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Archive - 2014

December 16th

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.

December 15th

Scientists Create “Green” Process to Reduce Waste from Molecular Switches; Significant Advance for Nanotechnology Solves Decades-Long Problem

Dartmouth researchers have found a solution using visible light to reduce waste produced in chemically activated molecular switches, opening the way for industrial applications of nanotechnology ranging from anti-cancer drug delivery to LCD displays and molecular motors. The study was published online on September 15, 2014 in the Journal of the American Chemical Society. Chemically activated molecular switches are molecules that can shift controllably between two stable states and that can be reversibly switched -- like a light switch -- to turn different functions "on" and "off." For example, light-activated switches can fine-tune anti-cancer drugs, so they target only cancer cells and not healthy ones, thereby eliminating the side effects of chemotherapy. But such switches typically generate waste and side products that are problematic. One way of making these processes cleaner is by using light energy, similar to how photosynthesis operates in nature. In their experiments, the researchers show that a merocyanine-based photoacid derivative can effectively be used in a switching process that is fast, efficient, and forms no wastes. "We address a bottleneck that's been hampering the field for decades -- what to do with the accumulated salts and side products when activating such switches," says co-author Dr. Ivan Aprahamian, an associate professor of chemistry. "Acids, bases, and other compounds need to be constantly added to the mix to make sure the system can be switched, but within a few cycles there is so much waste that it interferes with the switching process. We found a neat solution by coupling an efficient photoacid to our chemically activated hydrazone switch. We showed the system can be efficiently modulated more than 100 times with no accumulation of waste or degradation.

Pattern of 48 Long Noncoding RNAs Is Novel Prognostic Marker in Older Patients with Acute Myeloid Leukemia (AML)

A new study led by researchers at The Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC – James) describes a novel marker that may help doctors choose the least toxic, most effective treatment for many older patients with acute myeloid leukemia (AML). AML occurs mainly in older patients and has a three-year survival rate of just 5 to 15 percent. The researchers investigated patterns of molecules called long noncoding RNAs (lncRNAs), a class of RNA molecules more than 200 nucleotide units long that are involved in regulating genes. The researchers examined the abundance, or expression, of lncRNAs in patients who were 60 years and older and who had cytogenetically normal (CN) AML. The study was published online on December 15, 2014 in PNAS..“We have identified a pattern of 48 lncRNAs that predicted both response to standard chemotherapy and overall survival in older CN-AML patients,” says first author Ramiro Garzon, M.D., associate professor of internal medicine at Ohio State. “Patients in the favorable group had a high probability of responding to standard chemotherapy, while those in the unfavorable group generally responded poorly to the treatment and had worse overall survival,” he says. These findings are important for several reasons, says principal investigator Clara D. Bloomfield (photo), M.D., Distinguished University Professor, Ohio State University Cancer Scholar and holder of the William Greenville Pace III Endowed Chair in Cancer Research.

Sex and Relatedness Mediate Intensity of Egg Cannibalism by Ant Larvae

To the casual observer, the colonies of social insects like bees and ants appear to be harmonious societies where individuals work together for the common good. But appearances can be deceiving. In fact, individuals within nests compete over crucial determinants of fitness such as reproductive dominance and production of male eggs. The intensity of competition often depends on the level of kinship between colony members. This is because selfish individuals lose indirect fitness when their behavior harms close relatives. A new study by Dr. Eva Schultner and colleagues from the Universities of Helsinki, St. Andrews, and Oxford reveals that in ants, such social conflict occurs even among the youngest colony members: the eggs and developing larvae. In behavioral experiments conducted at Tvärminne Zoological Station in Finland, ant larvae acted selfishly by cannibalizing eggs, but levels of cannibalism were lower when relatedness among brood was high. In addition, male larvae engaged in cannibalism more often than female larvae. Using evolutionary modeling, the researchers show that cannibalism is predicted to evolve when it carries a benefit to the cannibal (for example in the form of increased survival), and that the costs of consuming kin influence the intensity of cannibalism behavior. Differences in cannibalism benefits for male and female larvae on the other hand may be responsible for higher levels of cannibalism in males. By exploring the evolutionary causes and consequences of selfish larvae behavior, the study published in The American Naturalist sheds new light on the evolutionary constraints of competition in social insect colonies, and demonstrates how in complex societies, even the youngest individuals are potential players in social conflict.

RNA-Binding Musashi Proteins Implicated in Regulation of Cancer

A new study from MIT and collaborating institutions implicates a family of RNA-binding proteins in the regulation of cancer, particularly in a subtype of breast cancer. These proteins, known as Musashi proteins, can force cells into a state associated with increased proliferation. Biologists have previously found that this kind of transformation, which often occurs in cancer cells as well as during embryonic development, is controlled by transcription factors — proteins that turn genes on and off. However, the new MIT research reveals that RNA-binding proteins also play an important role. Human cells have about 500 different RNA-binding proteins, which influence gene expression by regulating messenger RNA, the molecule that carries DNA’s instructions to the rest of the cell. “Recent discoveries show that there’s a lot of RNA-processing that happens in human cells and mammalian cells in general,” says Dr. Yarden Katz, a recent MIT Ph.D. recipient and one of the lead authors of the new paper. “RNA is processed at several points within the cell, and this gives opportunities for RNA-binding proteins to regulate RNA at each point. We’re very interested in trying to understand this unexplored class of RNA-binding proteins and how they regulate cell-state transitions.” Dr. Feifei Li of China Agricultural University is also a lead author of the paper, which was published online on November 7, 2014 in an open-access article in eLife. Senior authors of the paper are MIT biology professors Dr. Christopher Burge and Dr. Rudolf Jaenisch, and Dr. Zhengquan Yu of China Agricultural University. Until this study, scientists knew very little about the functions of Musashi proteins. These RNA-binding proteins have traditionally been used to identify neural stem cells, in which they are very abundant.

