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Archive - May 2011


May 11th

Evolutionary Adaptations Can Be Reversed, But Rarely

Ever since Charles Darwin proposed his theory of evolution in 1859, scientists have wondered whether evolutionary adaptations can be reversed. Answering that question has proved difficult, partly due to conflicting evidence. In 2003, scientists showed that some species of insects have gained, lost, and regained wings over millions of years. But a few years later, a different team found that a protein that helps control cells’ stress responses could not evolve back to its original form. Dr. Jeff Gore, assistant professor of physics at MIT, says the critical question to ask is not whether evolution is reversible, but under what circumstances it could be. “It’s known that evolution can be irreversible. And we know that it’s possible to reverse evolution in some cases. So what you really want to know is: What fraction of the time is evolution reversible?” he says. By combining a computational model with experiments on the evolution of drug resistance in bacteria, Dr. Gore and his students have, for the first time, calculated the likelihood of a particular evolutionary adaptation reversing itself. They found that a very small percentage of evolutionary adaptations in a drug-resistance gene can be reversed, but only if the adaptations involve fewer than four discrete genetic mutations. The findings will appear in the May 13 issue of the journal Physical Review Letters. Lead authors of the paper are two MIT juniors, Longzhi Tan and Stephen Serene. Dr. Gore and his students used an experimental model system developed by researchers at Harvard University to study the evolution of a gene conferring resistance to the antibiotic cefotaxime in bacteria. The Harvard team identified five mutations that are crucial to gaining resistance to the drug.

Beneficial Bacteria Help Repair Intestinal Injury by Inducing Reactive Oxygen Species

The gut may need bacteria to provide a little bit of oxidative stress to stay healthy, new research suggests. Probiotic bacteria promote healing of the intestinal lining in mice by inducing the production of reactive oxygen species, researchers at Emory University School of Medicine have shown. The results, published online on May 9, 2011, in PNAS, demonstrate a mechanism by which bacterial cultures in foods such as yogurt and kimchi have beneficial effects on intestinal health. The insights gained could also guide doctors to improved treatments for intestinal diseases, such as necrotizing enterocolitis in premature babies or intestinal injury in critically ill adults. The laboratories of Dr. Andrew Neish and Dr. Asma Nusrat, both professors of pathology and laboratory medicine, teamed up for the study. The paper’s co-first authors are postdoctoral fellow Dr. Philip Swanson and associate research professor Dr. Amrita Kumar. “It’s been known for years that probiotic bacteria can have these kinds of helpful effects, but it wasn’t really clear how this worked,” Dr. Neish says. “We’ve identified one example, among many, of how certain kinds of bacteria have specific biochemical functions in the body.” Recent research has shown that the bacteria in our intestines influence our metabolism and immune systems. For example, an imbalance in the proportions of harmful and beneficial bacteria seems to over-activate immune cells in the intestines, driving inflammatory bowel disease. Intestinal epithelial cells, the cells that line the intestine, live in close contact with bacteria and normally form a barrier that keeps bacteria away from other organs. They can repair small gaps in the barrier, which breaks down in intestinal diseases, by migrating into the gaps.

May 9th

Salmonella enterica Regulates Virulence Based on Iron Levels

Salmonella enterica, one of the main causes of gastrointestinal infections, modulates its virulence gene expression, adapting it to each stage of the infection process, depending on the free iron concentration found in the intestinal epithelium of its host. Researchers at Universitat Autònoma de Barcelona (UAB) have demonstrated for the first time that the pathogen activates these genes through the Fur protein, which acts as a sensor of iron levels in its surroundings. The research, published online on May 6, 2011, in the journal PLoS ONE and entitled "Fur activates the expression of Salmonella enterica pathogenicity island 1 by directly interacting with the hilD operator in vivo and in vitro," was carried out by the Molecular Microbiology Group of the UAB Department of Genetics and Microbiology and coordinated by Dr. Jordi Barbé. Dr Juan Carlos Alonso from the National Biotechnology Centre also collaborated in the research group. Iron is an essential part of the development of almost all living organisms. This is why all organisms have developed an iron uptake system which guarantees that they can acquire it from their external environment. However, too much iron in the cell interior can have harmful effects and organisms have systems to control this as well. In vertebrates, this control produces a first defense barrier known as nutritional immunity which limits the amount of free iron found in biological fluids and prevents the development of pathogens. Only the upper intestinal track, given its anaerobic condition, presents appreciable levels of free iron.

