resistance and grain yield.

Meharg, an internationally known arsenic-contamination authority, analyzed white rice samples from 10 countries. He determined that residents of Bangladesh and China were at the most risk, based on the arsenic content and the amount eaten.