college of science

Coral reefs fall victim to overfishing, pollution aggravated by ocean warming

CORVALLIS, Ore. – Coral reefs are declining  around the world because a combination of factors – overfishing, nutrient pollution, and pathogenic disease – ultimately become deadly in the face of higher ocean temperatures, researchers have concluded.

A study published today in Nature Communications, based on one of the largest and longest field experiments done on this topic, suggests that the widespread coral deaths observed in recent decades are being caused by this combination of multiple local stressors and global warming.

These forces greatly weaken corals, and allow opportunistic pathogens to build to such levels that corals cannot survive.

The findings were made by researchers from six institutions following a three-year experiment that simulated both overfishing and nutrient pollution on a coral reef in the Florida Keys. The large body of field data collected over an extended period of time helped resolve some of the fundamental questions about the cause of coral reef declines, scientists said.

“This is grim news, but at least it will help settle the argument over why corals are dying,” said Rebecca Vega Thurber, an assistant professor in the College of Science at Oregon State University and corresponding author on the study.

“This makes it clear there’s no single force that’s causing such widespread coral deaths. Loss of fish that help remove algae, or the addition of excess nutrients like those in fertilizers, can cause algal growth on reefs. This changes the normal microbiota of corals to become more pathogenic, and all of these problems reach critical levels as ocean temperatures warm.”

The end result, scientists say, is a global decline of coral reefs that is now reaching catastrophic proportions.

“We need to know how human activities are affecting coral reef ecosystems,” says David Garrison, program director in the National Science Foundation’s Division of Ocean Sciences, which funded the research.  “Coral reefs are among the most sensitive indicators of the health of the oceans. This report is a major contribution toward understanding how reefs will fare in the future.”

Scientists say the problems caused by bacterial infections due to local stressors and warm temperatures are in addition to damage from mass coral bleaching events already under way. Only in the early 1980’s did researchers observe the first mass bleaching event in recorded history. There have now been three such events just in the past 20 years.

“About 25-35 percent of the corals on the Great Barrier Reef are dying right now,” Vega-Thurber said. “In 2014-16 large portions of tropical reef across the planet experienced bleaching, and this past April, 90 percent of the Great Barrier Reef bleached as part of a massive El Nino event. Corals everywhere seem to be dying.”

In addition to helping to sort out the effects of known stressors like overfishing and nutrient pollution, the researchers made one bizarre and totally unexpected finding.

In normal conditions, parrotfish, like many other species, are essential to the health of coral reefs, nibbling at them to remove algae and causing no permanent damage. But in one part of the experiment corals were so weakened by nitrogen and phosphorus pollution that when parrot fish would bite them, 62 percent of the corals would die. A normally healthy fish-coral interaction had been turned into a deadly one.

“Normally benign predation by the parrotfish turned into coral murder,” said Deron Burkepile, also a corresponding author on the study at the University of California – Santa Barbara. “But it’s not the parrotfishes, they’re like the reef janitors, keeping it clean. Those extra nutrients — nutrient pollution — turn parrotfishes into an actual source of mortality by facilitating pathogens in the wounds left by their bites. Excess nutrients turn a coral accomplice into a coral killer.”

The researchers said they want to make it clear that parrotfish are not the problem, they are an essential part of healthy reef ecosystems.

“The problem is when corals are so weakened they cannot withstand normal impacts,” Vega-Thurber said. “And the solution will be to help those corals recover their health, by ensuring that their local environment is free of nutrient pollution and that fish stocks are not depleted.”

Among the findings of the study:

  • Overfishing, nutrient pollution and increased temperature all lead to an increase in pathogens;
  • The sheer abundance of pathogens is more important than what particular type or species they are;
  • Coral reef mortality mirrors the abundance of pathogens;
  • Heat exacerbates these problems, with 80 percent of coral deaths coming in the summer or fall, but only when fish are removed or nutrient pollution is present;
  • While high thermal stress has received the most attention, even modest temperature increases make corals more vulnerable to bacteria;
  • Loss of fish can increase algal cover up to six times;
  • In a distressed system with many algae, coral disease levels double and coral mortality increases eight times;
  • Increased algal cover or elevated temperature can reduce levels of naturally-secreted antibiotics that help protect corals from harmful bacteria;
  • Direct algal contact driven by overfishing and nutrient pollution destabilizes the coral microbiome, in some cases leading to a 6- to 9-time increase in mortality.

