Evolutionary Geneticist Helps to Find Butterfly Gene, Clue to Age-Old Question

Years after sleeping in hammocks in the wilds of Peru and Panama, collecting hundreds of thousands of samples of colorful insects, Mississippi State assistant professor Brian Counterman now is helping unlock a very difficult puzzle.

The more-than-century-long challenge has involved a secret of the Heliconius butterfly, the orange, black, yellow, and red insect that hasn't easily communicated how all its radiant colors came to be.

For evolutionary biologists, and especially geneticists like Counterman, the butterflies--commonly called passion vine butterflies--make perfect research subjects for better understanding the important scientific question: How do organisms change to survive?

Over the past decade, the researcher in the university's biological sciences department has been part of an international team using field experiments, genetic mapping, population genetics, and phylogenetics to study the butterflies' biology and history.

A Duke University doctoral graduate in biology and evolutionary genetics, Counterman studied genetics of adaptation as part of his post-doctoral research at North Carolina State University. He joined the MSU faculty in 2009.

Passion vine butterflies are found throughout South and Central America. Through the years, scientists observed that Heliconius butterflies with certain red patterns survived in certain areas, while others didn't.

"There are very few cases that we know what traits determine if an organism will survive in nature," Counterman said, adding that he and a team of researchers recently uncovered the gene responsible for the different red wing patterns.

Their finds were featured in the July issue of Science.

Counterman said the butterflies use red as a warning signal to birds and other predators that they are poisonous and should not be consumed.

"This is one of the first examples where we've found the genetic change that allowed (an organism) to live or die in nature," he observed, adding that finding the red gene was just the first step in understanding how they have survived.

Counterman and his team further analyzed the red gene to reconstruct when the different red patterns evolved, providing important clues into how rapidly new adaptations can arise and spread in populations that nearly encompass entire continents.

This research was showcased on the cover in a December issue of the Proceedings of the National Academy of Sciences.

For scientists like Counterman, finding answers to these questions may give insight about how and why the diversity in the world evolved. And, there is still more to come.

Counterman now is part of a team sequencing the entire Heliconius genome--one of the first butterfly genomes--that should open the door to a new level of questioning into the biological causes for one of the most charismatic groups of organisms on earth.

Read more at Science Daily

Online News Portals Get Credibility Boost from Trusted Sources

People who read news on the Web tend to trust the gate even if there is no gatekeeper, according to Penn State researchers. When readers access a story from a credible news source they trust through an online portal, they also tend to trust the portal, said S. Shyam Sundar, Distinguished Professor of Communications and co-director of the Media Effects Research Laboratory. Most of these portals use computers, not people, to automatically sort and post stories.

Sundar said this transfer of credibility provides online news portals -- Yahoo News and Google News -- with most of the benefits, but with little of the costs associated with online publishing.

"A news portal that uses stories from a credible source gets a boost in credibility and might even make money through advertising," said Sundar. "However, if there is a lawsuit for spreading false information, for example, it's unlikely that the portal will be named in the suit."

Sundar said the flow of credibility did not go both ways. He said that reading a low-credibility story on a high-credibility portal did not make the original source more trustworthy.

The researchers, who reported their findings in Journalism and Mass Communication Quarterly, asked a group of 231 students to read online news stories. After reading the stories, the students rated the credibility of the original source and the portal.

The researchers placed banners from Google News, which served as a high credibility portal, and the Drudge Report, which served as a low-credibility portal, on the pages. They also added banners to identify the New York Times -- the high-credibility source -- and the National Enquirer -- the low-credibility source.

The students were significantly more likely to consider a portal credible if the source of the story was trustworthy. The credibility of the portal suffered if the source lacked trustworthiness.

Sundar said that attention to sources depended on the involvement of the reader. When readers were particularly interested in the story, they tended to more thoroughly evaluate all the sources involved in the production and distribution of that news. People who are not interested in the story base their judgments on the credibility of the portal, which is the most immediately visible source.

Sundar, who worked with Hyunjin Kang and Keunmin Bae, both doctoral students in communications, and Shaoke Zhang, doctoral student in information sciences and technology, said that the way credibility is transferred from site to site shows the complexity of the relationship between online news readers and sources.

