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Archive - 2014

December 19th

Nobelist Leads Effort Revealing Beneficial Function of Endogenous Retroviruses in Immune Response

Retroviruses are best known for causing contagious scourges such as AIDS, or more sporadically, cancer. But researchers at the University of Texas (UT) Southwestern Medical Center and Karolinska Institutet in Stockholm, Sweden, have found that endogenous retroviruses (ERV) also play a critical role in the body’s immune defense against common bacterial and viral pathogens. “Most scientists have become used to the view that retroviruses are generally harmful,” said Nobel Laureate Dr. Bruce Beutler, Professor and Director of UT Southwestern’s Center for the Genetics of Host Defense. “We have found that ERV fulfill at least one beneficial function critical to producing protective antibodies.” Retroviruses are able to insert into the genomic DNA of cells they infect, including germ cells. In this way, and by a process called retrotransposition, they have become a major part of the genome of each person. About 45 percent of a person’s DNA is of retroviral origin, and some of the better preserved copies are termed “endogenous retroviruses” (ERV). Writing in the journal Science in an article published online on December 19, 2014, the researchers found that when B cells are activated by large polymeric antigens such as polysaccharides of bacteria, they rapidly produce protective antibodies in what is termed the Type II T-independent antibody response. This response, central to the body’s defense against common bacterial and viral pathogens, is dependent on ERV. Within activated B cells, the ERV are driven to express RNA copies of themselves, which in turn are copied into DNA by an enzyme called reverse transcriptase. The RNA copies of ERV are detected by a protein called RIG-I, and the DNA copies are detected by another protein called cGAS.

December 19th

New Hermit Cockroach Species Identified in China

Scientists from the Southwest University, Chongqing, China have found a new species and a new subspecies of cockroach. What makes these cockroaches distinct from the cockroaches most of us know is that they don't infest human houses. On the contrary, they prefer to live a hermit life drilling logs, hidden away from human eyes. The study was published online on December 19, 2014 in the open-access journal ZooKeys. Out of around 4,600 cockroach species worldwide, only 30 are the cockroaches associated with human habitats that gives a bad name to these creatures. The representatives of the genus Panesthia, to which the new species and subspecies belong, for example are distinctive for drilling logs and xylophagy (feeding on wood), rather than living in houses and eating rubbish. The new species, P. guizhouensis, was firstly collected from a rotten wood near a large pool where it was living undisturbed, and far away from cities in Guizhou Province. A colony of more than 60 nymphs and 52 adults, emerged from the log when the wood was split, quickly fleeing away. Up to now, 55 species and 9 subspecies have been reported in this genus, but because of their secluded lifestyle, these cockroaches are still mysterious to scientists, and their study had been nearly stagnant since 1999. "With this new discovery, we hope to reignite the scientific interest towards this peculiar and rather intriguing cockroach genus," comments Dr. Yanli Che, Southwest University, China. The image shows a cockroach belonging to the genus Panesthia. (Credit: Yanli Che).

[Press release] [Zoo Keys article]

Orphan Receptor Proteins Deliver Double Knock-Out Punch to Glioblastoma Cells in Vitro

Two related proteins exert a lethal double-whammy effect against glioblastoma cells when activated with a small molecule, say researchers at Georgetown Lombardi Comprehensive Cancer Center. The scientists report that, when activated, one protein, called the short form, stops glioblastoma cells from replicating their DNA, and the other, called the long form, prevents cell division if the DNA has already been replicated, explains Rebecca Riggins, Ph.D., Assistant Professor of Oncology at Georgetown Lombardi. The study was posted online on December 12, 2014 in an open-access article in the journal Cell Cycle. Both proteins are produced by the estrogen-related receptor beta (ERRβ) gene. They are known as "orphan receptors" because they are not known to bind to any substances naturally produced by the body. ERRβ proteins are similar in shape to the receptor that binds the hormone estrogen -- hence their name -- but they do not bind estrogen and are not otherwise related. Both men and women have ERRβ genes. In this study, Dr. Riggins and her co-author, postdoctoral fellow Mary Heckler, Ph.D., examined glioblastoma cells in the laboratory for the presence of ERRβ and found both long and short forms. To understand what these proteins were doing, they used a laboratory chemical, DY131, which had been designed to bind and activate these proteins. To their surprise, the researchers discovered that DY131 exerted a strong, but distinct, effect on both the short and long forms of ERRβ. The short form had been known to act as a tumor suppressor in prostate cancer, and a similar anti-cancer action was found by the researchers in glioblastoma. The study, however, is the first to find a function for the long form in cancer.