The findings, researchers say, make it clear that in the face of global warming, some of the best opportunities to protect coral reefs lie in careful management of fishing and protection of water quality. This would give corals their best chance to have a healthy microbiome and resist warmer conditions without dying.

Collaborators on this research were from Florida International University, the University of California/Santa Barbara, Penn State University, Rice University, the University of Florida/Gainsville, SymbioSeas and Marine Applied Research Center, and the Laboratoire d’Excellence.


Editor Notes: Video and audio are available to illustrate this story.


Interview with Rebecca Vega-Thurber:  http://bit.ly/1TSUe1N

Link to audio-only version of same interview: http://bit.ly/24ubTg0

YouTube view-only link of same video: https://youtu.be/dq8jtyuYp_U

Story By: 

Rebecca Vega-Thurber, 541-737-1851


Multimedia Downloads

Coral surveys

Divers in field study

Sampling coral microbiome

Testing coral microbiome

Experimental design

Study design

Parrot fish on coral reefs
Parrot fish cleaning coral

Common antimicrobial agent rapidly disrupts gut bacteria

CORVALLIS, Ore. – A new study suggests that triclosan, an antimicrobial and antifungal agent found in many consumer products ranging from hand soaps to toys and even toothpaste, can rapidly disrupt bacterial communities found in the gut.

The research was published today in PLOS ONE by scientists from Oregon State University. It was based on findings made with zebrafish, which researchers believe are an important animal model to help determine possible human biological and health impacts of this antimicrobial compound.

Triclosan was first used as a hospital scrub in the 1970s and now is one of the most common antimicrobial agents in the world, found in shampoos, deodorants, toothpastes, mouth washes, kitchen utensils, cutting boards, toys, bedding, socks and trash bags. It continues to be used in medical settings, and can be easily absorbed through the skin.

“There has been a legacy of concern about exposure to microbial pathogens, which has led to increased use of these antimicrobial products,” said Thomas Sharpton, an assistant professor of microbiology and statistics in the OSU Colleges of Science and Agricultural Sciences, and corresponding author on the new study.

“However, there’s now a growing awareness of the importance of the bacteria in our gut microbiome for human health, and the overuse of antibiotics that can lead to the rise of ‘superbugs.’ There are consequences to constantly trying to kill the bacteria in the world around us, aspects we’re just beginning to understand.”

In the new study, researchers found that triclosan exposure caused rapid changes in both the diversity and composition of the microbiome in the laboratory animals. It’s not clear what the implication may be for animal or human health, but scientists believe that compromising of the bacteria in the intestinal tract may contribute to the development or severity of disease.

Some bacteria were more susceptible to the impact of triclosan than others, such as the family Enterobacteriaceae; and others were more resilient, such as the genus Pseudomonas.

“Clearly there may be situations where antibacterial agents are needed,” said Christopher Gaulke, lead author on the study and a postdoctoral microbiology researcher in the OSU College of Science.

“However, scientists now have evidence that intestinal bacteria may have metabolic, cardiovascular, autoimmune and neurological impacts, and concerns about overuse of these agents are valid. Cumulative impacts are also possible. We need to do significantly more evaluation of their effects, some of which might be dramatic and long lasting.”

The gut-associated microbiome performs vital functions for human health, prevents colonization with pathogens, stimulates the development of the immune system, and produces micronutrients needed by the host. Dysfunction of this microbiome has been associated with human disease, including diabetes, heart disease, arthritis and malnutrition, the scientists pointed out in their study.

Humans are routinely exposed to an array of chemicals, metals, preservatives, microbes and nutrients, some of which may be beneficial, some innocuous, and others harmful, the researchers said. Part of the strength of the present study is developing improved ways, through rapid screening of zebrafish, to more easily determine which compounds may be acceptable and which are toxic, scientists say.

Triclosan has been a concern in part because it is so widely used, and it’s also readily absorbed through the skin and gastrointestinal tracts, showing up in urine, feces and breast milk. It also has been associated with endocrine disruption in fish and rats, may act as a liver tumor promoter, and can alter inflammatory responses.

This study showed it was quickly associated with shifts in the microbial community structure and can alter the abundance of specific taxa.

Collaborators on this research included scientists from the OSU Environmental Health Sciences Center and OSU College of Agricultural Sciences.