Evaluating credibility is difficult on the web because there are often chains of news sources for a story, Sundar said. For example, a person may find a story on an online news portal, forward the information to another friend through email, who then posts it on a social network. The identity of the original source may or may not be carried along this chain to the final reader.

Read more at Science Daily

Gorilla Grins Hint at Origin of Human Smiles

Psychologists from the University of Portsmouth have published a paper suggesting gorillas use human-like facial expressions to communicate moods with one another. Not only that, but two of the expressions, both of which resemble grinning, could show the origins of the human smile.

However, the findings published in the American Journal of Primatology show their smiles mean different things. The Portsmouth researchers found these expressions, observed in Western Lowland gorillas, expressed a number of emotions.

One, a “play face”, featuring an open mouth and showing no teeth, denotes a playful mood, usually accompanied with physical contact. Another, which is open-mouthed and displaying top teeth, could be a submissive smile — as it mixes the play face and a bared-teeth expression, which indicates appeasement.

“Many primate species also show their teeth when they scream,” Bridget Waller, the lead researcher told Wired.co.uk in an e-mail. “These expressions tend to look different to the expressions I studied in gorillas, as the upper and lower teeth are both exposed, and the mouth widely open. The expression is more tense, and accompanied by very different vocalisations. The vocalised element of the scream can differ depending on whether the screamer is an aggressor or a victim.”

In short: subtle differences in facial expression and vocals mean quite different things in primate posturing — one is obedient and appeasing, the other screaming and aggressive. But does this mean that our own smile is inherently passive and submissive?

“In some primate species the bared-teeth display (the expression similar to the human smile) is used only by subordinates, but these species have a very different social organisation to humans,” says Waller. “They tend to have very strict dominance hierarchies, whereas we have a more relaxed social structure. So, in some circumstances humans might use smiling as a subordinate signal, but is can also be used as a genuine signal of friendliness.”

Read more at Wired Science

Drug-Resistant Bugs Found in Organic Meat

If you’re paying premium prices for pesticide- and antibiotic-free meat, you might expect that it’s also free of antibiotic-resistant bacteria. Not so, according to a new study. The prevalence of one of the world’s most dangerous drug-resistant microbe strains is similar in retail pork products labeled “raised without antibiotics” and in meat from conventionally raised pigs, researchers have found.

Methicillin-resistant Staphylococcus aureus (MRSA), a drug-resistant form of the normally harmless S. aureus bacterium, kills 18,000 people in the United States every year and sickens 76,000 more. The majority of cases are linked to a hospital stay, where the combination of other sick people and surgical procedures puts patients at risk. But transmission also can happen in schools, jails, and locker rooms (and an estimated 1.5% of Americans carry MRSA in their noses). All of this has led to a growing concern about antibiotic use in agriculture, which may be creating a reservoir of drug-resistant organisms in billions of food animals around the world.

Tara Smith, an epidemiologist at the University of Iowa College of Public Health in Iowa City who studies the movement of staph bacteria between animals and people, wondered whether meat products might be another mode of transmission. For the new study, published this month in PLoS ONE, she and colleagues bought a variety of pork products—395 packages in all—from 36 different stores in two big pig farming states, Iowa and Minnesota, and one of the most densely populated, New Jersey.

In the laboratory, the team mixed meat samples “vigorously” with a bacterial growth medium and allowed any microbes present to grow. MRSA, which appears as mauve-colored colonies on agar plates, was genetically typed and tested for antibiotic susceptibility.

The researchers found that 64.8% of the samples were positive for staph bacteria and 6.6% were positive for MRSA. Rates of contamination were similar for conventionally raised pigs (19 of 300 samples) and those labeled antibiotic-free (seven of 95 samples). Results of genetic typing identified several well-known strains, including the so-called livestock-associated MRSA (ST398) as well as common human strains; all were found in conventional and antibiotic-free meat.

Smith says she was surprised by the results. In a related investigation, which has not been published, her group tested pigs living on farms and found that antibiotic-free pigs were free from MRSA, whereas the resistant bug is often found on conventional pig farms.

The study reveals an important data point on the path from farm to fork, yet the source of the MRSA on meat products is unknown, Smith says. “It’s difficult to figure out.” Transmission of resistant bugs might occur between antibiotic-using and antibiotic-free operations, especially if they’re near each other, or it could come from farm workers themselves. Another possibility is that contamination occurs at processing plants. “Processing plants are supposed to be cleaned between conventional and organic animals,” she says. “But how well does that actually happen?”