Scientists Discover Protein Protecting Against Chlorine

Chlorine is a common disinfectant that is used to kill bacteria, for example, in swimming pools and drinking water supplies. Our immune system also produces chlorine, which causes proteins in bacteria to lose their natural folding. These unfolded proteins then begin to clump and lose their function. Ruhr-Universitaet-Bochum (RUB) researchers in Germany, headed by Professor Dr. Lars Leichert, have discovered a protein (RidA) in the intestinal bacterium E. coli that protects bacteria from chlorine. In the presence of chlorine, this newly discovered protein tightly bonds with other proteins, thus preventing them from coagulating. Once the danger has passed, this protein releases the bound proteins and they can continue to work as usual. The researchers reported their findings online on December 17, 2014 in an open-access article in Nature Communications. The scientists look into oxidative stress, which affects cells when they encounter so-called “reactive oxygen species” (ROS), chemically reactive molecules containing oxygen. Oxidative stress plays a role during cell aging and in immune defense. By producing reactive oxygen species, immune cells subject bacteria to oxidative stress. But what happens inside those bacteria, and more specifically, what happens to their proteins? The researchers sought to answer this question by looking for proteins that change due to oxidative stress. This is how they discovered the protein RidA.

Adaptive Evolution of Human Color Vision

The evolution of trichromatic color vision in humans occurred by first switching from the ability to detect UV light to blue light (between 80-30 million years ago-MYA) and then by adding green-sensitivity (between 45-30 MYA) to the preexisting red-sensitivity in the vertebrate ancestor. The detailed molecular and functional changes of the human color vision have been revealed by lead author Dr. Shozo Yokoyama of Emory University and colleagues from Emory and other institutions. The article was published online on December 18, 2014 in the open-accessd journal PLOS Genetics. The molecular basis of functional differentiation is a fundamental question in biology. To fully appreciate how these changes are generated, it is necessary to evaluate the relationship between genes and functions. This is a difficult task because new mutations can produce different functional changes when they occur with different preexisting mutations, causing complex non-additive interactions. The blue-sensitive visual pigment in human evolved from the UV-sensitive pigment in the ancient Boreoeutherian ancestor by seven mutations. There are 5,040 possible evolutionary paths connecting them. The team examined experimentally the genetic composition and color perception of the visual pigment at every evolutionary step of all 5,040 trajectories. They found that 4,008 trajectories are terminated prematurely by containing a dehydrated nonfunctional pigment. Eight most likely trajectories reveal that the blue-sensitivity evolved gradually almost exclusively by non-additive interactions among the seven mutations.

Wild Blueberries May Reduce Adverse Effects of High-Fat Diet

Eating wild blueberries (bilberries) diminishes the adverse effects of a high-fat diet, according to a recent study at the University of Eastern Finland. For the first time, bilberries were shown to have beneficial effects on both blood pressure and nutrition-derived inflammatory responses. Low-grade inflammation and elevated blood pressure are often associated with obesity-related diseases. The current study focused on the health effects of bilberries on mice that were fed a high-fat diet for a period of three months. Some of the mice were fed either 5% or 10% of freeze-dried bilberries in the diet. The researchers assessed the effects of the diets by looking at inflammatory cell and cytokine levels, systolic blood pressure, glucose tolerance, insulin sensitivity, and weight gain. Mice on the high-fat diet experienced significant weight gain and detrimental changes in glucose and lipid metabolism, inflammation factors, and blood pressure. Bilberries diminished the pro-inflammatory effects of the high-fat diet, indicated by an altered cytokine profile and a reduced relative prevalence of inflammation supporting T-cells. Bilberries also prevented elevated blood pressure caused by the high-fat diet. Bilberries constitute an integral part of the Nordic diet and they could be better utilized also elsewhere in the world. Bilberries are associated with several beneficial health effects and their use involves plenty of traditional wisdom. The beneficial health effects of bilberries are thought to be explained by polyphenols, especially anthocyanins, the levels of which are significantly higher in bilberries than in commercially cultivated blueberries. The original article was published online on December 12, 2014 in the open-access journal PLOS ONE.

December 17th

New Coupling Technique May Have Immediate Applications in Pharmaceuticals, Materials, Agricultural, and Fragrance Chemistry

Chemists at The Scripps Research Institute (TSRI) in La Jolla, California, have invented a powerful method for joining complex organic molecules. This method is extraordinarily robust and can be used to make pharmaceuticals, fabrics, dyes, plastics, and other materials previously inaccessible to chemists. “We are rewriting the rules for how one thinks about the reactivity of basic organic building blocks, and in doing so we’re allowing chemists to venture where none has gone before,” said Dr. Phil S. Baran, the Darlene Shiley Chair in Chemistry at TSRI, whose laboratory reported the finding on functionalized olefin cross-coupling in an online article in Nature published on December 17, 2014. With the new technique, scientists can join two compounds known as olefins to create a new bond between their carbon-atom backbones. Carbon-to-carbon coupling methods are central to chemistry, but until now have been plagued by certain limitations: they often fail if either of the starting compounds contains small, reactive regions known as “functional groups” attached to their main structure. They also frequently don’t work well in the presence of “heteroatoms”—non-carbon atoms such as nitrogen, oxygen and iodine—despite the importance of these types of atoms in chemical synthesis. The new method is what chemists call “mild,” meaning that it doesn’t require the use of extreme temperatures or pressures, nor harsh chemicals. As a result, portions of the building blocks used that are particularly fragile remain unaltered by the reaction. “Functional groups that would be destroyed by other cross-coupling methods are totally unscathed when using our method,” said Julian C. Lo, a graduate student who was a co-lead author of the report with Research Associate Dr. Jinghan Gui.