Story By: 

Thomas Sharpton, 541-737-8623


Sea star juveniles abundant, but recovery is anything but guaranteed

CORVALLIS, Ore. – An unprecedented number of juvenile sea stars have been observed off the Oregon coast over the past several months – just two years after one of the most severe marine ecosystem epidemics in recorded history nearly wiped the population out.

The appearance of the juveniles does not mean the threat of “sea star wasting disease” is over, researchers caution. A second round of the disease could be disastrous to the purple ochre (Pisaster ochraceus) and other sea stars, some of which are considered “keystone” species in marine habitats because of their influence on the ecosystem.

A team of Oregon State University scientists who have been monitoring the sea stars for years reported on their status this week in the journal PLOS ONE.

“When we looked at the settlement of the larval sea stars on rocks in 2014 during the epidemic, it was the same or maybe even a bit lower than previous years,” said Bruce Menge, the Wayne and Gladys Valley Professor of Marine Biology at Oregon State University and lead author on the study. “But a few months later, the number of juveniles was off the charts – higher than we’d ever seen – as much as 300 times normal.”

“It wasn’t a case of high settlement, or more sea stars being born. They just had an extraordinary survival rate into the juvenile stage. Whether they can make it into adulthood and replenish the population without succumbing to sea star wasting disease is the big question.”

Menge and his colleagues believe the reason for the high survival rate is the availability of more food. The young sea stars feed on larval and juvenile mussels and barnacles, competing with adult sea stars for the same food source. The scarcity of adults provided a temporary smorgasbord for the juveniles.

Sea star wasting disease first appeared in Oregon in the summer of 2014. In rocky intertidal habitats, disease rapidly depleted populations of the dominant sea star, Pisaster ochraceus. The sea stars first developed twisted arms, then showed deflation and lesions, and eventually lost arms and the ability to grip onto the substrate before finally disintegrating completely.

Over a period of about 15 months, the disease reduced the overall sea star population by 63 to 84 percent at different site along the Oregon coast, and reduced the Pisaster ochraceus population by 80 to 99 percent. The epidemic ranged from Alaska to Baja California.

Scientists from Cornell University attributed the epidemic to a Sea Star-associated Densovirus and researchers in Washington say warmer water may have provided the trigger for the disease in that state.

But Menge’s research group found no association between water temperature and the disease outbreak in Oregon.

“The sea temperatures were warmer when the outbreak first began,” he said, “but Oregon wasn’t affected as early as other parts of the West Coast, and the outbreak reached its peak here when the sea temperature plummeted and was actually cooler than normal.”

The Cornell researchers found evidence of densovirus in the sea stars, the water column and in sediments. It occurs naturally and can become virulent, possibly as a result of stress.

“Something triggered that virulence and it happened on a coast-wide basis,” said Menge, a distinguished professor in the Department of Integrative Biology in OSU’s College of Science. “We don’t think it was a result of warming because conditions were different in Oregon than they were, for example, in Washington and likely other parts of the West Coast. Ocean acidification is one possibility and we’re looking at that now. Ultimately, the cause seems likely to be multi-faceted.”

Menge and his research team have been studying these intertidal rocky zones at different sites for as long as 32 years and analyzing the community structure. Historical research has shown that the ochre star is a “keystone” species because of its influence in these ecosystems, suggesting that the absence of so many adults could have a significant impact.

Ochre sea stars prey on barnacles and mussels and keep their populations under control. When left unchecked, mussel populations can explode, covering up algae and small invertebrates.

“The longer-term ecological consequences of this (disease) event could include wholesale elimination of many low zone species and a complete change in the zonation patterns of rocky intertidal communities along the West Coast of North America,” the authors wrote in their study.

Among the other findings the OSU researchers reported in PLOS One:

  • Sea stars that were continuously submerged, such as those in tidepools, had a higher rate of the disease than sea stars on rocks outside of tidepools where periodically they were above water;
  • During the last two years, the number of gooseneck barnacles has exploded along the coast – likely because they are not being preyed upon as heavily by adult sea stars;
  • Adult sea stars are much more likely to be affected by sea star wasting disease than juveniles, which may be because of longer exposure or some other factor.

The OSU research has been funded by the David and Lucile Packard Foundation, the National Science Foundation, the Kingfisher Foundation, and the Wayne and Gladys Valley Foundation.