In another recent study, researchers from Purdue University in West Lafayette, Indiana, found that beef products from conventionally raised and grass-fed animals were equally likely to be contaminated by antibiotic-resistant Escherichia coli. In a second study by the same group, poultry products labeled “no antibiotics added” carried antibiotic-resistant E. coli and Enterococcus (another bacteria that causes invasive disease in humans), although the microbes were less prevalent than on conventionally raised birds.

“The real question is, where is it coming from, on the farm or post-farm?” says Paul Ebner, a food safety expert who led the Purdue studies. And the biggest question of all, he says, “Is it impacting human health?”

“There’s a tremendous amount of interest in this issue—feeding antibiotics to food animals,” says Ellen Silbergeld, an expert on health and environmental impacts of industrial food animal production at the Johns Hopkins Bloomberg School of Public Health in Baltimore, Maryland. “Thus, determining when amending that practice makes a difference is important.”

Read more at Wired Science

Cutting Off the Oxygen Supply to Serious Diseases

A new family of proteins which regulate the human body’s ‘hypoxic response’ to low levels of oxygen has been discovered by scientists at Barts Cancer Institute at Queen Mary, University of London and The University of Nottingham.

The discovery has been published in the international journal Nature Cell Biology. It marks a significant step towards understanding the complex processes involved in the hypoxic response which, when it malfunctions, can cause and affect the progress of many types of serious disease, including cancer.

The researchers have uncovered a previously unknown level of hypoxic regulation at a molecular level in human cells which could provide a novel pathway for the development of new drug therapeutics to fight disease. The cutting-edge work was funded by the Biotechnology and Biological Sciences Research Council (BBSRC).

Proteins are biochemical compounds which carry out specific duties within the living cell. Every cell in our body has the ability to recognise and respond to changes in the availability of oxygen. The best example of this is when we climb to high altitudes where the air contains less oxygen. The cells recognise the decrease in oxygen via the bloodstream and are able to react, using the ‘hypoxic response’, to produce a protein called EPO. This protein in turn stimulates the body to produce more red blood cells to absorb as much of the reduced levels of oxygen as possible.

This response is essential for a normal healthy physiology but when the hypoxic response in cells malfunctions, diseases like cancer can develop and spread. Cancer cells have a faulty hypoxic response which means that as the cells multiply they highjack the response to create their own rogue blood supply. In this way the cells can form large tumours. The new blood supply also helps the cancer cells spread to other parts of the body, called ‘metastasis’, which is how ultimately cancer kills patients.

The scientists have identified a new family of hypoxic regulator proteins called ‘LIM domain containing proteins’ which function as molecular scaffolds or ‘adapters’ bringing together or bridging two key enzymes in the hypoxic response pathway, namely PHD2 and VHL. Both of these are involved in down-regulating the master regulator protein called Hypoxia-inducible factors (HIF1). The research has shown that loss of LIMD1 breaks down the bridge it creates between PHD2 and VHL and this then enables the master regulator to function out of control and thus contribute to cancer formation.

Read more at Science Daily

Was the Little Ice Age Triggered by Massive Volcanic Eruptions?

A new international study may answer contentious questions about the onset and persistence of Earth's Little Ice Age, a period of widespread cooling that lasted for hundreds of years until the late 19th century.

The study, led by the University of Colorado Boulder with co-authors at the National Center for Atmospheric Research (NCAR) and other organizations, suggests that an unusual, 50-year-long episode of four massive tropical volcanic eruptions triggered the Little Ice Age between 1275 and 1300 A.D. The persistence of cold summers following the eruptions is best explained by a subsequent expansion of sea ice and a related weakening of Atlantic currents, according to computer simulations conducted for the study.

The study, which used analyses of patterns of dead vegetation, ice and sediment core data, and powerful computer climate models, provides new evidence in a longstanding scientific debate over the onset of the Little Ice Age. Scientists have theorized that the Little Ice Age was caused by decreased summer solar radiation, erupting volcanoes that cooled the planet by ejecting sulfates and other aerosol particles that reflected sunlight back into space, or a combination of the two.

