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.
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.
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.
The humble butterfly could hold the key to unlocking new techniques to make solar energy cheaper and more efficient, according to the results of pioneering new research. A team of experts from the University of Exeter in the UK has examined new techniques for generating photovoltaic (PV) energy - or ways in which to convert light into power. The scientists showed that by mimicking the V-shaped posture adopted by Cabbage White butterflies when heating up their flight muscles before take-off, the amount of power produced by solar panels can be increased by almost 50 per cent. Crucially, by replicating this “wing-like” structure, the power-to-weight ratio of the overall solar energy structure is increased 17-fold, making it vastly more efficient. The research by the team from both the Environment and Sustainability Institute (ESI) and the Centre for Ecology and Conservation, based at the University of Exeter's Penryn Campus in Cornwall, UK, was published online on July 31, 2015 in an open-access article in Scientific Reports. The article is titled “White Butterflies As Solar Photovoltaic Concentrators.” Professor Tapas Mallick, lead author of the research said: "Biomimicry in engineering is not new. However, this truly multidisciplinary research shows pathways to develop low cost solar power that have not been done before." The Cabbage White butterflies are known to take flight before other butterflies on cloudy days - which limit how quickly the insects can use the energy from the sun to heat their flight muscles. This ability is thought to be due to the V-shaped posturing, known as reflectance basking, that these butteflies adopt on such days to maximize the concentration of solar energy onto their thorax, which allows for flight.
When it comes to vaccinating their babies, bees don't have a choice -- they naturally immunize their offspring against specific diseases found in their environments. And now for the first time, scientists have discovered how they do it. Researchers from Arizona State University (ASU), the University of Helsinki, the University of Jyväskylä, and the Norwegian University of Life Sciences made the discovery after studying a bee blood protein called vitellogenin. The scientists found that this protein plays a critical, but previously unknown, role in providing baby bees with protection against disease. The findings was published online on July 31, 2015 in the open-access journal PLOS Pathogens. The article is titled “Transfer of Immunity from Mother to Offspring Is Mediated via Egg-Yolk Protein Vitellogenin.” "The process by which bees transfer immunity to their babies was a big mystery until now. What we found is that it's as simple as eating," said Dr. Gro Amdam, a Professor with ASU's School of Life Sciences and co-author of the paper. "Our amazing discovery was made possible because of 15 years of basic research on vitellogenin. This exemplifies how long-term investments in basic research pay off." Co-author Dr. Dalial Freitak, a postdoctoral researcher with University of Helsinki adds: "I have been working on bee immune priming since the start of my doctoral studies. Now almost 10 years later, I feel like I've solved an important part of the puzzle. It's a wonderful and very rewarding feeling!" In a honey bee colony, the queen rarely leaves the nest, so worker bees must bring food to her. Forager bees can pick up pathogens in the environment while gathering pollen and nectar.
The American Society of Human Genetics (ASHG) has named Charles R. Scriver, M.D., Alva Professor Emeritus of Human Genetics, and Professor of Pediatrics, Biochemistry (Associate), Biology (Honorary), and Human Genetics at McGill University; as the 2015 recipient of the annual Victor A. McKusick Leadership Award (http://www.ashg.org/pages/awards_overview.shtml#mckuskick). This award, named in honor of the late and legendary Victor A. McKusick, M.D., widely and quite legitimately regarded as the “father of medical genetics” for his seminal work establishing the field, recognizes individuals whose professional achievements have fostered and enriched the development of human genetics as well as its assimilation into the broader context of science, medicine, and health. The ASHG will present the McKusick Award, which will include a plaque and monetary prize, to Dr. Scriver on Friday, October 9, during the ASHG’s 65th Annual Meeting (http://www.ashg.org/2015meeting/) in Baltimore. There is not an award in all of genetics that is more prestigious than one that bears the name, and honors the memory, of the great Victor McKusick. Dr. Scriver has worked at McGill University in Montreal for more than 50 years, having founded the deBelle Laboratory for Biochemical Genetics in 1961. He has dedicated his career as a clinician-scientist to discovering, training, treating, and educating the public about inherited metabolic and other genetic diseases. After a year of clinical work at Children’s Medical Center, Harvard, followed by two years in the laboratory at University College Hospital Medical School, London, Dr. Scriver unexpectedly encountered a recurrent seasonal epidemic in Quebec, which affected thousands of infants and children with Vitamin D deficiency.
A deadly fungus identified in 2013 could devastate native salamander populations in North America unless U.S. officials make an immediate effort to halt salamander importation, according to an urgent new report published in the July 31, 2015 issue of Science. The article is titled “Averting a North American Biodiversity Crisis.” San Francisco State University (SFSU) biologist Dr. Vance Vredenburg, his graduate student Tiffany Yap, and their colleagues at the University of California, Berkeley and the University of California, Los Angeles say the southeastern United States (particularly the southern extent of the Appalachian Mountain range and its southern neighboring region), the Pacific Northwest and the Sierra Nevada, and the central highlands of Mexico are at the highest risk for salamander declines and extinctions if the fatal Batrachochytrium salamandrivorans (Bsal) fungus makes its way into those regions. Salamanders are popular worldwide as pets, and frequently traded across borders. That has scientists worried that the fungus could spread from Asia, where it likely originated, to other parts of the globe. Dr. Vredenburg and his coauthors on the study are asking the U.S. Fish and Wildlife Service to place an immediate ban on live salamander imports to the U.S. until there is a plan in place to detect and prevent the spread of the Bsal fungus. Although the ban has been supported by key scientists for some time, including in a prominent op-ed in the New York Times last year, the government has been slow to act. "This is an imminent threat, and a place where policy could have a very positive effect," Dr. Vredenburg said. "We actually have a decent chance of preventing a major catastrophe."