Normally Solitary Desert Locust Transformed to Gregariousness by Activation of Specific Serotonin-Producing Nerve Cells

A team of biologists has identified a set of nerve cells in desert locusts that bring about ‘gang-like’ gregarious behavior when the insect are forced into a crowd. Dr. Swidbert Ott from the University of Leicester’s Department of Biology, working with Dr. Steve Rogers at the University of Sydney, Australia, has published a study, online on December 17, 2014 in an open-access article in The Royal Society Proceedings B, that reveals how newly identified nerve cells in locusts produce the neurochemical serotonin to initiate changes in their behavior and lifestyle. The findings demonstrate the importance of individual history for understanding how brain chemicals control behavior, which may apply more broadly to humans also. Locusts are normally shy, solitary animals that actively avoid the company of other locusts. But when they are forced into contact with other locusts, they undergo a radical change in behavior – they enter a “bolder” gregarious state in which they are attracted to the company of other locusts. This is the critical first step towards the formation of the notorious locust swarms. Dr. Ott said: “Locusts only have a small number of nerve cells that can synthesise serotonin. Now we have found that of these, a very select few respond specifically when a locust is first forced to be with other locusts. Within an hour, they produce more serotonin. It is these few cells that we think are responsible for the transformation of a loner into a gang member. In the long run, however, many of the other serotonin-cells also change, albeit towards making less serotonin.”

December 16th

Ancient DNA May Help Explain Extinction of Giant Lemurs

Ancient DNA extracted from the bones and teeth of giant lemurs that lived thousands of years ago in Madagascar may help explain why the giant lemurs became extinct. It also explains what factors make some surviving species more at risk today, says a study published online on December 16, 2014 in the Journal of Human Evolution. Most scientists agree that humans played a role in the giant lemurs' demise by hunting them for food and forcing them out of habitats. But an analysis of their DNA suggests that the largest lemurs were more prone to extinction than smaller-bodied species because of their smaller population sizes, according to a team of American and Malagasy researchers. By comparing the species that died out to those that survived, scientists hope to better predict which lemurs are most in need of protection in the future. The African island of Madagascar has long been known as a treasure trove of unusual creatures. More than 80 percent of the island's plants and animals are found nowhere else. But not long ago, fossil evidence showed there were even more species on the island than there are today. Before humans arrived on the island some 2,000 years ago, Madagascar was home to 10-foot-tall elephant birds, pygmy hippos, monstrous tortoises, a horned crocodile, and at least 17 species of lemurs that are no longer living -- some of which tipped the scales at 350 pounds, as large as a male gorilla. Using genetic material extracted from lemur bones and teeth dating back 550 to 5,600 years, an international team of researchers analyzed DNA from as many as 23 individuals from each of five extinct lemur species that died out after human arrival.

Mitochondrial DNA Content in Humans May Predict Risk of Frailty and Death

New research from The Johns Hopkins University suggests that the amount of mitochondrial DNA (mtDNA) found in peoples' blood directly relates to how frail they are medically. This DNA may prove to be a useful predictor of overall risk of frailty and death from any cause 10 to 15 years before symptoms appear. The investigators say their findings contribute to the scientific understanding of aging and may lead to a test that could help identify at-risk individuals whose physical fitness can be improved with drugs or lifestyle changes. A summary of the research was published online on December 4, 2014 in the Journal of Molecular Medicine. "We don't know enough yet to say whether the relationship is one of correlation or causation," says Dan Arking, Ph.D., associate professor of genetic medicine at Hopkins. "But either way, mitochondrial DNA could be a very useful biomarker in the field of aging." Mitochondria are structures within cells often referred to as "power houses" because they generate most of cells' energy. Unlike other cell structures, they contain their own DNA -- separate from that enclosed in the nucleus -- in the form of two to 10 small, circular chromosomes that code for 37 genes necessary for mitochondrial function. There are also genes important for mitochondrial function coded for by DNA in the cell nucleus. There are 10 to thousands of mitochondria per cell, depending on a cell's energy needs. Previous research from Dr. Arking's laboratory linked genetic differences in mtDNA to increased frailty and reduced muscle strength in older individuals. Medically speaking, frailty refers to a well-recognized collection of aging symptoms that include weakness, decreased energy, lower activity levels, and weight loss. To further test this link, Dr.