The Wildlife Conservation Society announced today that critically endangered alligators in China have a new chance for survival. The WCS's Bronx Zoo, in partnership with two other North American parks and the Department of Wildlife Conservation and Management of the State Forestry Administration of China, has successfully reintroduced alligators into the wild that are now multiplying on their own.

The alligator hatchlings—15 in number—are the offspring of a group of alligators that includes animals from the Wildlife Conservation Society's Bronx Zoo. The baby alligators represent a milestone for the 10-year effort to reintroduce the Chinese alligator on Chongming Island, located at the mouth of China's Yangtze River.

The announcement was made at the International Congress for Conservation Biology, convened by the Society for Conservation Biology in Beijing, China (July 11-16).

"We are grateful to our Chinese partners for their commitment to reintroduce Chinese alligators back into the wild," said Dr. Steven E. Sanderson, President and CEO of the Wildlife Conservation Society. "WCS has championed careful wildlife reintroductions for more than a century. The reintroduction of Chinese alligators is a great example of how WCS partners with governments and local communities around the world to save wildlife and wild places."

"This is fantastic news," said WCS researcher Dr. John Thorbjarnarson, one of the world's foremost experts on crocodilians and a participant in the project. "The success of this small population suggests that there's hope for bringing the Chinese alligator back to some parts of its former distribution."

Plans to reintroduce Chinese alligators started in 1999 with a survey conducted by WCS, the Anhui Forestry Bureau, and the East China Normal University in Anhui Province, the only remaining location where the reptiles are still found in the wild in what is a small fraction of the alligator's former range. The results of the survey were dire, with an estimate of fewer than 130 animals in a declining population.

An international workshop on the species was held in 2001, followed by recommendations for the reintroduction of captive bred alligators. The first three animals released in Hongxing Reserve of Xuancheng County in Anhui in 2003 were from the Anhui Research Center of Chinese Alligator Reproduction (ARCCAR).

To ensure the maximum genetic diversity for the effort, project participants imported 12 more animals to Changxing Yinjiabian Chinese Alligator Nature Reserve from North America, including four from the Bronx Zoo. From this group, three animals from the U.S. were released in 2007 along with three more alligators from Changxing. The alligators were given health examinations by veterinary professionals from WCS's Global Health Program and the Shanghai Wildlife Zoo and fitted with radio transmitters for remote monitoring before being released.

Experts reported that the reintroduced alligators successfully hibernated, and then in 2008, bred in the wild.

With a former range that covered a wide watershed area of East China, the Chinese alligator—or "tu long," which means "muddy dragon"—is now listed as "Critically Endangered" on IUCN's Red List of Threatened Species and is the most threatened of the 23 species of crocodilians in the world today. It is one of only two alligator species in existence (the other is the better known, and much better off, American alligator).

The Yangtze River, where the reintroduction of these alligators took place, is the third longest river in the world (after the Amazon and the Nile) and is China's most economically important waterway. The world's largest hydro-electric dam—the Three Gorges Dam—is also located on the river. The high levels of development along the river have become a challenge for native wildlife; in 2006, a comprehensive search for the Yangtze River dolphin, or baiji, didn't find any, although one isolated sighting of a dolphin was made in 2007.

Other participants in the project include the East China Normal University, Shanghai Forestry Bureau, Changxing Yinjiabian Chinese Alligator Nature Reserve, and Wetland Park of Shanghai Industrial Investment (Holdings) Co. Ltd.

The project is being supported by the Ocean Park Conservation Foundation, Hong Kong.

Researchers from the University of Southampton have drawn together 200 years' worth of oceanographic knowledge to investigate the distribution of a notorious deep-sea giant - the king crab. The results, published this week in the Journal of Biogeography, reveal temperature as a driving force behind the divergence of a major seafloor predator; globally, and over tens of millions of years of Earth's history.

In deep seas all over the world, around 100 species of king crabs live largely undiscovered. The fraction that have been found includes some weird and wonderful examples - Paralomis seagrantii has its eight walking legs and claws entirely covered in long fur-like setae; while related group Lithodes megacanthus grows to lengths of 1.5 metres, and has 15-20-cm long defensive spines covering its body. At temperatures of around 1- 4ºC, these crabs thrive in some of the colder waters on Earth; living and growing very slowly, probably to very old ages. Only in the cooler water towards the poles are king crabs found near the water surface - though temperatures found around some parts of the Antarctic (below 1ºC) are too extreme for their survival.

A paper, published 15 years ago in Nature is thought to show that king crabs evolved from shell-bound hermit crabs - similar to the familiar shoreline animals. Soft-bodied, but shell-free intermediate forms are found only in the shallow waters off Japan, Alaska, and Western Canada.

By looking at 200 years' worth of records from scientific cruises and museum collections, Sally Hall and Dr Sven Thatje from the University of Southampton's School of Ocean and Earth Science at the National Oceanography Centre, Southampton discovered that the soft-bodied forms can live at temperatures about ten degrees higher than the hard-bodied forms, but that both groups can only reproduce when temperature is between 1ºC up to 13-15ºC.

"It seems that most shallow-water representatives of this family are trapped in the coastal regions of the North Pacific because the higher sea surface temperatures further south prevent them from reproducing successfully and spreading," said Dr Thatje.

In order to leave this geographic bottleneck and spread around the world, the shallow water ancestors of current deep-sea groups had to go deep and adapt to the challenges of life in the deep sea. The process of adaptation to constant low temperatures (1-4ºC) prevailing in the deep sea seems to have narrowed the temperature tolerance range of the crabs where they have emerged to the surface waters in the Southern Hemisphere. With differences of only a couple of degrees in temperature affecting the distribution of the king crab, it is difficult to predict the consequences of range expansion in the warming waters around the Antarctic Peninsular region.

King crabs are of great commercial value, and fisheries are established in high latitude regions of both hemispheres. "Understanding their evolutionary history and ecology is key to supporting sustainable fisheries of these creatures," said research student Sally Hall. She adds: "Recent range extensions of king crabs into Antarctica, as well as that of the red king crab Paralithodes camtchaticus in the Barents Sea and along the coast off Norway emphasise the responsiveness of this group to rapid climate change."

This study reveals temperature as a driving force behind the speciation and radiation of a major seafloor predator globally and over tens of millions of years of Earth's history.

