A new species of a rugged darkling beetle that thrives in an arid region of the Chihuahuan Desert is being named in honor of Theodore Roosevelt on the 100th anniversary of a speech he gave at Tempe Normal School, now Arizona State University (ASU). The speech, delivered March 20, 1911, focused on the role of government, the importance of an educated citizenry, and the “far-sighted wisdom” of the Territory of Arizona. The new species of beetle, Stenomorpha roosevelti, covered in thick dark hair with golden setal pads on tarsal segments of legs, was discovered in the protected area of Cuatro Ciénegas, a biodiversity-rich oasis in Coahuila, Mexico. It was discovered and named by Dr. Aaron Smith, an authority on darkling beetles and a postdoctoral research associate at ASU; Dr. Kelly Miller, an assistant professor and curator of arthropods for the Museum of Southwestern Biology at the University of New Mexico; and Dr. Quentin Wheeler, a professor and founding director of the International Institute for Species Exploration at ASU. “We wanted to do something distinct and long lasting to mark Roosevelt’s impact on Arizona and conservation as we ramp up to the state centennial next year,” said Dr. Wheeler, an ASU vice president and dean of the College of Liberal Arts and Sciences. According to Douglas Brinkley’s book, “The Wilderness Warrior: Theodore Roosevelt and the Crusade for America,” it was Roosevelt’s executive orders that saved such natural treasures as Devils Tower, the Petrified Forest, and Arizona’s Grand Canyon. “Naming a new species for President Roosevelt honors his achievements as a pioneering conservationist, naturalist and explorer, and helps us bring attention to biodiversity and the field of taxonomy. The ruggedness of this darkling beetle reflects many of the hardy and resilient characteristics of President Roosevelt,” said Dr.
Exotic Kingfisher on Verge of Extinction
The Tuamotu kingfisher is a multicolored, tropical bird with bright blue feathers, a dusty orange head, and a bright green back. The entire population of these birds – fewer than 125 – lives on one tiny island in the south Pacific, and without serious intervention, they will soon no longer exist. One University of Missouri researcher is trying to stop the birds’ extinction by working with farmers and residents on the island inhabited by the kingfishers. “If we lose these birds, we lose 50,000 years of uniqueness and evolution,” said Dr. Dylan Kesler, assistant professor in fisheries and wildlife at the University of Missouri’s School of Natural Resources in the College of Agriculture, Food and Natural Resources. “Because it has lived in isolation for a very long time, it’s unlike any other bird. There is no other bird like this on the planet.” In new studies published in the journal The Auk (published by the American Ornithologists Union) and the Journal of Wildlife Management, Dr. Kesler and his team of researchers have uncovered important information to help ensure the birds’ survival and a unique way to attach radio transmitters to the birds to track them. To survive, the kingfishers need several specific habitat characteristics: (1) Hunting Perches about 5 feet off the ground – The birds hunt by “pouncing.” They watch their prey and then fall on them from hunting perches about 5 feet high. Without the perches in broadleaf trees at the appropriate height, the birds have no way to hunt. (2) Exposed ground – the birds’ food consists mainly of lizards, which are easier to spot where the ground is clear of vegetation. When coconut farmers conduct intermediate burns on their land – which are hot enough to kill brush, but do not lead to widespread fires or kill the lizards – it exposes more ground and the birds can see the lizards.
Jumping Gene Used in New Method to Study Gene Regulation
Scientists at the European Molecular Biology Laboratory (EMBL) in Heidelberg, Germany, have developed a new method for studying gene regulation, by employing a jumping gene as an informant. Described online on March 21, 2011, in Nature Genetics, the new method is called GROMIT. It enables researchers to systematically explore the very large part of our genome that does not code for proteins, and which likely plays a large role in making each of us unique, by controlling when, where, and to what extent genes are expressed. Thanks to GROMIT, scientists can also create mouse models for human diseases such as Down syndrome. “Our findings change how we think about gene regulation, and about how differences between individual genomes could lead to disease,” said Dr. François Spitz from EMBL, who led the study. Until now, scientists thought that regulatory elements essentially controlled a specific gene or group of genes. With GROMIT, Spitz and colleagues discovered that the genome is not organized in such a gene-centric manner. Instead, it appears that each regulatory element can potentially control whatever is within its reach. This means that mutations that simply shuffle genetic elements around (without deleting or altering them) can have striking effects, by bringing genes into or out of specific regulators’ zones of influence. The EMBL scientists also discovered that many of these regulatory elements act in specific tissues, which suggests that the expression levels of every gene, even those that are active all over the body, are fine-tuned at the tissue level. Jumping genes – or transposons – are sequences of DNA that can move from place to place within a cell’s genome. This can have detrimental effects, for example if this extra genetic material is inserted into an important gene, disrupting it. But Dr.
