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Archive - Aug 2015

August 10th

Whole Genome Duplication in Yeast Arose by Inter-Species Hybridization, Not Intra-Species Genome Duplication As Commonly Believed; Unexpected Findings Suggest New Paradigm for Evolution of Whole Genome Duplications

Researchers at the Centre for Genomic Regulation (CRG) in Barcelona, Spain, have proposed a new theory to explain the origin of whole-genome duplication at the beginning of the yeast lineage. Yeasts are single-celled fungi that originated over 100 million years ago. The ability of these organisms to ferment carbohydrates is widely used for food and drink fermentation. Yeasts are also one of the most commonly used model organisms in research. For example, the yeast Saccharomyces cerevisiae, which is used to make bread, wine, and beer, was the first eukaryotic organism to be sequenced (in 1996) and is a key model organism for studying molecular and cellular biology. Once the yeast genome sequences became available, researchers were able to determine that the yeast genome contains more than 50 repeated fragments. Since then, the scientific community has accepted the theory that yeast underwent a whole-genome duplication, a phenomenon that is not isolated and can also be found in other species. For instance, we know that whole-genome duplications were important in the early evolution of vertebrates and that it is a very common phenomenon in plants, especially cultivated ones. The CRG scientists Dr. Marina Marcet-Houben and Dr. Toni Gabaldón [CRG group leader and ICREA (Institució Catalana de Recerca i Estudis Avançats) Research Professor] have now studied the origins of the whole-genome duplication in yeast to gain a more thorough understanding of this phenomenon, which is thought to have played a key role the evolution and adaption of the species. Their results were published online on August 7, 2015 in the open-acces journal PLoS Biology.

August 6th

Double-Stranded RNA Activates Toll-Like Receptor 3 (TLR3) to Promote Regeneration of Skin and Hair Follicles During Wound Healing; Drugs to Turn On TLR3 Might Further Promote Tissue Regeneration in Patients Scarred from Injury, Hopkins Study Suggests

Johns Hopkins researchers have identified a novel cell signaling pathway in mice, through which mammals, presumably including humans, can regenerate hair follicles and skin while healing from wounds. The discovery, summarized in a featured, open-access article published online on August 6, 2015 in the journal Cell Stem Cell, could, the scientists say, eventually help spur the growth of new hair, skin, or other organ tissue in scarred victims of burns and other injuries. The article is titled “dsRNA Released by Tissue Damage Activates TLR3 to Drive Skin Regeneration.” The study "uncovers a novel role for a protein [TLR3] that works as a master regulator of regeneration in the skin," says senior study author Luis A. Garza, M.D., Ph.D., Associate Professor of Dermatology at the Johns Hopkins University School of Medicine. "Medications that turn on this protein have the powerful potential to decrease scarring as healing of wounds takes place, thereby promoting skin and hair follicle regeneration." Dr. Garza says his team's work is based on the knowledge that damaged skin releases double-stranded RNA (dsRNA) -- genetic information normally carried by some viruses -- that is sensed by a protein called toll-like receptor 3 (TLR3) (image illustrates structure of TLR3 protein). TLR3, which in other contexts plays a fundamental role in recognizing some disease-causing organisms and activating the immune system, also, in response to wounding activates the genes IL6 and STAT3 to promote hair follicle regeneration.

Exosome Diagnostics Demonstrates Technical Ability, Using Combined Exosomal RNA and Cell-Free DNA Capture from Plasma, to Detect EGFR-Activating Mutations and T790M Resistance Mutation in Patients with Non-Small Cell Lung Cancer (NSCLC)