The study has been supported by the National Environment Research Council (UK) through a PhD studentship to Sally Hall, and a Research Grant from the Royal Society awarded to Dr Thatje.

Suspending a life in time is a theme that normally finds itself in the pages of science fiction, but now such ideas have become a reality in the annals of science.

Cornell ecologist Nelson Hairston Jr. is a pioneer in a field known loosely as "resurrection ecology," in which researchers study the eggs of such creatures as zooplankton -- tiny, free-floating water animals -- that get buried in lake sediments and can remain viable for decades or even centuries. By hatching these eggs, Hairston and others can compare time-suspended hatchlings with their more contemporary counterparts to better understand how a species may have evolved in the meantime.

The researchers take sediment cores from lake floors to extract the eggs; the deeper the egg lies in the core, the older it is. They then place the eggs in optimal hatching conditions, such as those found in spring in a temperate lake, and let nature take its course.

"We can resurrect them and discover what life was like in the past," said Hairston, who came to Cornell in 1985 and is a professor and chair of Cornell's Department of Ecology and Evolutionary Biology. "Paleo-ecologists study microfossils, but you can't understand much physiologically or behaviorally" with that approach, he said.

Hairston first became interested in the possibilities of studying dormant eggs in the late 1970s, when he was an assistant professor of zoology at the University of Rhode Island. There, he noticed that the little red crustaceans -- known as copepods -- in the pristine lake behind his Rhode Island home disappeared in the summer, only to return as larvae in the fall.

The observation prompted him to study why they disappear, research that revealed the copepods stay active under the ice in the winter, but they die out as their eggs lie dormant on the lake floor through the summer when the lake's fish are most active. When the fish become less active in the fall, larvae hatch from the eggs, and the copepods continue their life cycle.

This time suspension, where zooplankton pause their life cycles to avoid heavy predation or harsh seasonal and environmental conditions, also increases a species' local gene pool, with up to a century's worth of genetic material stored in a lake bed, Hairston said. When insects, nesting fish and boat anchors stir the mud, they can release old eggs that hatch and offer a wider variety of genetic material to the contemporary population.

In 1999 Hairston and colleagues published a paper in Nature that described how 40-year-old resurrected eggs could answer whether tiny crustaceans called Daphnia in central Europe's Lake Constance had evolved to survive rising levels of toxic cyanobacteria, known as blue-green algae. In the 1970s, phosphorus levels from pollution rose in the lake, increasing the numbers of cyanobacteria. The researchers hatched eggs from the 1960s and found they could not survive the toxic lake conditions, but Daphnia from the 1970s had adapted and survived.

Hairston and colleagues have organized a resurrection ecology symposium in September 2009, in Herzberg, Switzerland, to bring together researchers in this growing new field.

If that office inkjet printer has become just another fixture, it's time to take a fresh look at it. Similar technology may soon be used to develop paper-based biosensors that can detect certain harmful toxins that can cause food poisoning or be used as bioterrorism agents.

In a paper published in the July issue of Analytical Chemistry, John Brennan and his research team at McMaster University, working with the Sentinel Bioactive Paper Network, describe a method for printing a toxin-detecting biosensor on paper using a FujiFilm Dimatix Materials Printer.

The researchers demonstrated the concept on the detection of acetylcholinesterase (AChE) inhibitors such as paraoxon and aflatoxin B1 on paper using a "lateral flow" sensing approach similar to that used in a home pregnancy test strip.

The process involves formulating an ink like the one found in computer printer cartridges but with special additives to make the ink biocompatible. An ink comprised of biocompatible silica nanoparticles is first deposited on paper, followed by a second ink containing the enzyme, and the resulting bio-ink forms a thin film of enzyme that is entrapped in the silica on paper. When the enzyme is exposed to a toxin, reporter molecules in the ink change colour in a manner that is dependent on the concentration of the toxin in the sample.

This simple and cost-effective method of adhering biochemical reagents to paper is expected to bring the concept of bioactive paper a significant step closer to commercialization. The goal for bioactive paper is to provide a rapid, portable, disposable and inexpensive way of detecting harmful substances, including toxins, pathogens and viruses, without the need for sophisticated instrumentation. The research showed that the printed enzyme retains full activity for at least two months when stored properly, suggesting that such sensor strips should have a good shelf life.

Portable bio-sensing papers are expected to be extremely useful in monitoring environmental and food-based toxins, as well as in remote settings in less industrialized countries where simple bioassays are essential for the first stages of detecting disease.

Applications for bioactive paper also include clinical applications in neuroscience, drug assessment, and pharmaceutical development.

Bacteria know that they are too small to make an impact individually. So they wait, they multiply, and then they engage in behaviors that are only successful when all cells participate in unison. There are hundreds of behaviors that bacteria carry out in such communities. Now researchers at Rockefeller University have discovered one that has never been observed or described before in a living system.

In research published in the May 12 issue of Physical Review Letters, Albert J. Libchaber, head of the Laboratory of Experimental Condensed Matter Physics, and his colleagues, including first author Carine Douarche, a postdoctoral associate in the lab, show that when oxygen penetrates a sample of oxygen-deprived Escherichia coli bacteria, they do something that no living community had been seen to do before: The bacteria accumulate and form a solitary propagating wave that moves with constant velocity and without changing shape. But while the front is moving, each bacterium in it isn’t moving at all.

“It’s like a soliton,” says Douarche. “A self-reinforcing solitary wave.”

Unlike the undulating pattern of an ocean wave, which flattens or topples over as it approaches the shore, a soliton is a solitary, self-sustaining wave that behaves like a particle. For example, when two solitons collide, they merge into one and then separate into two with the same shape and velocity as before the collision. The first soliton was observed in 1834 at a canal in Scotland by John Scott Russell, a scientist who was so fascinated with what he saw that he followed it on horseback for miles and then set up a 30-foot water tank in his yard where he successfully simulated it, sparking considerable controversy.

The work began when Libchaber, Douarche and their colleagues placed E. coli bacteria in a sealed square chamber and measured the oxygen concentration and the density of bacteria every two hours until the bacteria consumed all the oxygen. (Bacteria, unlike humans, don’t die when starved for oxygen, but switch to a nonmotile state from which they can be revived.) The researchers then cracked the seals of the chamber, allowing oxygen to flow in.