Other authors on the study, all from OSU, include Elizabeth Cerny-Chipman, Angela Johnson, Jenna Sullivan, Sarah Gravem and Francis Chan.

Story By: 

Bruce Menge, 541-737-5358, mengeb@oregonstate.edu

Multimedia Downloads




This photograph of a disintegrating adult purple sea star, Pisaster ochraceus, is available at: https://flic.kr/p/nzd81S

West Coast scientists sound alarm for changing ocean chemistry

CORVALLIS, Ore. – The ocean chemistry along the West Coast of North America is changing rapidly because of global carbon dioxide emissions, and the governments of Oregon, California, Washington and British Columbia can take actions now to offset and mitigate the effects of these changes.

That is the conclusion of a 20-member panel of leading West Coast ocean scientists, who presented a comprehensive report on Monday outlining a series of recommendations to address the increase in ocean acidification and hypoxia, or extremely low oxygen levels.

“Ocean acidification is a global problem that is having a disproportionate impact on productive West Coast ecosystems,” said Francis Chan, an Oregon State University marine ecologist and co-chair of the West Coast Ocean Acidification and Hypoxia Science Panel. “There has been an attitude that there is not much we can do about this locally, but that just isn’t true. A lot of the solutions will come locally and through coordinated regional efforts.”

Ocean acidification and hypoxia are distinct phenomena that trigger a wide range of effects on marine ecosystems. They frequently occur together and represent two important facets of global ocean changes that have important implications for Oregon’s coastal oceans.

Among the panel’s recommendations:

  • Develop new benchmarks for near-shore water quality as existing criteria were not developed to protect marine organisms from acidification;
  • Improve methods of removing carbon dioxide from seawater through the use of kelp beds, eel grass and other plants;
  • Enhance coastal ecosystems’ ability to adapt to changing ocean chemistry through better resource management, including marine reserves, adaptive breeding techniques for shellfish, and other methods.

“Communities around the country are increasingly vulnerable to ocean acidification and long-term environmental changes," said Richard Spinrad, chief scientist for the National Oceanic and Atmospheric Administration, and former OSU vice president for research. “It is crucial that we comprehend how ocean chemistry is changing in different places, so we applaud the steps the West Coast Ocean Acidification and Hypoxia Science Panel has put forward in understanding and addressing this issue. We continue to look to the West Coast as a leader on understanding ocean acidification.”

Chan said regional awareness of the impact of changing ocean chemistry started in Oregon. Some of the first impacts were seen about 15 years ago when the state began experiencing seasonal hypoxia, or low-oxygen water, leading to some marine organism die-offs. Then the oyster industry was confronted with high mortality rates of juvenile oysters because of increasingly acidified water. It turns out that Oregon was on the leading edge of a much larger problem.

“It was a wakeup call for the region, which since has spread up and down the coast,” said Chan, an associate professor in the Department of Integrative Biology in OSU’s College of Science.

California responded to this call, and in partnership with Oregon, Washington and British Columbia, convened a panel of scientific experts to provide advice on the issue. The panel worked with federal and state agencies, local organizations and higher education institutions to identify concerns about ocean acidification and hypoxia, then developed a series of recommendations and actions that can be taken today.

“One of the things all of the scientists agree on is the need for better ocean monitoring or ‘listening posts,’ up and down the West Coast,” said Jack Barth, a professor and associate dean in OSU’s College of Earth, Ocean, and Atmospheric Sciences and a member of the panel. “It is a unifying issue that will require participation from state and federal agencies, as well as universities, ports, local governments and NGOs.”

Barth said one such “listening post” has been the Whiskey Creek Shellfish Hatchery in Netarts Bay, Oregon, which was able to solve the die-off of juvenile oysters with the help of OSU scientists George Waldbusser and Burke Hales, who both served on the 20-member panel. Together, they determined that the ocean chemistry changed throughout the day and by taking in seawater in the afternoon, when photosynthesis peaked and CO2 levels were lower, juvenile oysters could survive.

The West Coast is a hotspot for acidification because of coastal upwelling, which brings nutrient-rich, low-oxygen and high carbon dioxide water from deep in the water column to the surface near the coast. These nutrients fertilize the water column, trigger phytoplankton blooms that die and sink to the bottom, producing even more carbon dioxide and lowering oxygen further.