On August 5, 2015, Exosome Diagnostics, Inc., a developer of what it terms “revolutionary, biofluid-based molecular diagnostics,” announced data demonstrating the ability of its proprietary exosomal RNA (exoRNA) plus cell-free DNA (cfDNA) platform to detect, with high sensitivity, EGFR-activating mutations and the EGFR T790M resistance mutation in the blood plasma of patients with non-small cell lung cancer (NSCLC). The data were first presented on July 31, 2015 at a poster session (http://www.exosomedx.com/sites/default/files/uploads/publications/ilcc_e...) titled, “Detection of EGFR-Activating and T790M Resistance Mutation in Plasma of NSCLC Patients Using Combined Exosomal RNA and cfDNA capture,” presented during the 16th Annual International Lung Cancer Congress (http://www.gotoper.com/conferences/ilc/meetings/16th-international-lung-...), which took place July 30 – August 1, 2015 in Huntington Beach, California. “Unfortunately, non-small cell lung cancer is very smart; it develops new mutations over time to resist treatment, including the EGFR T790M mutation,” said Vince O’Neill, M.D., Chief Medical Officer at Exosome Diagnostics. “Based on these new data we presented, we’re highly encouraged that our EGFR T790M test will give medical oncologists a critical new tool to non-invasively, and with high sensitivity, detect the development of this resistance mutation over time through a simple blood draw, helping inform the most appropriate, targeted, and timely treatment decisions for patients, as their disease progresses.” In the study, Exosome Diagnostics applied its exoRNA plus cfDNA platform to isolate exoRNA and cfDNA from 21 blood plasma samples from NSCLC patients collected at the time of clinical resistance to EGFR tyrosine kinase inhibitor (TKI) therapy.

Why the Long Face? Horses Share Similar Facial Expressions with Humans and Chimps; Use of New Facial Action Coding System Adds to Evidence That Social Factors Have Significantly Influenced Evolution of Facial Expression

Horses share some surprisingly similar facial expressions with humans and chimps, according to new research from the Mammalian Communication and Cognition University group in the School of Psychology at the University of Sussex in the UK, and colleagues. Mammal communication researchers have shown that, as do humans, horses use muscles underlying various facial features - including their nostrils, lips, and eyes - to alter their facial expressions in a variety of social situations. The findings, published online in the open-access journal PLOS ONE on August 5, 2015, suggest evolutionary parallels in different species in how the face is used for communication. The article is titled “'EquiFACS: The equine Facial Actin Coding System.” [Note that links to multiple popular press articles on this new work are provided at the end of this BioQuick article, as are links to the press release and to the full research article in PLOS ONE.] The study builds on previous research, which had shown that that cues from the face are important for horses to communicate, by developing the first objective coding system to identify different individual facial expressions on the basis of underlying muscle movement. The Equine Facial Action Coding System (EquiFACS), as devised by the Sussex team in collaboration with researchers at the University of Portsmouth in the UK and at Duquesne University in the United States, identified 17 "action units" (discrete facial movements) in horses. This compares with 27 in humans, 13 in chimps, and 16 in dogs. The study's co-lead author, doctoral researcher Jennifer Wathan, said: "Horses are predominantly visual animals, with eyesight that's better than [that of] domestic cats and dogs, yet their use of facial expressions has been largely overlooked.

August 3rd

Seeds of Parasitic Plants Can Detect Hormones Released by Roots of Host Plant, Enabling Identification, and Stimulating Germination and Attack; System Developed by Duplications and Evolution of Gene Used to Sense Fire; Related Crop Losses Now in Billions

An international team of researchers, led by scientists at the University of Georgia (UGA), has discovered how parasitic plants, which steal their nutrients from other living plants, evolved the ability to detect and attack their hosts. The team’s findings, published in the July 31, 2015 issue of Science, could lead to new techniques to control the destructive plant parasites. The article is titled “Convergent Evolution of Strigolactone Perception Enabled Host Detection in Parasitic Plants.” There are thousands of parasitic plant species, but the most burdensome for humans are those that infiltrate farmland and destroy crops. Parasite infestations reduce crop yields by billions of dollars each year, particularly in developing nations where access to advanced herbicides and other control methods is limited, according to the researchers. "In the simplest terms, these are plants that eat other plants," said Dr. David Nelson, co-author of the Science article and Assistant Professor of Genetics in UGA's Franklin College of Arts and Sciences. "The seeds of some parasitic plants, like witchweed (image is of purple witchweed) for example, can lie dormant in soil for more than a decade, waiting to grow until they detect the presence of a host. We wanted to understand how the parasites know other plants are nearby so we could develop new ways of combating them." As plant roots grow, they release hormones called strigolactones into the soil. This is a signal that normally helps fungi form a beneficial connection to the plant, in which they each trade nutrients. But the seeds of parasitic plants also possess the ability to sense strigolactones, which prompt them to germinate, attach to the host root, and syphon off nutrients.