The result: The motionless bacteria, which had spread out uniformly, began to move; first those around the perimeter, nearest to the seals, and then those further away. A few hours later, the bacteria began to spatially segregate into two domains of moving and nonmoving bacteria and pile up into a ring at the border of low-oxygen and no-oxygen. There they formed a solitary wave that propagated slowly but steadily toward the center of the chamber without changing its shape.

The effect, which lasted for more than 15 hours and covered a considerable distance (for bacteria), could not be explained by the expression of new proteins or by the addition of energy in the system. Instead, the creation of the front depends on the dispersion of the active bacteria and on the time it takes for oxygen-starved bacteria to completely stop moving, 15 minutes. The former allows the bacteria to propagate at a constant velocity, while the latter keeps the front from changing shape.

However, a propagating front of bacteria wasn’t all that was created. “To me, the biggest surprise was that the bacteria control the flow of oxygen in the regime,” says Libchaber. “There’s a propagating front of bacteria, but there is a propagating front of oxygen, too. And the bacteria, by absorbing the oxygen, control it very precisely.”

Oxygen, Libchaber explains, is one of the fastest-diffusing molecules, moving from regions of high concentration to low concentration such that the greater the distance it needs to travel, the faster it will diffuse there. But that is not what they observed. Rather, oxygen penetrated the chamber very slowly in a linear manner. Equal time, equal distance. “This pattern is not due to biology,” says Libchaber. “It has to do with the laws of physics. And it is organized in such an elegant way that the only thing it tells us is that we have a lot to learn from bacteria.”

If you are a cricket and it is a dry season on the San Pedro River in Arizona, on your nighttime ramblings to eat leaves, you are more likely to be ambushed by thirsty wolf spiders, or so a June 19 study suggests, published in the journal Ecology, and featured as an editor's choice in the journal Science.

A potential horror story for any cricket. However, it is also a tale of water limitation that looks beyond how most ecosystem studies are considered. Much current work about the relationships between predators and prey is based on nutrients or energy limitation – via a food web.

The research, performed by graduate student Kevin McCluney and associate professor John Sabo in School of Life Sciences at Arizona State University, demonstrates that under restricted water conditions, crickets consume more moist green leaves and wolf spiders more crickets. This distinct increase is driven by water limitation and the connectivity between organisms based on water – a water web.

With water the key ingredient to life, especially in the desert, why the focus on crickets and spiders and water webs? Studies on insects and riparian ecosystems such as these lend specific insights into how arid and semi-arid environments and their flora and fauna may be specifically affected by global climate change.

The authors note: "Water seems to be the ecological currency governing consumption behavior at multiple trophic levels, which indicates a role for water in understanding effects of global change on animal communities."

This article coincides with the June 18 release of the national report "Global Climate Change Impacts in the United States," funded by the National Science and Technology Council and authored by members of the U.S. Global Change Research Program, including ASU professor Nancy Grimm. The report contains a special section on the Southwest. Major changes in soil moisture and precipitation are expected as a result of climate change. McCluney and Sabo's study highlights one way ecological communities may be affected.

"Kevin's experiments suggest that by understanding water webs, we can find clues about how biodiversity may change as our region experiences drier climates under climate change," adds Sabo.

In that way, this study of crickets and spiders offers a looking glass into a future that extend much farther than the banks of one of the last undammed perennial rivers in the Southwest and the vibrant riparian community it supports.

"Drylands constitute more than one third of the land mass on Earth," McCluney notes. "While further testing is needed, our study may have implications for other ecosystems in light of recent reports of droughts and rivers drying up globally."

In addition to examining the water ties that bind inhabitants of terrestrial systems, Sabo and his students also examine aquatic ecosystems and the effects of human activity and water policy in the Southwest. In 2008, with funding from the National Science Foundation, Sabo launched a series of workshops to examine the impacts of dams on waterways in the United States held at the National Center for Ecological Synthesis and Analysis at University of California, Santa Barbara. Participants are working to define the ecological footprint that dams have had on water quantity and quality, the number of native and non-native species in rivers, the salinity of soils in some of the most productive agricultural areas, and the demand for irrigated water by the 100 largest cities in the United States. Along with studies by his ASU colleagues in the Global Institute of Sustainability and the College of Liberal Arts and Sciences, such as Juliet Stromberg, author of "The Ecology and Conservation of the San Pedro," Sabo seeks to illuminate the complexity of relationships behind developing sustainable management of water resources for both human and biodiversity needs.

Scientists have long suspected that the sex chromosome that only males carry is deteriorating and could disappear entirely within a few million years, but until now, no one has understood the evolutionary processes that control this chromosome's demise. Now, a pair of Penn State scientists has discovered that this sex chromosome, the Y chromosome, has evolved at a much more rapid pace than its partner chromosome, the X chromosome, which both males and females carry.

This rapid evolution of the Y chromosome has led to a dramatic loss of genes on the Y chromosome at a rate that, if maintained, eventually could lead to the Y chromosome's complete disappearance. The research team, which includes Associate Professor of Biology Kateryna Makova, the team's leader, and National Science Foundation Graduate Research Fellow Melissa Wilson, will publish its results in the 17 July 2009 issue of the journal PLoS Genetics.

"There are three classes of mammals," said Makova, "egg-laying mammals, like the platypus and the echidna; marsupials, like the opossum and the wallaby; and all other mammals -- called eutherians -- which include humans, dogs, mice, and giraffes. The X and Y chromosomes of marsupials and eutherians evolved from a pair of non-sex chromosomes to become sex chromosomes."

Humans have 23 pairs of chromosomes, which are the structures that hold our DNA, but just one pair of these chromosomes are sex chromosomes, while the others are referred to as non-sex chromosomes. "In eutherian mammals, the sex chromosomes contain an additional region of DNA whereas, in the egg-laying mammals and marsupials, this additional region of DNA is located on the non-sex chromosomes," said Makova. "At first, bits of DNA within this additional region were readily swapped between the X and Y chromosomes, but some time between 80 and 130 million years ago, the region became two completely separate entities that no longer swapped DNA. One of the regions became specifically associated with the X chromosome and the other became specifically associated with the Y chromosome."