“We’re just starting to see the impacts now, and we need to accelerate what we know about how increasingly acidified water will impact our ecosystems,” said panel member Waldo Wakefield, a research fisheries biologist with NOAA Fisheries in Newport and courtesy associate professor in OSU’s College of Earth, Ocean, and Atmospheric Sciences.

“There’s a lot at stake. West Coast fisheries are economic drivers of many coastal communities, and the seafood we enjoy depends on a food web that is likely to be affected by more corrosive water.”

Last year, OSU researchers completed the deployment of moorings, buoys and gliders as part of the Endurance Array – a component of the $386 million National Science Foundation-funded Ocean Observatories Initiative, created to address ocean issues including acidification.

These and other ocean-monitoring efforts will be important to inform policy-makers about where to best focus their adaptation and mitigation strategies.

“The panel’s findings provide a road map to help us prepare for the changes ahead,” said Gabriela Goldfarb, natural resource policy adviser to Oregon Gov. Kate Brown. “How Oregon and the West Coast address ocean acidification will inform those confronting this issue around the country and world.”

“With the best scientific recommendations in hand from the science panel, we now have the information on which to base our future management decisions,” added Caren Braby, marine resource manager at the Oregon Department of Fish and Wildlife. “These are practical recommendations natural resource managers and communities can use to ensure we continue to have the rich and productive ecosystem Oregonians depend on for healthy fisheries, our coastal culture and economy.”

Story By: 

Francis Chan, 541-844-8415, chanft@science.oregonstate.edu;

Jack Barth, 541-737-1607, barth@coas.oregonstate.edu

Multimedia Downloads


An oyster at Whiskey Creek Shellfish Hatchery

An ancient killer: ancestral malarial organisms traced to age of dinosaurs

CORVALLIS, Ore. – A new analysis of the prehistoric origin of malaria suggests that it evolved in insects at least 100 million years ago, and the first vertebrate hosts of this disease were probably reptiles, which at that time would have included the dinosaurs.

Malaria, a scourge on human society that still kills more than 400,000 people a year, is often thought to be of more modern origin - ranging from 15,000 to 8 million years old, caused primarily by one genus of protozoa, Plasmodium, and spread by anopheline mosquitoes.

But the ancestral forms of this disease used different insect vectors and different malarial strains, and may literally have helped shape animal survival and evolution on Earth, according to George Poinar, Jr., a researcher in the College of Science at Oregon State University.

Poinar suggested in the journal American Entomologist that the origins of this deadly disease, which today can infect animals ranging from humans and other mammals to birds and reptiles, may have begun in an insect such as the biting midge more than 100 million years ago. And in previous work, Poinar and his wife, Roberta, implicated malaria and the evolution of blood-sucking insects as disease vectors that could have played a significant role in the extinction of the dinosaurs.

“Scientists have argued and disagreed for a long time about how malaria evolved and how old it is,” Poinar said. “I think the fossil evidence shows that modern malaria vectored by mosquitoes is at least 20 million years old, and earlier forms of the disease, carried by biting midges, are at least 100 million years old and probably much older.”

Since the sexual reproduction stage of malaria only occurs in insects, Poinar said in the new study that they must be considered the primary hosts of the disease, not the vertebrate animals that they infect with disease-causing protozoa. And he believes the evidence points toward the Gregarinida as a protozoan parasite group that could have been the progenitors of malaria, since they readily infect the insects that vector malaria today.

Understanding the ancient history of malaria evolution, Poinar said, might offer clues to how its modern-day life cycle works, how it evolved, and what might make possible targets to interrupt its transmission through its most common vector, the Anopheles mosquito.

Understanding the evolution of malaria also takes one on a worldwide journey, according to evidence found in insects preserved in amber. Poinar is an international expert in using plant and animal life forms preserved in this semi-precious stone to help learn more about the biology and ecology of the distant past.

Poinar was the first to discover a type of malaria in a 15-20 million-year-old fossil from the New World, in what is now the Dominican Republic. It was the first fossil record of Plasmodium malaria, one type of which is now the strain that infects and kills humans.

Even further back, malaria may have been one of the diseases that arose, along with the evolution of insects, and had a huge impact on animal evolution. In a 2007 book, “What Bugged the Dinosaurs? Insects, Disease and Death in the Cretaceous,” George and Roberta Poinar argued that insects carried diseases that contributed to the widespread extinction of the dinosaurs around the “K-T boundary” about 65 million years ago.