"This is the first time anyone has clearly identified the specific onset of the cold times marking the start of the Little Ice Age," says lead author Gifford Miller of the University of Colorado Boulder. "We also have provided an understandable climate feedback system that explains how this cold period could be sustained for a long period of time. If the climate system is hit again and again by cold conditions over a relatively short period -- in this case, from volcanic eruptions -- there appears to be a cumulative cooling effect."

"Our simulations showed that the volcanic eruptions may have had a profound cooling effect," says NCAR scientist Bette Otto-Bliesner, a co-author of the study. "The eruptions could have triggered a chain reaction, affecting sea ice and ocean currents in a way that lowered temperatures for centuries."

The study appears this week in Geophysical Research Letters. The research team includes co-authors from the University of Iceland, the University of California Irvine, and the University of Edinburgh in Scotland. The study was funded in part by the National Science Foundation, NCAR's sponsor, and the Icelandic Science Foundation.

Far-flung regions of ice

Scientific estimates regarding the onset of the Little Ice Age range from the 13th century to the 16th century, but there is little consensus, Miller says. Although the cooling temperatures may have affected places as far away as South America and China, they were particularly evident in northern Europe. Advancing glaciers in mountain valleys destroyed towns, and paintings from the period depict people ice-skating on the Thames River in London and canals in the Netherlands, places that were ice-free before and after the Little Ice Age.

"The dominant way scientists have defined the Little Ice Age is by the expansion of big valley glaciers in the Alps and in Norway," says Miller, a fellow at CU's Institute of Arctic and Alpine Research. "But the time in which European glaciers advanced far enough to demolish villages would have been long after the onset of the cold period."

Miller and his colleagues radiocarbon-dated roughly 150 samples of dead plant material with roots intact, collected from beneath receding margins of ice caps on Baffin Island in the Canadian Arctic. They found a large cluster of "kill dates" between 1275 and 1300 A.D., indicating the plants had been frozen and engulfed by ice during a relatively sudden event.

The team saw a second spike in plant kill dates at about 1450 A.D., indicating the quick onset of a second major cooling event.

To broaden the study, the researchers analyzed sediment cores from a glacial lake linked to the 367-square-mile Langjökullice cap in the central highlands of Iceland that reaches nearly a mile high. The annual layers in the cores -- which can be reliably dated by using tephra deposits from known historic volcanic eruptions on Iceland going back more than 1,000 years -- suddenly became thicker in the late 13th century and again in the 15th century due to increased erosion caused by the expansion of the ice cap as the climate cooled.

"That showed us the signal we got from Baffin Island was not just a local signal, it was a North Atlantic signal," Miller says. "This gave us a great deal more confidence that there was a major perturbation to the Northern Hemisphere climate near the end of the 13th century."

The team used the Community Climate System Model, which was developed by scientists at NCAR and the Department of Energy with colleagues at other organizations, to test the effects of volcanic cooling on Arctic sea ice extent and mass. The model, which simulated various sea ice conditions from about 1150 to 1700 A.D., showed several large, closely spaced eruptions could have cooled the Northern Hemisphere enough to trigger the expansion of Arctic sea ice.

Read more at Science Daily

Speed Limits on the Evolution of Enormousness

If you’ve ever wondered whether mammalian evolution has a speed limit, here’s a number for you: 24 million.

That’s how many generations a new study estimates it would take to go from mouse- to elephant-sized while operating on land at the maximum velocity of change. The figure underscores just how special a trait sheer bigness can be.

“Big animals represent the accumulation of evolutionary change, and change takes time,” said evolutionary biologist Alistair Evans of Australia’s Monash University.

Evans and co-authors revisit a fossil record dataset of mammal body size during the last 70 million years, in a study published Jan. 31 in Proceedings of the National Academy of Sciences. The data was originally used to describe the evolutionary growth spurts experienced by mammals soon after dinosaurs ceased to be Earth’s dominant animals.

For the previous 140 million years, mammals had been rat-sized or smaller. With dinosaurs significantly reduced, mammals had a chance to fill newly vacant ecological niches, particularly that of the large-bodied plant-eater.

In this context, size isn’t simply a visible sign of change, but a proxy for modifications to diet, metabolism and body structure. To become big is to change, radically and fundamentally.