By comparing the DNA of the X and Y chromosomes in eutherian mammals to the DNA of the non-sex chromosomes in the opossum and platypus, the team was able to go back in time to the point when the X and Y chromosomes were still swapping DNA, just like the non-sex chromosomes in the opossum and platypus. The scientists then were able to observe how the DNA of the X and Y chromosomes changed over time relative to the DNA of the non-sex chromosomes. "Our research revealed that the Y-specific DNA began to evolve rapidly at the time that the DNA region split into two entities, while the X-specific DNA maintained the same evolutionary rate as the non-sex chromosomes," said Makova.

Once the biologists determined that the Y chromosome has been evolving more rapidly and has been losing more genes as a result, they wanted to find out why the Y chromosome has not already disappeared entirely. "Today, the human Y chromosome contains less than 200 genes, while the human X chromosome contains around 1,100 genes," said Wilson. "We know that a few of the genes on the Y chromosome are important, such as the ones involved in the formation of sperm, but we also know that most of the genes were not important for survival because they were lost, which led to the very different numbers of genes we observe between the once-identical X and Y. Although there is evidence that the Y chromosome is still degrading, some of the surviving genes on the Y chromosome may be essential, which can be inferred because these genes have been maintained for so long."

The team then decided to test the hypothesis that some of the genes on the Y chromosome are being maintained because they are essential. The team's approach was to compare the expression and function of genes on the Y chromosome with analogous genes on the X chromosome. "If the genes' expressions and/or functions were different, then it would make sense that the genes on the Y chromosome would be maintained because they are doing something that the genes on the X chromosome can't do," said Makova. "This hypothesis turned out to be correct."

Although some of the genes on the Y chromosome have been maintained, most of them have died, and the team found evidence that some others are on track to disappear, as well. "Even though some of the genes appear to be important, we still think there is a chance that the Y chromosome eventually could disappear," said Makova. "If this happens, it won't be the end of males. Instead, a new pair of non-sex chromosomes likely will start on the path to becoming sex chromosomes."

In the future, the team plans to use its newly generated data to create a computer model that tracks the degeneration of the Y chromosome. The scientists hope to determine how long it will take for the Y chromosome to disappear. They also hope to identify the processes that are most important for degeneration of the Y chromosome.

This research was funded by the National Institutes of Health, Penn State, and the National Science Foundation.

A single evolutionary event appears to explain the short, curved legs that characterize all of today's dachshunds, corgis, basset hounds and at least 16 other breeds of dogs, a team led by the National Human Genome Research Institute (NHGRI), part of the National Institutes of Health, reported July 16. In addition to what it reveals about short-legged dogs, the unexpected discovery provides new clues about how physical differences may arise within species and suggests new approaches to understanding a form of human dwarfism.

In a study published in the advance online edition of the journal Science, the researchers led by NHGRI's Elaine Ostrander, Ph.D., examined DNA samples from 835 dogs, including 95 with short legs. Their survey of more than 40,000 markers of DNA variation uncovered a genetic signature exclusive to short-legged breeds. Through follow-up DNA sequencing and computational analyses, the researchers determined the dogs' disproportionately short limbs can be traced to one mutational event in the canine genome — a DNA insertion — that occurred early in the evolution of domestic dogs.

"Every species, including canine and human, carries an amazing record of evolution scripted in its genome that can teach us about the mechanisms at work in biology, as well as about human health and disease," said NHGRI Scientific Director Eric Green, M.D., Ph.D. "This work provides surprising evidence of a new way in which genome evolution may serve to generate diversity within a species."

Specifically, the researchers found that in contrast to other dog breeds, all short-legged dog breeds have an extra copy of the gene that codes for a growth-promoting protein called fibroblast growth factor 4 (FGF4). Although functional, the extra gene lacks certain parts of the DNA code, called introns, found in normal genes. These characteristics led researchers to conclude that the extra gene is a so-called retrogene that was inserted into the dog genome some time after the ancestor of modern dog breeds diverged from wolves.

To understand retrogenes, one first needs to understand how the cell normally makes proteins. To produce a protein, a gene's DNA code is transcribed into a molecule called messenger RNA (mRNA). The mRNA then leaves the cell's nucleus and enters the outer region of the cell, called the cytoplasm. There the mRNA is read by tiny molecular machines, called ribosomes, which use the information to assemble proteins.

Retrogenes are formed when the mRNA encounters something — often a type of virus called a retrovirus — that turns it back into DNA through a process referred to as reverse transcription. This new piece of DNA, which contains the same protein-coding information as the gene that produced the mRNA, may then be inserted back into the genome, usually at a much different place than the original gene. Depending on where it is inserted, this piece of DNA may or may not be capable of producing proteins. If it is functional, it is called a retrogene.

In the case of short-legged dogs, the inserted retrogene results in the overproduction of the FGF4 protein, which researchers hypothesize may turn on key growth receptors at the wrong times during fetal development. Veterinary researchers already know that in certain dog breeds the development of long bones is curtailed due to calcification of growth plates, resulting in short legs with a curved appearance. The trait, called disproportional dwarfism, or chondrodysplasia, is an American Kennel Club standard for more than a dozen domestic dog breeds, including the dachshund, corgi, Pekingese and basset hound. This trait is distinct from the uniformly miniature size of toy breeds, such as the toy poodle.

"Our findings suggest that retrogenes may play a larger role in evolution than has been previously thought, especially as a source of diversity within species," said the study's first author, Heidi G. Parker, Ph.D. of NHGRI. "We were surprised to find that just one retrogene inserted at one point during the evolution of a species could yield such a dramatic physical trait that has been conserved over time."

In the past, retrogenes have been recognized as an important source of changes that have fueled the divergence of species. However, the dog findings are the first example of a retrogene that has spurred significant and long-lasting variation within a single species.

The findings also may have implications for understanding human biology and disease. Researchers note that some people are affected by a similar appearing growth disorder, called hypochondroplasia, which belongs to a group of conditions commonly referred to as dwarfism. While about two-thirds of cases of human hypochondroplasia have been linked to a different gene, the cause of the other one-third remains a mystery.

"This study points to a new gene that should be investigated for its possible role in human hypochondroplasia," said Dr. Ostrander, the study's senior author and a senior investigator in NHGRI's Division of Intramural Research. "Our findings may prove valuable to scientists studying other aspects of human growth and development. The work also underscores the value of canine studies for uncovering new biological mechanisms that are likely relevant to human disease."