LincRNA Plays Key Role in Determining Cell Identity
If some of your brain cells suddenly decided to become fat cells, it could cloud your decision-making capacity. Fortunately, early in an organism’s development, cells make firm and more-or-less permanent decisions about whether they will live their lives as, say, skin cells, brain cells, or fat cells. These decisions essentially boil down to which proteins, among all the possible candidates encoded in a cell’s genes, the cell will tend to make under ordinary circumstances. But exactly how a cell chooses its default protein selections from an overwhelmingly diverse genetic menu is somewhat mysterious. A new study from the Stanford University School of Medicine and collaborating institutions may help solve the mystery. The researchers discovered how a particular variety of the biomolecule RNA that had been thought to be largely irrelevant to cellular processes plays a dynamic regulatory role in protein selection. In unraveling this molecular mechanism, the study also offers enticing clues as to how certain cancers may arise. Dr. Howard Chang, associate professor of dermatology at Stanford, is the senior author of the study, published online on March 20, 2011, in Nature. “All the cells in your body have the same genes, but they don’t all make the same proteins,” said Dr. Chang, who is also a Howard Hughes Medical Institute Early Career Scientist. In this new study, Dr. Chang and his colleagues identified a novel action by a subset of RNA that reinforces cells’ decisions about which combinations of their genes are to be active and which must stay silent. RNA, according to older textbooks, mainly functions as a messenger: a copy of a gene, made by a cell’s gene-reading machinery, that can float away from the chromosomes where genes reside to other places in the cell where proteins are made.
Mutant Prions Can Help Correct Misfolding of Proteins
Clumps of misfolded proteins are prime suspects in many neurological disorders including Alzheimer’s, Parkinson’s, and Creutzfeld-Jakob disease. Those diseases are devastating and incurable, but a team of biologists at Brown University reports that cells can fix the problems themselves with only a little bit of help. The insight suggests that there are more opportunities to develop a therapy for protein misfolding than scientists had thought. “There are multiple steps that you could target,” said Susanne DiSalvo, a Brown biology graduate student and lead author of a paper published online on March 20, 2011, in Nature Structural & Molecular Biology. In the study, the research team, led by Dr. Tricia Serio, associate professor of medical science, explains how two different beneficial mutant prions managed to foil the amplification of harmful clumps of misfolded proteins in yeast. Cells have an internal quality assurance system to break up and refold misfolded proteins, but that system can be overwhelmed by diseases. DiSalvo was the first to observe that the mutants act at distinct stages to tip the balance back in favor of the cells, allowing them to overcome the problem. Dr. Serio says the molecular mechanisms appear to explain how similar mutants solve protein misfolding in mammals, including people. The phenomenon had been poorly understood and has never been exploited to develop a successful therapy. Until now most scientists guessed that the only way to stop the runaway misfolding was right at the beginning and assumed the mutants must be blocking that first step to keep the protein in a harmless form. DiSalvo’s work instead suggests that there are many opportunities throughout the process where even a mild intervention could give cells what they need to gain the upper hand, Dr. Serio said.
LNA-Based Compounds Can Inhibit Entire Disease-Associated MicroRNA Families
A study published online on March 20, 2011, in Nature Genetics demonstrates that tiny locked nucleic acid (LNA)-based compounds developed by Santaris Pharma A/S can inhibit entire disease-associated microRNA families. This provides a potential new approach for treating a variety of diseases including cancer, viral infections, cardiovascular and muscle diseases. Santaris Pharma A/S, a clinical-stage biopharmaceutical company focused on the research and development of mRNA and microRNA targeted therapies, developed the tiny LNA-based compounds, which are 8-mer LNA oligonucleotides, using its proprietary LNA Drug Platform. The high affinity and target specificity of tiny LNA-based compounds enabled functional inhibition of both single microRNAs and entire microRNA families in a range of tissues in vivo without off-target effects. MicroRNAs have emerged as an important class of small regulatory RNAs encoded in the genome. They act to control the expression of sets of genes and entire pathways and are thus thought of as master regulators of gene expression associated with many diseases. Because they dictate the expression of fundamental regulatory pathways, microRNAs represent potential drug targets in the treatment of many disease processes. “Using tiny LNA-based compounds to successfully inhibit entire disease-associated microRNA families provides a new range of opportunities to develop novel microRNA-targeted drugs for both in-house drug discovery programs, as well as with our partners,” said Dr. Henrik Ørum, Vice President and Chief Scientific Officer of Santaris Pharma A/S.
Berkeley Scientists Discuss Systems Biology Advances in Review Issue of Cell
Dr. Adam Arkin, director of the Physical Biosciences Division of the U.S. Department of Energy (DOE)’s Lawrence Berkeley National Laboratory and a leading computational biologist, is the corresponding author of an essay in the March 18, 2011 issue of Cell which describes in detail key technologies and insights that are advancing systems biology research. The paper is titled “Network News: Innovations in 21st Century Systems Biology.” Co-authoring the article is Dr. David Schaffer, a chemical engineer with Berkeley Lab’s Physical Biosciences Division. Both Drs. Arkin and Schaffer also hold appointments with the University of California (UC) Berkeley. The Cell issue is devoted to reviews of systems biology. “System biology aims to understand how individual elements of the cell generate behaviors that allow survival in changeable environments, and collective cellular organization into structured communities,” Dr. Arkin says. “Ultimately, these cellular networks assemble into larger population networks to form large-scale ecologies and thinking machines, such as humans.” In their essay, Drs. Arkin and Schaffer argue that the ideas behind systems biology originated more than a century ago and that the field should be viewed as “a mature synthesis of thought about the implications of biological structure and its dynamic organization.” Research into the evolution, architecture, and function of cells and cellular networks in combination with ever expanding computational power has led to predictive genome-scale regulatory and metabolic models of organisms. Today systems biology is ready to “bridge the gap between correlative analysis and mechanistic insights” that can transform biology from a descriptive science to an engineering science.