May 9th

Nerve Cells’ Navigation System Revealed

Johns Hopkins scientists have discovered how two closely related proteins guide projections from nerve cells with exquisite accuracy, alternately attracting and repelling these axons as they navigate the most miniscule and frenetic niches of the nervous system to make remarkably precise connections. The discovery, reported April 28 in the journal Neuron and featured on the cover, reveals that proteins belonging to the "semaphorin" family of guidance cues are crucial for getting neuronal projections exactly where they need to be, not only across long distances, but also in the short-range wiring of tiny areas fraught with complex circuitry, such as the central nervous system of the fruit fly. Because signaling that affects the growth and steering of neuronal processes is critical for repairing and regenerating damaged or diseased nerve cells, this research suggests that a more refined understanding of how semaphorin proteins work could contribute to treatment strategies, according to Dr. Alex Kolodkin, a professor in the neuroscience department at Johns Hopkins and a Howard Hughes Medical Institute investigator. Using embryonic flies, some native (normal) and others genetically altered to lack a member of the semaphorin gene family or the receptor that binds to the semaphorin and signals within the responding neuron, the team labeled particular classes of neurons and then observed them at high resolution using various microscopy strategies to compare their axon projections. In the native developing flies, the team saw how certain related semaphorins, proteins that nerve cells secrete into the intracellular space, work through binding their plexin receptor. First, a semaphorin-plexin pair attracts a certain class of extending neurons in the embryonic fly central nervous system to assemble a specific set of target projections.

May 7th

Personalized Medicine 4.0 Conference: Focus on Pharmacogenomics & Consumer Genetic Testing

This year’s Personalized Medicine Conference (4.0) will be held Thursday, May 26 from 8 am to 7 pm at the South San Francisco Conference Center on the campus of San Francisco State University. This fourth annual conference on personalized medicine focuses on two exciting areas – pharmacogenomics (the right drug, at the right dose, for the right patient, at the right time) and the controversial topic of direct-to-consumer genetic testing, examining the science, the business, and the social dimensions of each. Personalized Medicine 4.0 is a one-day conference and networking opportunity for health and industry professionals, educators, and scientists. Learn how the new genomic medicine will affect your work and your life. Seating is limited. Register now at For additional information or to sponsor this event, please e-mail or call Arlene Essex at 415-405-4107. Advance registration is $495 through 5/16. Save $100 – Early registration is $395 ending soon! Contact us for academic rates.

Temperature Shifts Prime Immune Response

Researchers at The Scripps Research Institute and the Novartis Research Foundation have found a temperature-sensing protein within immune cells that, when tripped, allows calcium to pour in and activate an immune response. This process can occur as temperature rises, such as during a fever, or when it falls—such as when immune cells are "called" from the body's warm interior to a site of injury on cooler skin. The study, published online on April 17, 2011 in Nature Chemical Biology, is the first to find such a sensor in immune cells—specifically, in the T lymphocytes that play a central role in activation of killer immune cells. The protein, STIM1, previously known as an endoplasmic reticulum (ER) calcium sensor, had been thought to be important in immune function, and now the scientists show it is also a temperature sensor. "Temperature has a profound effect on all biological processes including immune responses, but surprisingly little is known about molecules in immune cells that sense temperature shifts," said the study's principal investigator, Scripps Research Professor Ardem Patapoutian. "Here we show that STIM1 senses temperature and has a profound impact on immune cells." This is the second family of thermosensation molecules that the Patapoutian laboratory has uncovered. The team has isolated and characterized three of six members of the transient receptor potential (TRP) family of ion channels—the so-called thermoTRPs. "These proteins translate temperature, which is a physical stimulus, into a chemical signal—ions flowing into cells," said Dr. Patapoutian. "ThermoTRPs mainly function in specialized sensory neurons that relay environmental temperature information to the brain." In this study, the researchers turned to immune cells to look for temperature sensors.

May 6th

Sequencing of Single-Cell Marine Organisms Offers Clues to How Cells Interact within the Environment

From a bucket of seawater, scientists have unlocked information that may lead to deeper understanding of organisms as different as coral reefs and those that cause human disease. By analyzing genomes of a tiny, single-celled marine animal, they have demonstrated a possible way to address diverse questions such as how diseased cells differ from neighboring healthy cells and what it is about some Antarctic algae that allows them to live in warming waters while other algae die out. Dr. Debashish Bhattacharya, professor of ecology, evolution and natural resources in Rutgers' School of Environmental and Biological Sciences, and Dr. Ramunas Stepanauskas and Dr. Hwan Su Yoon of the Bigelow Laboratory of Ocean Sciences, and colleagues, have published their results in the May 6, 2011 issue of Science. They used sophisticated new technologies to sequence the genomes of individual picobilophytes, tiny microbes first discovered in 2007. At less than 10 micrometers across, they are some of the tiniest marine animals known to science. "If we can peer inside the genome of a single cell and reconstruct its history, we can do that for many cells and figure out their interactions with other cells in the environment," Dr. Bhattacharya said. For example, why do different cancer cells from the same tumor grow at different rates? Their genomes might contain the answer, and the answer might lead to more effective treatment strategies. "Our results demonstrate how single cell genomics opens a window into the natural drama that constantly takes place in each drop of seawater – a drama featuring predation, viral infections, and the divergent fate of close relatives," Dr. Stepanauskas said. "The outcomes of this drama have profound effects on the lives of larger marine organisms, such as commercially valuable fish." Dr. Bhattacharya and Dr.