“How fast can all of these interconnected changes be made? This to me is the main question that drives why maximum evolutionary rates are fascinating,” said Evans.

In the new study, Evans’ team measures the time taken, in total years and likely number of generations, for 28 mammal lineages to become larger and smaller over the fossil record.

Odd-toed ungulates, including horses and rhinoceroses, had the highest maximum rates of growth. (The largest land mammal ever, the now-extinct Paraceratherium, was part of this group.) Rodents placed in the middle of the pack, while carnivores changed quite slowly, and primates even more slowly.

At the fastest observed terrestrial rates, going from rabbit- to elephant-sized takes roughly 10 million generations, while the aforementioned mouse- to elephant-sized jump takes 24 million generations. In the oceans, however, body size could change twice as fast, perhaps because water’s support of body weight lessened physiological constraints.

The researchers also found that mammals shrink more rapidly than they grow, with size lost 100 times faster than it’s gained. An implicit conservation message: Treasure bigness, because it’s difficult to achieve, and won’t likely happen again so long as humans remain Earth’s dominant species.

Read more at Wired Science

Humans Tamed Horses All Over the World

The domestication of wild horses had a profound effect on human history -- offering nutrition, transportation and a leg up in warfare, among other advantages. But there are still many unanswered questions about when and where our species began its long love affair with horses.

A new genetic study offers some clues. Through the first complete analysis of equestrian mitochondrial DNA -- a kind of genetic material that is passed directly from mother to offspring -- an international group of scientists was able to trace all modern horses to an ancestor that lived about 140,000 years ago.

After horse domestication began about 10,000 years ago, the study also discovered, horses diverged into at least 18 distinct genetic lines. Those findings suggest that, unlike cows and other animals, horses may have been tamed independently in many different places around Europe and Asia.

The new research could help scientists decode the genetic secrets of modern horse breeds and top racehorses.

“Horse domestication had major cultural, socioeconomic, and even genetic implications for the numerous prehistoric and historic human populations that at different times adopted horse breeding,” said Alessandro Achilli, a geneticist at the University of Perugia in Italy. “Thus, our results will have a major impact in many areas of biological science, ranging from the field of animal and conservation genetics to zoology, veterinary science, paleontology, human genetics and anthropology.”

Cows, sheep, and goats had simple beginnings as livestock, with evidence suggesting that a small number of animals of each species were domesticated in just a few places between about 8,000 and 10,000 years ago. Today, genetic diversity among these creatures remains low.

Horse DNA tells a different story, according to a new paper published today in the Proceedings of the National Academy of Sciences. After analyzing mitochondrial DNA from a wide range of horse breeds across Asia, Europe, the Middle East and the Americas, and then using the known mutation rate of this kind of DNA as a sort of clock, Achilli and colleagues were able to connect all modern horses to a common ancestor that lived between 130,000 and 160,000 years ago. By comparison, modern humans first evolved about 200,000 years ago.

Previous research focused only on limited regions of mitochondrial DNA in horses. But by looking at the entire mitochondrial genome, the new study was able to categorize horses into at least 18 different groups that evolved independently.

One possible explanation for those findings is that many different groups of people independently discovered the dramatic benefits of taming wild horses thousands of years ago.

“The very fact that many wild mares have been independently domesticated in different places testifies to how significant horses have been to humankind,” Achilli said. “It means that the ability of taming these animals was badly needed by different groups of people in different regions of Eurasia, from the Asian steppes to Western Europe, since they could generate the food surplus necessary to support the growth of human populations and the capability to expand and adapt into new environments or facilitate transportation.”

Results also showed that horses managed to survive in modern-day Spain and Portugal during a glacial period more than 13,000 years ago, when horses, humans and other mammals disappeared north of the Pyrenees. The area has shown to be an important refuge during that time for people, who later went on to repopulate Europe when conditions improved. The new study suggests that horses may have followed a similar pattern.

The new findings offer another potential explanation for the origins of domesticated horses, said Alan Outram, an archaeologist at the University of Exeter in the United Kingdom. Horses may have been originally domesticated in one area, he said, such as the central Asian steppe. Then, people could have transported tamed stallions to other cultures in other places, where they were bred with local, wild mares. That scenario would also create multiple distinct female genetic lines.

