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Archive - Dec 16, 2014

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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.

Naming People and Things for Babies Provides Key Learning Benefits Later

In a follow-up to her earlier studies of learning in infancy, developmental psychologist Dr. Lisa Scott (photo) and colleagues at the University of Massachusetts-Amherst (U Mass-Amherst) are reporting that talking to babies in their first year, in particular naming things in their world, can help them make connections between what they see and hear, and these learning benefits can be seen as much as five years later. "Learning in infancy between the ages of six to nine months lays a foundation for learning later in childhood," Dr. Scott says. "Infants learn labels for people and things at a very early age. Labeling helps them recognize people and objects individually and helps them decide how detailed their understanding of the object or face needs to be." Details of Scott's research, conducted with U Mass-Amherst psychological and brain science doctoral students Hillary Hadley and Charisse Pickron, were published online on November 29, 2014 in Developmental Science. Dr. Scott's own earlier experiments, as well as work by others, shows that before they are six months old, babies can easily tell faces apart within familiar (e.g., human faces) and unfamiliar (e.g, monkey faces) groups. But by nine months, they are no longer as good at distinguishing faces outside their own species compared to faces from their own species. This decline in recognizing unfamiliar individuals is called "perceptual narrowing" and is driven by the infants' experience interacting with some groups more than others and learning the names of individuals in some groups more than others during the six- to nine-month window, the neuroscience researchers say.

Gene Defect Alters Ion Channel in Melanosomes to Cause Form of Albinism

A team led by Brown University biologists, together with colleagues, has discovered the way in which a specific genetic mutation appears to lead to the lack of melanin production underlying a form of albinism. Newly published research provides the first demonstration of how a genetic mutation associated with a common form of albinism leads to the lack of melanin pigments that characterizes the condition. Approimately 1 in 40,000 people worldwide have type 2 oculocutaneous albinism, which has symptoms of unusually light hair and skin coloration, vision problems, and reduced protection from sunlight-related skin or eye cancers. Scientists have known for about 20 years that the condition is linked to mutations in the gene that produces the OCA2 protein, but they hadn’t yet understood how the mutations lead to a melanin deficit. In the new research, a team led by Brown University biologists Nicholas Bellono and Dr. Elena Oancea shows that the protein is necessary for the proper functioning of an ion channel on the melanosome organelle (image), the little structure in a cell where melanin is made and stored. The ion channel is like a gate that lets electrically charged chloride molecules flow into and out of the melanosome. When the melanosome lacks OCA2 or contains OCA2 with an albinism-associated mutation, the researchers found, the chloride flow doesn’t occur and the melanosome fails to produce melanin, possibly because its acidity remains too high. The discovery could inspire new ideas for treating albinism, said Dr. Oancea, assistant professor of medical science and senior author of the paper published online on December 16, 2014 in the open-access journal eLife. “From a therapeutic point of view, we now have a channel that’s a possible drug target,” she said.

Discovery of Pathogen Toxin May Help Fight Destructive Honeybee Disease

University of Guelph researchers in Canada hope their new discovery will help combat a disease killing honeybee populations around the world. The researchers have found a toxin released by the pathogen that causes American foulbrood disease — Paenibacillus larvae (P. larvae) — and developed a lead-based inhibitor against it. The study was published online on December 4, 2014 in the Journal of Biological Chemistry. The finding provides much-needed insight into how the infection occurs, said Dr. Rod Merrill, a professor in Guelph’s Department of Molecular and Cellular Biology and a study co-author. It also could lead to natural and more effective approaches for fighting the most widespread and destructive of bee brood diseases. “We are the first to do this,” said Dr. Merrill, who conducted the study with graduate student Daniel Krska. Also involved were post-doctoral researchers Drs. Ravi Ravulapalli and Miguel Lugo, technician Tom Keeling, and Harvard Medical School’s Dr. Rob Fieldhouse. American foulbrood is found throughout Ontario and Canada, and affects both the honeybee industry and pollinator populations. Honeybees are among the world’s most important pollinators, and their numbers are already falling globally because of disease, pesticide use, climate change, and other factors. The disease spreads readily through spores transmitted within and between colonies by adult bee carriers, Dr. Merrill said. Developing larvae are infected by eating the spores. The larvae die but not before releasing millions of additional spores into the colony. As well, the hive’s weakened state attracts “robber bees” looking for honey, which then spread the disease to other colonies.