Scientist Discover On-Off Switch for Key Stem Cell Gene (Sox2)

Consider the relationship between between an air traffic controller and a pilot. The pilot gets the passengers to their destination, but the air traffic controller decides when the plane can take off and when it must wait. The same relationship plays out at the cellular level in animals, including humans. A region of an animal's genome - the controller - directs when a particular gene - the pilot - can perform its prescribed function. A new study by cell and systems biologists at the University of Toronto (U of T) investigating stem cells in mice shows, for the first time, an instance of such a relationship between the Sox2 gene which is critical for early development, and a region elsewhere on the genome that effectively regulates its activity. The discovery could mean a significant advance in the emerging field of human regenerative medicine, as the Sox2 gene is essential for maintaining embryonic stem cells that can develop into any cell type of a mature animal. "We studied how the Sox2 gene is turned on in mice, and found the region of the genome that is needed to turn the gene on in embryonic stem cells," said Professor Jennifer Mitchell of U of T's Department of Cell and Systems Biology, lead invesigator of a study published online December 15, 2014 in Genes & Development. "Like the gene itself, this region of the genome enables these stem cells to maintain their ability to become any type of cell, a property known as pluripotency. We named the region of the genome that we discovered the Sox2 control region, or SCR," said Dr. Mitchell. Since the sequencing of the human genome was completed in 2003, researchers have been trying to figure out which parts of the genome make some people more likely to develop certain diseases.

December 14th

Baby Cells Learn to Communicate Using the Lsd1 Protein

We would not expect a baby to join a team or participate in social situations that require sophisticated communication. Yet, most developmental biologists have assumed that young cells, only recently born from stem cells and known as "progenitors," are already competent at inter-communication with other cells. New research from Carnegie's Dr. Allan Spradling and postdoctoral fellow Dr. Ming-Chia Lee shows that infant cells have to go through a developmental process that involves specific genes before they can take part in the group interactions that underlie normal cellular development and keep our tissues functioning smoothly. The existence of a childhood state where cells cannot communicate fully has potentially important implications for our understanding of how gene activity on chromosomes changes both during normal development and in cancerous cells. The work is published in Genes and Development. The way that the molecules that package a cell's chromosomes are organized in order to control gene activity is known as the cell's "epigenetic state." The epigenetic state is fundamental to understanding Dr. Spradling’s and Dr. Lee's findings. To developmental biologists, changes in this epigenetic state ultimately explain how the cell's properties are altered during tissue maturation. "In short, acquired epigenetic changes in a developing cell are reminiscent of the learned changes the brain undergoes during childhood," Dr. Spradling explained. "Just as it remains difficult to map exactly what happens in a child's brain as it learns, it is still very difficult to accurately measure epigenetic changes during cellular development. Not enough cells can usually be obtained that are at precisely the same stage for scientists to map specific molecules at specific chromosomal locations." Dr. Lee and Dr.

Landmark Mitochonrdrial Studies at UW-Madison Continue 60-Year Tradition

Dr. Frederick Crane was a researcher under Dr. David E. Green in the mid-1950s, during the early days of the University of Wisconsin-Madison (UW-Madison) Enzyme Institute, when he made his defining discovery. The lab group was on a mission to determine, bit by bit, how mitochondria -- the power plants of cells -- generate the energy required to sustain life. What Dr. Crane found, a compound called coenzyme Q, was a missing piece of the puzzle and became a major part of the legacy of mitochondrial research at UW-Madison. But it was no accident. "It was the result of a long train of investigation into a mechanism of, and compounds involved in, biological energy conversion," Dr. Crane wrote in a 2007 review article of his discovery. Almost six decades later, that "long train" has grown even longer. Dr. Dave Pagliarini, a UW-Madison assistant professor of biochemistry, has established a new laboratory studying these dynamic organelles, the mitochondria. He recently published two studies shedding more light on coenzyme Q and how it's made, one in PNAS online on October 22, 2014. and another on December 11, 2014 in Molecular Cell. "Mitochondria are tiny structures in nearly all of our cells that are essential for producing our cellular energy and that house a wide array of metabolic processes," Dr. Pagliarini says. "When mitochondria don't work properly, many different human diseases can arise." These include cerebellar ataxia, certain kidney diseases, and severe childhood-onset multisystemic diseases. Coenzyme Q deficiency is a hallmark of these diseases, but scientists aren't sure why. "Nearly 60 years later, there is still much we don't know about how mitochondria make coenzyme Q and that has complicated our ability to target this pathway therapeutically," Dr. Pagliarini says.