New Strategy for Extending Useful Life of Antibiotics
A team of scientists from the University of Oxford, U.K., has devised a new strategy that could one day slow, possibly even prevent, the spread of drug-resistant bacteria. In a new research report published in the March 2011 issue of GENETICS, the scientists show that bacterial gene mutations that lead to drug resistance come at a biological cost not borne by nonresistant strains. They speculate that by altering the bacterial environment in such a way to make these costs too great to bear, drug-resistant strains would eventually be unable to compete with their nonresistant neighbors and die off. “Bacteria have evolved resistance to every major class of antibiotics, and new antibiotics are being developed very slowly; prolonging the effectiveness of existing drugs is therefore crucial for our ability to treat infections,” said Dr. Alex Hall, a researcher involved in the work from the Department of Zoology at the University of Oxford. “Our study shows that concepts and tools from evolutionary biology and genetics can give us a boost in this area by identifying novel ways to control the spread of resistance.” The research team measured the growth rates of resistant and susceptible Pseudomonas aeruginosa bacteria in a wide range of laboratory conditions. They found that antibiotic resistance has a cost to bacteria, and this cost can be eliminated by adding chemical inhibitors of the enzyme responsible for resistance to the drug. Leveling the playing field increased the ability of resistant bacteria to compete effectively against sensitive strains in the absence of antibiotics. Given that the cost of drug resistance plays an important role in preventing the spread of resistant bacteria, manipulating the cost of resistance may make it possible to prevent resistant bacteria from persisting after the conclusion of antibiotic treatment.
New Blood Analysis Chip Could Yield Diagnoses in Minutes
A major milestone in microfluidics could soon lead to stand-alone, self-powered chips that can diagnose diseases within minutes. A new device, developed by an international team of researchers from the University of California, Berkeley, Dublin City University in Ireland, and Universidad de Valparaíso Chile, is able to process whole blood samples without the use of external tubing and extra components. The researchers have dubbed the device SIMBAS, which stands for Self-powered Integrated Microfluidic Blood Analysis System. The report on SIMBAS was featured as the cover story of the March 7, 2011 issue of the peer-reviewed journal Lab on a Chip. “The dream of a true lab-on-a-chip has been around for a while, but most systems developed thus far have not been truly autonomous,” said Dr. Ivan Dimov, UC Berkeley post-doctoral researcher in bioengineering and co-lead author of the study. “By the time you add tubing and sample prep setup components required to make previous chips function, they lose their characteristic of being small, portable and cheap. In our device, there are no external connections or tubing required, so this can truly become a point-of-care system.” Dr. Dimov works in the lab of the study’s principal investigator, Dr. Luke Lee, UC Berkeley professor of bioengineering and co-director of the Berkeley Sensor and Actuator Center. “This is a very important development for global healthcare diagnostics,” said Dr. Lee. “Field workers would be able to use this device to detect diseases such as HIV or tuberculosis in a matter of minutes. The fact that we reduced the complexity of the biochip and used plastic components makes it much easier to manufacture in high volume at low cost.
Llama Antibodies Provide Clues to Novel Treatment of Virulent Hospital Infection
Clostridium difficile is a health problem that affects hundreds of thousands of patients and costs $10 billion to $20 billion every year in North America. Researchers from the University of Calgary and the National Research Council of Canada and colleagues say they are gaining a deeper understanding of this disease and are closer to developing a novel treatment using antibodies from llamas. “We have found that relatively simple antibodies can interfere with the disease-causing toxins from C. difficile,” said paper co-author Dr. Kenneth Ng, an associate professor of biological sciences at the University of Calgary and principal investigator of the Alberta Ingenuity Centre for Carbohydrate Science. “This discovery moves us a step closer to understanding how to neutralize the toxins and to create novel treatments for the disease.” His research is part of a paper published in the March 18, 2011 issue of the Journal of Biological Chemistry. Approximately two percent of all patients admitted to hospital may be infected by C. difficile, which thrives when healthy bacteria in the gut are weakened by antibiotics, thus allowing spores from Clostridium to germinate and colonize the large intestine. “This research is significant because C. difficile is an increasing heath care problem and many people may experience multiple infections,” said Dr. Glen Armstrong, head of the Department of Microbiology, Immunology, and Infectious Diseases in the Faculty of Medicine at the University of Calgary. “The current treatments are becoming less effective and C. difficile is developing resistance to conventional antibiotics. This research promises to provide a much-needed alternate treatment option that will overcome the failings of conventional antibiotics.” C.