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Archive - May 2013

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May 9th

DNA Analysis Reveals Hidden Fungal Species

Our ability to assess biological diversity, ecosystem health, ecological interactions, and a wide range of other important processes is largely dependent on accurately recognizing species. However, identifying and describing species is not always a straightforward task. In some cases, a single species may show a high level of morphological variation, while in other cases, multiple morphologically similar species may be hidden under a single species name. Cryptic species, two or more distinct species that are erroneously classified under a single species name, are found in all major groups of living things. As an alternative to traditional morphology-based species delimitation, an international research group, including scientists from Germany, Iran, Spain, and the USA, describes five new species of lichen-forming fungi from what was traditionally considered a single species using differences in DNA sequence data. The authors state that "the effective use of genetic data appears to be essential to appropriately and practically identify natural groups in some phenotypically cryptic lichen-forming fungal lineages." The study was published online on May 9, 2013 in the open access journal MycoKeys. The scientists also provide a reference DNA sequence database for specimen identification using DNA barcoding, making specimen identification more accessible and more reliable at the same time. The application of DNA-based identification can potentially be used as a way for both specialists and nonspecialists alike to recognize species that are otherwise difficult to identify. Lichens are commonly used to monitor ecosystem health and the impact of atmospheric pollution. In addition, some lichens are potentially valuable sources of pharmaceutical products, including antibiotics, antioxidants, etc.

Taiwanese Scientists Develop Ultra-Fast DNA Sequencing Technique

Professor G. Steven Huang from the Department of Materials Science and Engineering and Professor Yu-Shiun Chen from the Department of Biological Science and Technology of National Chiao Tung University (NCTU) in Taiwan have successfully developed a more rapid, precise, and economic technique of singe-molecule DNA sequencing. By combining a protein transistor with biological technologies, they can accelerate the process of DNA sequencing in order to provide a better tool for personalized medicine and genetic research. The research was published online on May 5, 2013 in Nature Nanotechnology. DNA sequencing is a key to unveiling the mystery of life. A gene is formed by a sequence of bases (G, A, T, C) and locates in the double helix of DNA. It is the basic unit that determines the genetic characteristics of a creature. A human genome consists of approximately 3 billion DNA base pairs. Even with current technology, the process of DNA sequencing still takes a significant amount of time. The innovative technique developed by the team from NCTU stands out becuse it can significantly reduce the time of the sequencing process and meanwhile also lower the error rate. With this technique, single DNA molecules can be sequenced by monitoring the electrical conductance of a phi29 DNA polymerase as it incorporates unlabelled nucleotides into a template strand of DNA. The conductance of the polymerase is measured by attaching it to a protein transistor. According to Professor Chen, with this technology, they can overcome the obstacles from which other techniques suffer. This will be the very first time that people can see the entire process of polymerase synthesis without the use of fluorescence and other external aids.

May 9th

Study Discovers Organizing Principle of Bacteria in Biofilms

Bacteria on a surface wander around and often organize into highly resilient communities known as biofilms. It turns out that they organize in a rich-get-richer pattern similar to many economies, according to a new study by researchers at UCLA, Northwestern University, and the University of Washington. The study, published online on May 8, 2013 in Nature, is the first to identify the strategy by which bacteria form the micro-colonies that become biofilms, which can cause lethal infections. The research may have significant implications for battling stubborn bacterial infections that do not respond to antibiotics. Bacteria in biofilms behave very differently from free-swimming bacteria. Within biofilms, bacteria change their gene expression patterns and are far more resistant to antibiotics and the body's immune defenses than individual, free-swimming bacteria, because they mass together and are protected by a matrix of proteins, DNA, and long, chain-like sugar molecules called polysaccharides. This makes seemingly routine infections potentially deadly. Dr. Gerard Wong, professor of bioengineering at the UCLA Henry Samueli School of Engineering and Applied Science, member of the California NanoSystems Institute, and professor of chemistry and biochemstry at UCLA; Erik Luijten, professor of materials science and engineering and of applied mathematics at Northwestern University; and Matthew R. Parsek, professor of microbiology at the University of Washington, led a team of researchers that elucidated the early formation of biofilms by developing algorithms that describe the movements of the different strains of the bacterium Pseudomonas aeruginosa and by conducting computer simulations to map the bacteria's movements. P. aeruginosa can cause lethal, difficult-to-treat infections, including those found in cystic fibrosis and AIDS patients.