August 1st

Vision-Restoring Retinal Gene Therapy Also Strengthens Visual Processing Pathways in Brain; Rapid Regrowth of Unused Brain Connections Seen After Decades of Near Blindness in Treated LCA2 Patients

Since 2007, clinical trials using gene therapy have resulted in often-dramatic sight restoration for dozens of children and adults who were otherwise doomed to blindness. Now, researchers from the Perelman School of Medicine at the University of Pennsylvania (Penn) and The Children’s Hospital of Philadelphia (CHOP), together with colleagues, have found evidence that this sight restoration leads to strengthening of visual pathways in the brain, published in the July 15, 2015 issue of Science Translational Medicine. The article is titled “Plasticity of the Human Visual System after Retinal Gene Therapy in Patients with Leber’s Congenital Amaurosis.” “The patients had received the gene therapy in just one eye (their worse seeing eye), and though we imaged their brains only about two years later, on average, we saw big differences between the side of the brain connected to the treated region of the injected eye and the side connected to the untreated eye,” said lead author Manzar Ashtari, Ph.D., Director of CNS Imaging at the Center for Advanced Retinal and Ocular Therapeutics in the Department of Ophthalmology at Penn. Ashtari is the former Director of Diffusion Tensor Image Analyses and Brain Morphometry at CHOP. “It’s an elegant demonstration that these visual processing pathways can be restored even long after the period when it was thought there would be a loss of plasticity,” said senior author Jean Bennett, M.D., Ph.D., the F.M. Kirby Professor of Ophthalmology at Penn and Director of the Center for Advanced Retinal and Ocular Therapeutics. The team examined ten patients who have Leber’s congenital amaurosis Type 2 (LCA2), a rare disease that afflicts those who inherit one bad copy of an LCA2 gene from each parent.

NIH Images Show How Neurotensin Hormone May Activate Its G-Protein-Coupled Receptor (GPCR); Binding Changes GPCR Shape and It Moves Through Membrane into Cell to Likely Activate G Proteins

Many hormones and neurotransmitters work by binding to receptors on a cell's exterior surface. This activates the receptors causing them to twist, turn, and spark chemical reactions inside cells. NIH scientists used atomic level images to show how the neuropeptide hormone neurotensin might activate its receptors. Their description is the first of its kind for a neuropeptide-binding G protein-coupled receptor (GPCR), a class of receptors involved in a wide range of disorders and the target of many drugs. "G protein-coupled receptors are found throughout the body. Knowing how they work should help scientists devise better treatments," said Reinhard Grisshammer, Ph.D., an investigator at the NIH's National Institute of Neurological Disorders and Stroke (NINDS) and the senior author of the study published online on July 24, 2015 in an open-access article in Nature Communications. The article is titled “Structural Prerequisites for G-Protein Activation by the Neurotensin Receptor.” Neurotensin is believed to be involved in Parkinson's disease, schizophrenia, temperature regulation, pain, and cancer cell growth. Previously, Dr. Grisshammer and his colleagues showed how neurotensin binds to the part of its receptor located on a cell's surface. In the current study, the scientists demonstrated how binding changes the structure of the rest of the receptor, which then passes through a cell's membrane and into its interior. There, neurotensin receptors activate G proteins, a group of molecules inside cells that control a series of chemical chain reactions. For these experiments, scientists shot X-rays at crystallized neurotensin receptor molecules. Making crystals of receptors that activate G proteins is difficult. In most studies, scientists have investigated inactive receptors.