In addition to Ostrander and her colleagues at NHGRI, the team included researchers from Cornell University in Ithaca, N.Y.; the University of California, Los Angeles; Oregon Health and Science University, Portland; the Waltham Center for Pet Nutrition in Leicestershire, England; and Affymetrix Corporation, Santa Clara, Calif.

Plant roots provide the crops we eat with water, nutrients and anchorage. Understanding how roots grow and how hormones control that growth is crucial to improving crop yields, which will be necessary to address food security and produce better biofuels.

Now an international group of scientists, led by the Centre for Plant Integrative Biology at The University of Nottingham, has shed light on how a plant hormone is crucial in controlling the growth of plant roots.

Plant growth is driven by an increase in two factors: the number of cells, and their size. It is already known that the plant hormone gibberellin controls how root cells elongate as the root grows in the model plant Arabidopsis thaliana. Now a paper appearing in Current Biology describes for first time how this hormone also regulates the number of cells in the root in order to control root growth.

Gibberellin normally acts by signaling the removal of proteins which repress growth, and so promotes root cell production. The new research shows that mutant plants that do not produce gibberellin are unable to increase their cell production rate and the size of the root meristem, the zone of cell proliferation.

Plants in which the cells in the meristem were made to express a mutant version of the growth-repressing protein GAI not degraded by gibberellin showed disrupted cell proliferation. Expressing this mutant form, gai, in only one tissue, the endodermis (the innermost layer of the root cortex of a plant), was sufficient to stop the meristem enlarging. In effect, the rate of expansion of dividing endodermal cells dictates the equivalent rate in other tissues.

This research was headed by Dr Susana Ubeda-Tomás and Professor Malcolm Bennett of the Centre for Plant Integrative Biology, in collaboration with scientists in Nottingham, Cambridge, Edinburgh, Spain, Belgium and Sweden.

Professor Malcolm Bennett, Biology Director for the Centre for Plant Integrative Biology and Professor of Plant Sciences in the Division of Plant and Crop Sciences, said: “We have shown that gibberellin plays a crucial role in controlling the size of the root meristem, and that it is the endodermis which sets the pace for expansion rates in the other tissues.

“Understanding precisely how hormones regulate plant growth is one of the key areas of fundamental plant biology which will underpin crop improvements in the future.”

Amid reports that swine flu viruses are developing the ability to shrug off existing antiviral drugs, scientists in Japan are reporting a first-of-its kind discovery that could foster a new genre of antivirals that sidestep resistance problems, according to a new article.

Toshinori Sato and colleagues note in the new study that current antiviral drugs, including Tamiflu and Relenza, fight influenza by blocking key proteins that viruses need to reproduce. As the viruses reproduce, however, they can mutate into drug-resistant strains.

The researchers describe discovery of a new way to prevent flu viruses from infecting cells in the first place. They identified potential drugs that can block the first step in the infection process, and demonstrated that the substances work in cell cultures. "These results may lead to a new approach in the design of antiviral drugs," they state, noting that it could be used to develop new drugs for a variety of other medical problems.

Research by a group of Montreal scientists calls into question one of the most basic assumptions of human genetics: that when it comes to DNA, every cell in the body is essentially identical to every other cell. Their results appear in the July issue of the journal Human Mutation.

This discovery may undercut the rationale behind numerous large-scale genetic studies conducted over the last 15 years, studies which were supposed to isolate the causes of scores of human diseases.

Except for cancer, samples of diseased tissue are difficult or even impossible to take from living patients. Thus, the vast majority of genetic samples used in large-scale studies come in the form of blood. However, if it turns out that blood and tissue cells do not match genetically, these ambitious and expensive genome-wide association studies may prove to have been essentially flawed from the outset.

This discovery sprang from an investigation into the underlying genetic causes of abdominal aortic aneurysms (AAA) led by Dr. Morris Schweitzer, Dr. Bruce Gottlieb, Dr. Lorraine Chalifour and colleagues at McGill University and the affiliated Lady Davis Institute for Medical Research at Montreal's Jewish General Hospital. The researchers focused on BAK, a gene that controls cell death.

What they found surprised them.

AAA is one of the rare vascular diseases where tissue samples are removed as part of patient therapy. When they compared them, the researchers discovered major differences between BAK genes in blood cells and tissue cells coming from the same individuals, with the suspected disease "trigger" residing only in the tissue. Moreover, the same differences were later evident in samples derived from healthy individuals.

"In multi-factorial diseases other than cancer, usually we can only look at the blood," explained Gottlieb, a geneticist with McGill's Centre for Translational Research in Cancer. "Traditionally when we have looked for genetic risk factors for, say, heart disease, we have assumed that the blood will tell us what's happening in the tissue. It now seems this is simply not the case."

"From a genetic perspective, therapeutic implications aside, the observation that not all cells are the same is extremely important. That's the bottom line," he added. "Genome-wide association studies were introduced with enormous hype several years ago, and people expected tremendous breakthroughs. They were going to draw blood samples from thousands or hundreds of thousands of individuals, and find the genes responsible for disease.

"Unfortunately, the reality of these studies has been very disappointing, and our discovery certainly could explain at least one of the reasons why."

AAA is a localized widening and weakening of the abdominal aorta, and primarily affects elderly Caucasian men who smoke, have high blood pressure and high cholesterol levels. It often has no symptoms, but can lead to aortic ruptures which are fatal in 90 per cent of cases.

If the mutations discovered in the tissue cells actually predispose for AAA, they present an ideal target for new therapies, and may have even wider therapeutic implications.

"This will probably have repercussions for vascular disease in general," said Schweitzer, of McGill's Department of Medicine. "We have not yet looked at coronary or cerebral arteries, but I would suspect that this mutation may be present across the board."

Schweitzer is optimistic that this discovery may lead to new treatments for vascular disease in the near to medium term.

"The timeline might be five to 10 years," he said. "We have to do in-vitro cell culture experiments first, prove it in an animal model, and then develop a molecule or protein which will affect the mutated gene product. This is the first step, but it's an important step."

Scientists at NOAA's National Centers for Coastal Ocean Science and the Monterey Bay Aquarium Research Institute (MBARI) have successfully conducted the first remote detection of a harmful algal species and its toxin below the ocean's surface. The achievement was recently reported in the June issue of Oceanography.