Read more at Discovery News

Astronomers Solve Mystery of Vanishing Electrons in Earth's Outer Radiation Belt

UCLA researchers have explained the puzzling disappearing act of energetic electrons in Earth's outer radiation belt, using data collected from a fleet of orbiting spacecraft.

In a paper published Jan. 29 in the advance online edition of the journal Nature Physics, the team shows that the missing electrons are swept away from the planet by a tide of solar wind particles during periods of heightened solar activity.

"This is an important milestone in understanding Earth's space environment," said lead study author Drew Turner, an assistant researcher in the UCLA Department of Earth and Space Sciences and a member of UCLA's Institute for Geophysics and Planetary Physics (IGPP). "We are one step closer towards understanding and predicting space weather phenomena."

During powerful solar events such as coronal mass ejections, parts of the magnetized outer layers of sun's atmosphere crash onto Earth's magnetic field, triggering geomagnetic storms capable of damaging the electronics of orbiting spacecraft. These cosmic squalls have a peculiar effect on Earth's outer radiation belt, a doughnut-shaped region of space filled with electrons so energetic that they move at nearly the speed of light.

"During the onset of a geomagnetic storm, nearly all the electrons trapped within the radiation belt vanish, only to come back with a vengeance a few hours later," said Vassilis Angelopoulos, a UCLA professor of Earth and space sciences and IGPP researcher.

The missing electrons surprised scientists when the trend was first measured in the 1960s by instruments onboard the earliest spacecraft sent into orbit, said study co-author Yuri Shprits, a research geophysicist with the IGPP and the departments of Earth and space sciences, and atmospheric and oceanic sciences.

"It's a puzzling effect," he said. "Oceans on Earth do not suddenly lose most of their water, yet radiation belts filled with electrons can be rapidly depopulated."

Even stranger, the electrons go missing during the peak of a geomagnetic storm, a time when one might expect the radiation belt to be filled with energetic particles because of the extreme bombardment by the solar wind.

Where do the electrons go? This question has remained unresolved since the early 1960s. Some believed the electrons were lost to Earth's atmosphere, while others hypothesized that the electrons were not permanently lost at all but merely temporarily drained of energy so that they appeared absent.

"Our study in 2006 suggested that electrons may be, in fact, lost to the interplanetary medium and decelerated by moving outwards," Shprits said. "However, until recently, there was no definitive proof for this theory."

To resolve the mystery, Turner and his team used data from three networks of orbiting spacecraft positioned at different distances from Earth to catch the escaping electrons in the act. The data show that while a small amount of the missing energetic electrons did fall into the atmosphere, the vast majority were pushed away from the planet, stripped away from the radiation belt by the onslaught of solar wind particles during the heightened solar activity that generated the magnetic storm itself.

A greater understanding of Earth's radiation belts is vital for protecting the satellites we rely on for global positioning, communications and weather monitoring, Turner said. Earth's outer radiation belt is a harsh radiation environment for spacecraft and astronauts; the high-energy electrons can penetrate a spacecraft's shielding and wreak havoc on its delicate electronics. Geomagnetic storms triggered when the oncoming particles smash into Earth's magnetosphere can cause partial or total spacecraft failure.

"While most satellites are designed with some level of radiation protection in mind, spacecraft engineers must rely on approximations and statistics because they lack the data needed to model and predict the behavior of high-energy electrons in the outer radiation belt," Turner said.

During the 2003 "Halloween Storm," more than 30 satellites reported malfunctions, and one was a total loss, said Angelopoulos, a co-author of the current research. As the solar maximum approaches in 2013, marking the sun's peak activity over a roughly 11-year cycle, geomagnetic storms may occur as often as several times per month.

"High-energy electrons can cut down the lifetime of a spacecraft significantly," Turner said. "Satellites that spend a prolonged period within the active radiation belt might stop functioning years early."

While a mechanized spacecraft might include multiple redundant circuits to reduce the risk of total failure during a solar event, human explorers in orbit do not have the same luxury. High-energy electrons can punch through astronauts' spacesuits and pose serious health risks, Turner said.

"As a society, we've become incredibly dependent on space-based technology," he said. "Understanding this population of energetic electrons and their extreme variations will help create more accurate models to predict the effect of geomagnetic storms on the radiation belts."