Researchers have recreated the evolutionary lineage of adeno-associated viruses (AAVs) for the purpose of reconstructing an ancient viral particle that is highly effective at delivering gene therapies targeting the liver, muscle, and retina. This approach, published on July 30, 2015 in an open-access article in Cell Reports, could be used to design a new class of genetic drugs that are safer and more potent than those currently available. The article is titled “In Silico Reconstruction of the Viral Evolutionary Lineage Yields a Potent Gene Therapy Vector.” "Our novel methodology allows us to understand better the intricate structure of viruses and how different properties arose throughout evolution," says senior study author Dr. Luk H. Vandenberghe of Harvard Medical School. "We believe our findings will teach us how complex biological structures, such as AAVs, are built. From this knowledge, we hope to design next-generation viruses for use as vectors in gene therapy." Viruses need to efficiently transfer their genetic material into host cells in order to replicate and survive. Researchers have taken advantage of this natural property to develop viral vectors, or carriers, capable of shuttling therapeutic genes to the appropriate cells or tissues. Early-stage clinical trials have demonstrated the safety and effectiveness of this approach for treating inherited blindness and hemophilia. But so far, AAVs used for gene therapy have been chosen from naturally circulating viral strains, which patients may already have been exposed to, which means they would have natural immunity. Because natural immunization blocks the transfer of the therapeutic gene, these individuals are often ineligible for gene therapy.
Patients with type 1 diabetes have significantly lower blood levels of four proteins that help protect their tissue from attack by their immune system, scientists report. Conversely, the patients’ first-degree relatives, who share some of the high-risk genes but do not have the disease, have high levels of these proteins circulating in their blood, said Dr. Jin-Xiong She, Director of the Center for Biotechnology and Genomic Medicine at the Medical College of Georgia (MCG) at Georgia Regents University. Healthy individuals without the risky genes also have higher levels of the four proteins, IL8, IL-1Ra, MCP-1, and MIP-1β, according to the study published online on July 9, 2015 in the Journal of Clinical Endocrinology & Metabolism. The article is titled “Large-Scale Discovery and Validation Studies Demonstrate Significant Reductions in Circulating Levels of IL8, IL-1Ra, MCP-1, and MIP-1 in Type-1 Diabetes Patients.” The findings point toward a sort of protein cocktail that could help at-risk children avoid disease development, as well as new biomarkers in the blood that could aid disease diagnosis, prognosis, and management, said Dr. She, Georgia Research Alliance Eminent Scholar in Genomic Medicine and the study's corresponding author. The scientists looked at a total of 13 cytokines and chemokines, which are cell signaling molecules involved in regulating the immune response. They first looked at blood samples from 697 children with type 1 diabetes and from 681 individuals without antibodies to insulin-producing pancreatic beta cells, a hallmark of this generarally autoimmune disease. The scientists then analyzed the blood of a second and larger set of individuals, which included 1,553 children with type 1 diabetes and 1,493 individuals without any sign of anti-beta-cell antibodies.
In a project spearheaded by investigators at the University of California (UC) San Francisco (UCSF), scientists and collaborators have devised a new strategy to precisely modify human T cells using the genome-editing system known as CRISPR/Cas9. Because these immune-system cells play important roles in a wide range of diseases, from diabetes to AIDS to cancer, the achievement provides a versatile new tool for research on T cell function, as well as a path toward CRISPR/Cas9-based therapies for many serious health problems. Using their novel approach, the scientists were able to disable a protein on the T-cell surface called CXCR4, which can be exploited by HIV when the virus infects T cells and causes AIDS. The group also successfully shut down PD-1, a protein that has attracted intense interest in the burgeoning field of cancer immunotherapy, as scientists have shown that using drugs to block PD-1 coaxes T cells to attack tumors. The CRISPR/Cas9 system has captured the imagination of both scientists and the general public, because it makes it possible to easily and inexpensively edit genetic information in virtually any organism. T cells, which circulate in the blood, are an obvious candidate for medical applications of the technology, as these cells not only stand at the center of many disease processes, but could be easily gathered from patients, edited with CRISPR/Cas9, then returned to the body to exert therapeutic effects. But in practice, editing T cell genomes with CRISPR/Cas9 has proved surprisingly difficult, said Alexander Marson, Ph.D., a UCSF Sandler Fellow, and senior and co-corresponding author of the new study. "Genome editing in human T cells has been a notable challenge for the field," Dr. Marson said.