This achievement represents a significant milestone in NOAA's effort to monitor the type and toxicity of harmful algal blooms (HABs). HABs are considered to be increasing not only in their global distribution, but also in the frequency, duration, and severity of their effects. HABs damage coastal ecosystem health and pose threats to humans as well as marine life. Climate change is expected to exacerbate this trend, since many critical processes that govern HABs dynamics, such as water temperature and ocean circulation, are influenced by climate.

A MBARI-designed robotic instrument called the Environmental Sample Processor, or 'ESP,' designed as a fully-functional analytical laboratory in the sea, lets researchers collect the algal cells and extract the genetic information required for organism identification as well as the toxin needed to assess the risk to humans and wildlife. The ESP then conducts specialized, molecular-based measurements of species and toxin abundance, and transmits results to the laboratory via radio signals.

"This represents the first autonomous detection of both a HAB species and its toxin by an underwater sensor," notes Greg Doucette, Ph.D., a research oceanographer at NOAA's Center for Coastal Environmental Health and Biomolecular Research laboratory in Charleston, S.C. "It allows us to determine not only the organism causing a bloom, but also the toxicity of the event, which ultimately dictates whether it is a threat to the public and the ecosystem."

For the first demonstration of the ESP's ability to detect HABs and their toxins, Doucette and his MBARI colleague, Chris Scholin, Ph.D., targeted certain members of the algal genus Pseudo-nitzschia and their neurotoxin, domoic acid in Monterey Bay, Calif.

Pseudo-nitzschia and domoic acid have been a concern in the Monterey Bay area for well over a decade. In 1991, the first U.S. outbreak of domoic acid poisoning was documented in Monterey Bay. This outbreak resulted in the unusual deaths of numerous pelicans and cormorants that ingested sardines and anchovies, which had accumulated the domoic acid by feeding on a bloom of the toxic algae.

In the spring of 1998, a mass mortality of sea lions in and around the Monterey Bay area was attributed to the sea lions' feeding on domoic acid contaminated anchovies. Since that time, Pseudo-nitzschia and domoic acid have appeared on virtually an annual basis in California coastal waters and are the objects of an intensive statewide monitoring program run by the California Dept. of Public Health. Humans also can be affected by the toxin through consumption of contaminated seafood such as shellfish.

"Our public health monitoring program is one of the many groups that can benefit directly from the ESP technology and ability to provide an early warning of impending bloom activity and toxicity," said Gregg Langlois, director of the state of California's Marine Biotoxin Monitoring Program. "This is critical information for coastal managers and public health officials in mitigating impacts on the coastal ecosystem, since the toxicity of these algae can vary widely from little or no toxicity to highly toxic."

Beyond improving forecasting of HABs, this research will contribute to the rapidly emerging U.S. Integrated Ocean Observing System (IOOS) by adding a new way to make coastal ocean observations.

Bordetella hinzii just may be the Eddie Haskell of avian bacteria. Like the notoriously sneaky character from the iconic 1950s television show "Leave It to Beaver," B. hinzii has been causing trouble and dodging the blame.

Until recently, B. hinzii was believed to be nonpathogenic in poultry. But Agricultural Research Service (ARS) scientists have shown that the bacterium caused severe disease in turkeys that was attributed to another Bordetella species.

B. avium is a pathogenic bacterium that causes upper respiratory disease in poultry and wild birds. It is very similar to B. hinzii, and the two species are difficult to distinguish without using highly specific, DNA-based tests.

Scientists at the ARS National Animal Disease Center (NADC) in Ames, Iowa, used these tests to examine several Bordetella isolates, including some that had caused 100 percent morbidity in turkey poults. Although the isolates had been labeled as B. avium, the scientists found that they were actually B. hinzii, flouting conventional wisdom that the bacterium could not cause disease in poultry.

B. hinzii has been found in poultry with respiratory disease, but was believed to be nonpathogenic because previous attempts to cause disease in chickens and turkeys with the bacterium have failed.

To test the bacterium's pathogenicity, NADC microbiologist Karen Register and veterinary medical officer Robert Kunkle selected six genetically distinct strains of B. hinzii and attempted to infect turkeys with them. Four of the strains were able to grow and persist in the trachea and also caused clinical disease. The strains varied in severity, although none demonstrated 100 percent morbidity.

This study showed for the first time that some strains of B. hinzii can cause disease in turkeys. The results of the study were published in the March 2009 issue of Avian Diseases.

In a related study with chickens, no birds developed clinical disease, suggesting that the pathogenicity of B. hinzii does not extend to chickens.

Now, NADC scientists are examining how the disease-causing strains of the bacterium differ. They are also working to identify virulence factors that influence disease development in turkey poults.

Varroa mites could literally be walking into a trap—thanks to a new attractant developed by Agricultural Research Service (ARS) scientists in Gainesville, Fla.

The 1/16-inch long parasite, Varroa destructor, is a top pest of honey bees nationwide, hindering the beneficial insects' ability to pollinate almonds, blueberries, apples, zucchini and many other flowering crops.

At the ARS Chemistry Research Unit in Gainesville, research leader Peter Teal and colleagues are testing a bait-and-kill approach using sticky boards and natural chemical attractants called semiochemicals.

In nature, Varroa mites rely on these semiochemicals to locate—and then feed on—the bloodlike hemolymph of both adult honey bees and their brood. Severe infestations can decimate an affected hive within several months—and rob the beekeeper of profits from honey or pollinating services. But in this case, the mites encounter a more heady bouquet of honey bee odors that lure the parasites away from their intended hosts and onto the sticky boards, where they starve.

In preliminary tests, 35 to 50 percent of mites dropped off the bees when exposed to the attractants. Free-roving mites found the semiochemicals even more attractive, according to Teal.

Moreover, the extra dose of semiochemicals wafting through hives didn't appear to significantly interfere with the honey bees' normal behavior or activity, added Teal who, along with postdoctoral associate Adrian Duehl and University of Florida collaborator Mark Carroll, reported the results this past January at the 2009 North American Beekeeping Conference in Reno, Nev.

The team hopes ARS' patenting of the Varroa mite attractants will encourage an industrial partner to develop the technology further.

Biologically speaking, many animals besides dogs bark, according to Kathryn Lord at the University of Massachusetts Amherst, but the evolutionary biologist also says domestic dogs vocalize in this way much more than birds, deer, monkeys and other wild animals that use barks. The reason is related to dogs’ 10,000-year history of hanging around human food refuse dumps, she suggests.