Read more at Science Daily

That Which Does Not Kill Yeast Makes It Stronger

Cells trying to keep pace with constantly changing environmental conditions need to strike a fine balance between maintaining their genomic integrity and allowing enough genetic flexibility to adapt to inhospitable conditions. In their latest study, researchers at the Stowers Institute for Medical Research were able to show that under stressful conditions yeast genomes become unstable, readily acquiring or losing whole chromosomes to enable rapid adaption.

The research, published in the January 29, 2012, advance online issue of Nature, demonstrates that stress itself can increase the pace of evolution by increasing the rate of chromosomal instability or aneuploidy. The observation of stress-induced chromosome instability casts the molecular mechanisms driving cellular evolution into a new perspective and may help explain how cancer cells elude the body's natural defense mechanisms or the toxic effects of chemotherapy drugs.

"Cells employ intricate control mechanisms to maintain genomic stability and prevent abnormal chromosome numbers," says the study's leader, Stowers investigator Rong Li, Ph.D. "We found that under stress cellular mechanisms ensuring chromosome transmission fidelity are relaxed to allow the emergence of progeny cells with diverse aneuploid chromosome numbers, producing a population with large genetic variation."

Known as adaptive genetic change, the concept of stress-induced genetic variation first emerged in bacteria and departs from a long-held basic tenet of evolutionary theory, which holds that genetic diversity -- evolution's raw material from which natural selection picks the best choice under any given circumstance -- arises independently of hostile environmental conditions.

"From an evolutionary standpoint it is a very interesting finding," says graduate student and first author Guangbo Chen. "It shows how stress itself can help cells adapt to stress by inducing chromosomal instability."

Aneuploidy is most often associated with cancer and developmental defects and has recently been shown to reduce cellular fitness. Yet, an abnormal number of chromosomes is not necessarily a bad thing. Many wild yeast strains and their commercial cousins used to make bread or brew beer have adapted to their living environs by rejiggering the number of chromosomes they carry. "Euploid cells are optimized to thrive under 'normal' conditions," says Li. "In stressful environments aneuploid cells can quickly gain the upper hand when it comes to finding creative solutions to roadblocks they encounter in their environment."

After Li and her team had shown in an earlier Nature study that aneuploidy can confer a growth advantage on cells when they are exposed to many different types of stress conditions, the Stowers researchers wondered whether stress itself could increase the chromosome segregation error rate.

To find out, Chen exposed yeast cells to different chemicals that induce various types of general stress and assessed the loss of an artificial chromosome. This initial screen revealed that many stress conditions, including oxidative stress, increased the rate of chromosome loss ten to 20-fold, a rate typically observed when cells are treated with benomyl, a microtubule inhibitor that directly affects chromosome segregation.

The real surprise was radicicol, a drug that induces proteotoxic stress by inhibiting a chaperone protein, recalls Chen. "Even at a concentration that barely slows down growth, radicicol induced extremely high levels of chromosome instability within a very short period of time," he says.

Continued growth of yeast cells in the presence of radicicol led to the emergence of drug-resistant colonies that had acquired an additional copy of chromosome XV. Yeast cells pretreated briefly with radicicol to induce genomic instability also adapted more efficiently to the presence of other drugs including fluconazole, tunicamycin, or benomyl, when compared to euploid cells.

Interestingly, certain chromosome combinations dominated in colonies that were resistant to a specific drug. Fluconazole-resistant colonies typically gained an extra copy of chromosome VIII, tunicamycin-resistant colonies tended to lose chromosome XVI, while a majority of benomyl-resistant colonies got rid of chromosome XII. "This suggested to us that specific karyotypes are associated with resistance to certain drugs," says Chen.

Digging deeper, Chen grew tunicamycin-resistant yeast cells, which had adapted to the presence of the antibiotic by losing one copy of chromosome XVI, under drug-free conditions. Before long, colonies of two distinct sizes emerged. He quickly discovered that the faster growing colonies had regained the missing chromosome. By returning to a normal chromosome XVI number, these newly arisen euploid cells had acquired a distinctive growth advantage over their aneuploid neighbors. But most importantly, the fast growing yeast cells were no longer resistant to tunicamycin and thus clearly linking tunicamycin resistance to the loss of chromosome XVI.

Read more at Science Daily