May 2nd

Antioxidant May Prevent Alcohol-Induced Liver Disease

An antioxidant may prevent damage to the liver caused by excessive alcohol, according to new research from the University of Alabama at Birmingham (UAB) and collaborating institutions. The findings, published in the May 2011 issue of the journal Hepatology, may point the way to treatments to reverse steatosis, or fatty deposits in the liver that can lead to cirrhosis and cancer. The research team, led by Dr. Victor Darley-Usmar, professor of pathology at UAB, introduced an antioxidant called mitochondria-targeted ubiquinone, or MitoQ, to the mitochondria of rats that were given alcohol every day for five to six weeks in an amount sufficient to mirror excessive intake in a human. Chronic alcoholics, those who drink to excess every day, experience a buildup of fat in the liver cells. When alcohol is metabolized in the liver, it creates free radicals that damage mitochondria in the liver cells and prevent them from using sufficient amounts of oxygen to produce energy. Moreover, the low-oxygen condition called hypoxia worsens mitochondrial damage and promotes the formation of the fatty deposits that can progress to cirrhosis. Dr. Darley-Usmar and his collaborators say that the antioxidant MitoQ is able to intercept and neutralize free radicals before they can damage the mitochondria, preventing the cascade of effects that ultimately leads to steatosis. "There has not been a promising pharmaceutical approach to preventing or reversing the long-term damage associated with fatty deposits in the liver that result from excessive consumption of alcohol," said Dr. Darley-Usmar. "Our findings suggest that MitoQ might be a useful agent for treating the liver damage caused by prolonged, habitual alcohol use." "Previous studies have shown that MitoQ can be safely administered long-term to humans," said Dr.

Scientists Track Evolution and Spread of Deadly Fungus

New research has shed light on the origins of a fungal infection which is one of the major causes of death from AIDS-related illnesses. The study, published on April 28, 2011, in the journal PLoS Pathogens, shows how the more virulent forms of Cryptococcus neoformans evolved and spread out of Africa and into Asia. Cryptococcus neoformans is a species of often highly aggressive fungi. One particular strain of the fungus – known as Cryptococcus neoformas varietygrubii (Cng) – causes meningitis amongst patients with compromised immune systems following HIV infection. There are believed to be up to a million cases of cryptococcal meningitis each year, resulting in over 600,000 deaths. Infection with the fungus, which invades the central nervous system, is treated with a life-long therapy of antifungal drugs, which can have highly unpleasant side effects. Sitali Simwami and Dr. Matthew Fisher from Imperial College London, together with colleagues from St Georges, University of London, Naresuan University, Thailand, and the CBS Fungal Biodiversity Centre, The Netherlands, used genetic sequencing techniques to compare the genetic diversity of Cng in 183 samples taken from the clinic and the environment in Thailand against the 77 samples from a global database. Thailand has an emerging HIV epidemic and nearly one in five HIV-infected patients is affected by cryptococcal infection. "Cryptococcal meningitis kills hundreds of thousands of people each year, almost as many as malaria, yet gets little attention," explains Dr. Fisher. "We know very little about where it originated from and how it evolved. If we can track its evolution and diversity, then we can begin to understand where the pathogen originates from, how it infects people, and how it adapts to become more – or less – virulent.

May 1st

DNA Reveals Convergent Evolution in Lichen

Lichen, those drab, fuzzy growths found on rocks and trees, aren't as cuddly and charismatic as kangaroos or intriguing as opossums, but they could be a fungal equivalent, at least evolutionarily. A Duke research team has found that lichen that seem identical in all outward appearances and produce the same internal chemicals are in fact two different species, one living in North America and one in Australia. They're an example of "convergent evolution," in which two species evolve separately but end up looking very similar, like the Tasmanian wolf and the American wolf. The lichens developed the same adaptations to survive and thrive in vastly different regions of the world. Because they show the same evolutionary patterns as marsupials and mammals, but are easier to study, they could become model organisms to further probe how mammals and other groups of organisms evolve, said Duke biologist Brendan Hodkinson. "Lichen can often seem dull and uncharismatic, but these two species turned out to be quite intriguing," said Hodkinson, a graduate student in the lab of Duke lichenologist Dr. François Lutzoni. "They're like sugar gliders and flying squirrels or wombats and groundhogs. They're fungal examples of convergent evolution." Scientists originally labeled specimens from both continents Xanthoparmelia tasmanica, which, like all lichen, is a type of fungus that "farms" algae. The lichen specimens were thought to be one species because they shared the same body plan and produced the same chemicals. But given the lichens' geography and the natural history of other species, some scientists still questioned whether the organisms were truly identical, even though previous tests showed that they were.