Sweeping Analysis of the Embryonic Epigenome

A large, multi-institutional research team involved in the NIH Epigenome Roadmap Project has published a sweeping analysis online on May 9, 2013 in Cell of how genes are turned on and off to direct early human development. Led by Dr. Bing Ren of the Ludwig Institute for Cancer Research, Dr. Joseph Ecker of The Salk Institute for Biological Studies, and Dr. James Thomson of the Morgridge Institute for Research, the scientists also describe novel genetic phenomena likely to play a pivotal role not only in the genesis of the embryo, but in that of cancer as well. Their publicly available data, the result of more than four years of experimentation and analysis, will contribute significantly to virtually every subfield of the biomedical sciences. After an egg has been fertilized, it divides repeatedly to give rise to every cell in the human body—from the patrolling immune cell to the pulsing neuron. Each functionally distinct generation of cells subsequently differentiates itself from its predecessors in the developing embryo by expressing only a selection of its full complement of genes, while actively suppressing others. "By applying large-scale genomics technologies," explains Dr. Ren, Ludwig Institute member and a professor in the Department of Cellular and Molecular Medicine at the UC San Diego School of Medicine, "we could explore how genes across the genome are turned on and off as embryonic cells and their descendant lineages choose their fates, determining which parts of the body they would generate." One way cells regulate their genes is by DNA methylation, in which a molecule known as a methyl group is tacked onto cytosine—one of the four DNA bases that write the genetic code.

May 7th

Researchers Describe a Way That Breast Cancer Cells Acquire Drug Resistance

A seven-year quest to understand how breast cancer cells resist treatment with the targeted therapy lapatinib has revealed a previously unknown molecular network that regulates cell death. The discovery provides new avenues to overcome drug resistance, according to researchers at Duke Cancer Institute. "We've revealed multiple new signaling pathways that regulate cell death," said Sally Kornbluth, Ph.D., vice dean of Basic Science and professor of Pharmacology and Cancer Biology at the Duke University School of Medicine. "And we've shown, at least in one disease, these signaling pathways can go awry in drug resistance. It also suggests you could manipulate these other pathways to overcome drug resistance." The researchers -- co-directed by Dr. Kornbluth and Neil Spector, M.D., associate professor of medicine at Duke -- identified a protein that effectively shuts down the signals that tell a cell to die, enabling cancer cells to keep growing. That protein, MDM2 (image), is already generating intense interest in the cancer research community because it is a master regulator of the tumor suppressor protein called p53. The new findings are published online on May 7, 2013 in Science Signaling. The Duke research team, with assistance from collaborators at the University of Michigan, identified a new role for MDM2 in activating cell death pathways independent of its role in regulating p53, a known initiator of cell death. More than half of all human tumors contain a mutation or deletion of the gene that controls p53. The researchers began by studying four different types of breast cancer cells that were able to keep growing despite treatment with lapatinib, a powerful drug that targets two growth pathways commonly disrupted in breast cancer, HER2 and epidermal growth factor receptor.

Advance in Understanding of Restless Legs Syndrome

Johns Hopkins researchers believe they may have discovered an explanation for the sleepless nights associated with restless legs syndrome (RLS), a symptom that persists even when the disruptive, overwhelming nocturnal urge to move the legs is treated successfully with medication. Neurologists have long believed RLS is related to a dysfunction in the way the brain uses the neurotransmitter dopamine, a chemical used by brain cells to communicate and produce smooth, purposeful muscle activity and movement. Disruption of these neurochemical signals, characteristic of Parkinson's disease, frequently results in involuntary movements. Drugs that increase dopamine levels are mainstay treatments for RLS, but studies have shown they don't significantly improve sleep. An estimated 5 percent of the U.S. population has RLS. The small new study, headed by Richard P. Allen, Ph.D., an associate professor of neurology at the Johns Hopkins University School of Medicine, used MRI to image the brain and found glutamate — a neurotransmitter involved in arousal — in abnormally high levels in people with RLS. The more glutamate the researchers found in the brains of those with RLS, the worse their sleep. The findings were published in the May 2013 issue of Neurology. "We may have solved the mystery of why getting rid of patients' urge to move their legs doesn't improve their sleep," Dr. Allen says. "We may have been looking at the wrong thing all along, or we may find that both dopamine and glutamate pathways play a role in RLS." For the study, Dr. Allen and his colleagues examined MRI images and recorded glutamate activity in the thalamus, the part of the brain involved with the regulation of consciousness, sleep, and alertness. They looked at images of 28 people with RLS and 20 people without.