In her recent paper in a special issue of the journal, Behavioural Processes, Lord and co-authors from nearby Hampshire College also provide the scientific literature with its first consistent, functional and acoustically precise definition of this common animal sound.

As Lord, a doctoral candidate in organismic and evolutionary biology at UMass Amherst, explains, “We suggest an alternative hypothesis to one that many biologists seem to accept lately, which seeks to explain dog barking in human-centric terms and define it as an internally motivated vocalization strategy.” In the researchers’ view, however, barking is not a special form of communication between dogs and humans. “What we’re saying is that the domestic dog does not have an intentional message in mind, such as, ‘I want to play’ or ‘the house is on fire,’” explains Lord.

Rather, she and colleagues say barking is the auditory signal associated with an evolved behavior known as mobbing, a cooperative anti-predator response usually initiated by one individual who notices an approaching intruder. A dog barks because she feels an internal conflict―an urge to run plus a strong urge to stand her ground and defend pups, for example. When the group joins in, the barks intimidate the intruder, who often flees.

“We think dogs bark due to this internal conflict and mobbing behavior, but domestic dogs bark more because they are put, and put themselves into, conflicting situations more often,” she says.

The reason traces back to the first dogs that started hanging around human food dumps about 8,000 to 10,000 years ago. They would have experienced a serious disadvantage if they had run a mile away every time a human or other animal approached. As Lord explains, “In evolutionary terms, dogs self-selected the behavior of sticking around, overcoming their fear and being rewarded by getting to eat that meal before some other dog got it. Thus these animals allow people to get unusually close. The scared ones die while those less scared stay, eat, survive and reproduce. So they inherit the tendency.”

She adds, “By contrast, wild animals like wolves have a very long flight distance. They hear something and they run before you’d ever see them. Dogs hang around, but now they have committed to holding their ground and the closer an ‘intruder’ gets, the more likely mobbing is to occur rather than running away.”

An example of the domestic environment (rather than the dog’s own behavior) that increases barking is the animal stuck behind a fence with a person approaching, says Lord. “The dog may either feel anxiety or excitement at seeing a stranger but in either case the dog is prevented from approaching or fleeing. This creates conflict, and thus barking.”

Several technical pages of the researchers’ recent paper identify eight different parameters in three categories which must be met in order to classify a given vocalization as a bark. These include tonality, noise, pitch, volume or amplitude, abrupt onset and pulse duration, for example.

In their view, barking is not self-referential communication to convey a message, but a short, loud sound characterized by combining both noise and tonal sounds, which is unusual in animal calls. This definition widens the bark’s usefulness as a functional behavior seen in many animals, though domesticated dogs display it more often. “Using this definition, even birds bark, and certainly many mammals besides canines, including baboons and monkeys, rodents and deer also bark,” Lord explains. “In a whole bunch of mammals and birds, what they do in such conflicted situations is bark.”

This evolutionary view of barking does not sit well with some pet owners who insist that Buffy communicates with them by barking, the researchers acknowledge. “We understand the objection when people say their dogs bark for supper or to get out and play,” Lord says. “Dogs do quickly learn the simple cause-and-effect relationship between their bark at 10 p.m. and the fact that you’ll get right up and take them outdoors. It’s true, but in our view it’s going too far to suggest the animal is intentionally referring to a specific activity. Rather, it has just learned cues, as it does when it learns to sit or beg for a treat.”

Forget the old folk tales about snakes hypnotizing their prey. The tentacled snake from South East Asia has developed a more effective technique. The small water snake has found a way to startle its prey so that the fish turn toward the snake's head to flee instead of turning away. In addition, the fish's reaction is so predictable that the snake actually aims its strike at the position where the fish's head will be instead of tracking its actual movement.

"I haven't been able to find reports of any other predators that exhibit a similar ability to influence and predict the future behavior of their prey," says Kenneth Catania, associate professor of biological sciences at Vanderbilt University, who has used high-speed video to deconstruct the snake's unusual hunting technique.

His observations are published the week of June 15 in the online early edition of the Proceedings of the National Academy of Sciences.

Catania, who is the recipient of a MacArthur "genius" award, studies the brains and behavior of species with extreme specializations. He was attracted to the tentacled snake because it is the only snake that comes equipped with a pair of short tentacles on its nose and he was curious about their function.

"Before I begin a study on a new species, it is my practice to spend some time simply observing its basic behavior," Catania explains. The snake forms an unusual "J" shape with its head at the bottom of the "J" when it is fishing. Then it remains completely motionless until a fish swims into the area near the hook of the "J." That is when the snake strikes.

The snakes' motions take only a few hundredths of a second and are too fast for the human eye to follow. However, its prey reacts even faster, in a few thousandths of a second. In fact, fish are famous for the rapidity of their escape response and it has been extensively studied. These studies have found that many fish have a special circuit in their brains that initiates the escape, which biologists call the "C-start." Fish ears sense the sound pressure on each side of their body. When the ear on one side detects a disturbance, it sends a message to the fishes' muscles causing its body to bend into a C-shape facing in the opposite direction so it can begin swimming away from danger as quickly as possible.

Catania is the first scientist to study this particular predator-prey interaction with the aid of a high-speed video camera. When he began examining the movements of the snake and its prey in slow motion, he saw something peculiar. When the fish that the snake targets turn to flee, most of them turn toward the snake's head and many literally swim into its jaws! In 120 trials with four different snakes, in fact, he discovered that an amazing 78 percent of the fish turned toward the snake's head instead of turning away.

Next, the biologist noticed that the first part of its body that the snake moves is not its head. Instead, it flexes a point midway down its body. Using a sensitive hydrophone that he put in the aquarium, he confirmed that this body fake produces sound waves intense enough to trigger the fish's C-start response. Because these sound waves come from the side opposite the snake's head, this reflex action drives the fish to turn and swim directly toward the snake's mouth.

"Once the C-start begins, the fish can't turn back," Catania says. "The snake has found a way to use the fish's escape reflex to its advantage."

As he studied the snake's actions even closer, he made an even more remarkable discovery. When it strikes, the snake doesn't aim for the fish's initial position and then adjust its direction as the fish moves – the way most predators do. Instead it heads directly for the location where it expects the fish's head to be.