May 6th

Personalized Medicine Conference Will Focus on Next-Gen Sequencing for Targeted Therapeutics

The sixth annual Personalized Medicine Conference (6.0) organized by San Francisco State University will focus on the amazing technological challenges and advances of “next-generation sequencing,” examining the very latest approaches and how they are leading to profound changes in our understanding of basic biological questions and to more efficacious and cost-effective therapies. The conference is entitled, “Next-Generation Sequencing for Targeted Therapeutics.” Featured speakers include Kimberly J. Popovits, Chairman of the Board, Chief Executive Officer & President of Genomic Health; Dr. Mark Sliwkowski, Distinguished Staff Scientist at Genentech; Professor Atul Butte of Stanford University; and Dr. Carl Borrebaeck, Professor & Chair of Immunotechnology and Director of CREATE Health at Lund University in Sweden. The conference will take place at the South San Francisco Conference Center (http://www.ssfconf.com/directions-top) from 8:00 am to 5:30 pm on Thursday, May 30, 2013, with a reception to follow. Those wishing to attend are urged to register as soon as possible (http://personalizedmedicine.sfsu.edu/register.html). For additional information, to help sponsor the event, or to inquire about special academic rates, contact dnamed@sfsu.edu. The conference organizers, including Michael Goldman, Ph.D., Professor and Chair of San Francisco State’s Department of Biology, noted that with the price of sequencing a complete human genome falling into the $1,000 range, stunning advances are sure to come over the next few years. It is likely that a detailed genome sequence will soon be part of a routine medical history, allowing unprecedented precision in diagnosis and treatment. The DNA and RNA signatures of both complex, common diseases and rare, elusive conditions will yield their secrets.

May 5th

Portable Device Provides Rapid, Accurate Diagnosis of TB, Other Bacterial Infections

A handheld diagnostic device that Massachusetts General Hospital (MGH) investigators first developed to diagnose cancer has been adapted to rapidly diagnose infections by Mycobacterium tuberculosis (TB) and other important infectious bacteria. Two papers, one appearing in the journal Nature Communications, and the other in Nature Nanotechnology describe portable devices that combine microfluidic technology with nuclear magnetic resonance (NMR) to not only diagnose these important infections, but also determine the presence of antibiotic-resistant bacterial strains. "Rapidly identifying the pathogen responsible for an infection and testing for the presence of resistance are critical not only for diagnosis but also for deciding which antibiotics to give a patient," says Ralph Weissleder, M.D., Ph.D., director of the MGH Center for Systems Biology (CSB) and co-senior author of both papers. "These described methods allow us to do this in two to three hours, a vast improvement over standard culturing practice, which can take as much as two weeks to provide a diagnosis." Investigators at the MGH CSB previously developed portable devices capable of detecting cancer biomarkers in the blood or in very small tissue samples. Target cells or molecules are first labeled with magnetic nanoparticles, and the sample is then passed through a micro NMR system capable of detecting and quantifying levels of the target. But initial efforts to adapt the system to bacterial diagnosis had trouble finding antibodies – the detection method used in the earlier studies – that would accurately detect the specific bacteria. Instead the team switched to targeting specific nucleic acid sequences. The system described in the Nature Communications paper, published online on April 23, 2013, detects DNA from the tuberculosis bacteria in small sputum samples.

Genetics of Pulmonary Fibrosis

Researchers from the University of Colorado Denver and colleagues have carried out a genome-wide association study to identify susceptibility loci for fibrotic idiopathic pneumonia. Their results sugget that genes involved in host defense, cell-cell adhesion, and DNA repair contribute to risk for this disease. Specifically, the scientists confirmed association with TERT at 5p15, MUC5B at 11p15, and the 3q26 region near TERC. In addition, they identified seven newly associated loci: FAM13A at 4q22, DSP at 6p24, OBFC1 at 10q24, ATP11A at 13q34,DPP9 at 19p13, and chromosomal regions 7q22 and 15q14-15. The results of this study were published online in Nature Genetics on April 14, 2013. [Nature Genetics abstract]

Platyfish Genome Sequenced

The sequence and analysis of the platyfish genome was published in the May 2013 issuee of Nature Genetics. The work represents the first genome sequence of a poeciliid fish and provides insights into evolutionary adaptation in this freshwater fish as well as a potential model for cancer research. Dr. Wesley Warren of the Genome Institue, the Washington University School of Medicine, and an international group of colleagues report the sequencing. The authors use this as a model to examine the evolution of a number of traits, including a live-bearing reproductive mode, pigmentation patterns, cancer, and behavioral traits. They identify a gene implicated in both pigmentation patterning and melanoma development in the platyfish. They also find evidence for selection of genes associated with viviparity—the development of the embryo inside the body of the mother, eventually leading to a live birth. In addition, they identify selective retention of duplicate genes implicated in cognition during the evolution of teleost fish, suggesting a model for the evolution of behavioral complexity in fish. [Press release] [Nature Genetics abstract]