"The best evidence for this is the cases when the snake misses," says Catania. "Not all the targeted fish react with a C-start and the snake almost always misses those that don't react reflexively."

Catania's next step will be to determine whether this predictive capability is hard-wired or learned. To do so, he hopes to obtain some baby snakes that have just hatched and videotape their first efforts to catch prey.

The research was supported by a grant from the National Science Foundation.

A new, highly detailed study of the H1N1 flu virus shows that the pathogen is more virulent than previously thought.

Writing in a fast-tracked report published July 13, 2009 in the journal Nature, an international team of researchers led by UW-Madison virologist Yoshihiro Kawaoka provides a detailed portrait of the pandemic virus and its pathogenic qualities.

In contrast with run-of-the-mill seasonal flu viruses, the H1N1virus exhibits an ability to infect cells deep in the lungs, where it can cause pneumonia and, in severe cases, death. Seasonal viruses typically infect only cells in the upper respiratory system.

"There is a misunderstanding about this virus," says Kawaoka, a professor of pathobiological sciences at the UW-Madison School of Veterinary Medicine and a leading authority on influenza. "People think this pathogen may be similar to seasonal influenza. This study shows that is not the case. There is clear evidence the virus is different than seasonal influenza."

The ability to infect the lungs, notes Kawaoka, is a quality frighteningly similar to those of other pandemic viruses, notably the 1918 virus, which killed tens of millions of people at the tail end of World War I. There are likely other similarities to the 1918 virus, says Kawaoka, as the study also showed that people born before 1918 harbor antibodies that protect against the new H1N1 virus.

And it is possible, he adds, that the virus could become even more pathogenic as the current pandemic runs its course and the virus evolves to acquire new features. It is now flu season in the world's southern hemisphere, and the virus is expected to return in force to the northern hemisphere during the fall and winter flu season.

To assess the pathogenic nature of the H1N1 virus, Kawaoka and his colleagues infected different groups of mice, ferrets and non-human primates — all widely accepted models for studies of influenza — with the pandemic virus and a seasonal flu virus. They found that the H1N1 virus replicates much more efficiently in the respiratory system than seasonal flu and causes severe lesions in the lungs similar to those caused by other more virulent types of pandemic flu.

"When we conducted the experiments in ferrets and monkeys, the seasonal virus did not replicate in the lungs," Kawaoka explains. "The H1N1 virus replicates significantly better in the lungs."

The new study was conducted with samples of the virus obtained from patients in California, Wisconsin, the Netherlands and Japan.

The new Nature report also assessed the immune response of different groups to the new virus. The most intriguing finding, according to Kawaoka, is that those people exposed to the 1918 virus, all of whom are now in advanced old age, have antibodies that neutralize the H1N1 virus. "The people who have high antibody titers are the people born before 1918," he notes.

Kawaoka says that while finding the H1N1 virus to be a more serious pathogen than previously reported is worrisome, the new study also indicates that existing and experimental antiviral drugs can form an effective first line of defense against the virus and slow its spread.

There are currently three approved antiviral compounds, according to Kawaoka, whose team tested the efficacy of two of those compounds and the two experimental antiviral drugs in mice. "The existing and experimental drugs work well in animal models, suggesting they will work in humans," Kawaoka says.

Antiviral drugs are viewed as a first line of defense, as the development and production of mass quantities of vaccines take months at best.

The appearance of many species of flowering plants on Earth, and especially their relatively rapid dissemination during the Cretaceous (approximately 100 million years ago) can be attributed to their capacity to transform the world to their own needs.

In an article in Ecology Letters, Wageningen ecologists Frank Berendse and Marten Scheffer postulate that flowering plants changed the conditions during the Cretaceous period to suit themselves. The researchers have consequently provided an entirely new explanation for what Charles Darwin considered to be one of the greatest mysteries with which he was confronted.

During the Cretaceous, the Earth's surface underwent one of its greatest changes in vegetation composition, a change which also took place with unprecedented speed. Frank Berendse (Professor of Nature Conservation and Plant Ecology), and Marten Scheffer, (Professor of Aquatic Ecology), both at Wageningen University, wanted to understand how this happened. They looked for the explanation in a totally unconventional direction.

Before the early Cretaceous, the vegetation consisted primarily of gymnosperms and ferns. These plants were largely replaced by an entirely new group of plants: the angiosperms (flowering plants). During the early Cretaceous – approximately 125 million years ago – the first flowering plants evolved. Soon thereafter, the gymnosperms in the tropics were replaced almost entirely by the angiosperms. And by the end of the Cretaceous (65 million years ago), the empire of the flowering plants had become definitively established in much of the rest of the world. The gymnosperms continued to exist only in the far north – which is the case even today.

The rapid increase in the fantastic diversity of flowering plants – linked to their rapid conquest of the Earth – was one of the greatest puzzles faced by Charles Darwin. In a letter to Joseph Hooker dated 22 July 1879, he referred to an "abominable mystery". The great diversity of fossil flowering plants from the late Cretaceous, while there were virtually no fossils known from the early Cretaceous, appeared to be completely in conflict with his vision that the emergence of new species could only take place very gradually.

The big question was how this massive change could have taken place with such unprecedented speed. Was it because – just before the Cretaceous – that the big Sauropods were forced out by the much smaller Ornithischian dinosaurs, which then systematically ate all the seedlings of the gymnosperms? Or was it because the flowering plants could evolve simultaneously with many insect species that could pollinate their flowers?

According to Berendse and Scheffer, we must think in a totally different direction. They postulate that the flowering plants were able to change the world to suit their own needs. They grew more rapidly and therefore required more nutrients. In a world that was poor in nutrients and was entirely dominated by the gymnosperms, that kept the soil poor - with their poorly degradable litter - flowering plants had great difficulties to establish. But at some locations where the gymnosperms had temporarily disappeared, for example due to floods, fires or storms, the angiosperms could increase so that they were capable of improving their own conditions with their easily degradable litter.

According to the theory of Berendse and Scheffer, this led to positive feedback; as a result, the flowering plants could increase even more rapidly and were capable of replacing the angiosperms in much of the world. Ultimately, the improved edibility of the leaves and fruits of the flowering plants led to a tremendous increase in the number of plant eaters on the Earth, which opened the way to the rapid evolution of mammals, and finally to the appearance of humans.