“There were catastrophic events known to have happened around that time, such as asteroid impacts and lava flows,” Poinar said. “But it’s still clear that dinosaurs declined and slowly became extinct over thousands of years, which suggests other issues must also have been at work. Insects, microbial pathogens and vertebrate diseases were just emerging around that same time, including malaria.”

Avian malaria has been implicated in the extinction of many bird species in Hawaii just in recent decades, especially in species with no natural resistance to the disease. Different forms of malaria, which is now known to be an ancient disease, may have been at work many millions of years ago and probably had other implications affecting the outcome of vertebrate survival, Poinar said.

The first human recording of malaria was in China in 2,700 B.C., and some researchers say it may have helped lead to the fall of the Roman Empire. In 2015 there were 214 million cases worldwide, according to the World Health Organization. Immunity does not occur naturally and the search for a vaccine has not yet been achieved.

Story By: 
Multimedia Downloads

Biting midge

Biting midge
with ancestral malaria

Oldest fossil showing Plasmodium malaria
Oldest fossil with
Plasmodium malaria

DNA evidence shows that salmon hatcheries cause substantial, rapid genetic changes

CORVALLIS, Ore. – A new study on steelhead trout in Oregon offers genetic evidence that wild and hatchery fish are different at the DNA level, and that they can become different with surprising speed.

The research, published today in Nature Communications, found that after one generation of hatchery culture, the offspring of wild fish and first-generation hatchery fish differed in the activity of more than 700 genes.

A single generation of adaptation to the hatchery resulted in observable changes at the DNA level that were passed on to offspring, scientists reported.

This research was conducted at Oregon State University in collaboration with the Oregon Department of Fisheries and Wildlife. Scientists say the findings essentially close the case on whether or not wild and hatchery fish can be genetically different.

Differences in survival and reproductive success between hatchery and wild fish have long offered evidence of rapid adaptation to the hatchery environment. This new DNA evidence directly measured the activity of all genes in the offspring of hatchery and wild fish. It conclusively demonstrates that the genetic differences between hatchery and wild fish are large in scale and fully heritable.

“A fish hatchery is a very artificial environment that causes strong natural selection pressures,” said Michael Blouin, a professor of integrative biology in the OSU College of Science. “A concrete box with 50,000 other fish all crowded together and fed pellet food is clearly a lot different than an open stream.”

It’s not clear exactly what traits are being selected for, but the study was able to identify some genetic changes that may explain how the fish are responding to the novel environment in the hatchery.

“We observed that a large number of genes were involved in pathways related to wound healing, immunity, and metabolism, and this is consistent with the idea that the earliest stages of domestication may involve adapting to highly crowded conditions,” said Mark Christie, lead author of the study.

Aside from crowding, which is common in the hatchery, injuries also happen more often and disease can be more prevalent.

The genetic changes are substantial and rapid, the study found. It’s literally a process of evolution at work, but in this case it does not take multiple generations or long periods of time.

“We expected hatcheries to have a genetic impact,” Blouin said. “However, the large amount of change we observed at the DNA level was really amazing. This was a surprising result.”

With the question put to rest of whether hatchery fish are different, Blouin said, it may now be possible to determine exactly how they are different, and work to address that problem. When the genetic changes that occur in a hatchery environment are better understood, it could be possible to change the way fish are raised in order to produce hatchery fish that are more like wild fish. This research is a first step in that direction.

This work was performed using steelhead trout from the Hood River in Oregon. It was supported by the Bonneville Power Administration and the Oregon Department of Fish and Wildlife.

Story By: 

Michael Blouin, 541-737-2362

Multimedia Downloads


Steelhead trout

Juvenile steelhead trout
Juvenile steelhead

Ancient flowering plant was beautiful - but probably poisonous

CORVALLIS, Ore. – Researchers today announced in the journal Nature Plants the discovery of the first-ever fossil specimens of an “asterid” – a group of flowering plants that gave us everything from the potato to tomatoes, tobacco, petunias and our morning cup of coffee.

But these two 20-30 million-year-old fossil flowers, found perfectly preserved in a piece of amber, came from the dark side of the asterid group – they belong to the genus Strychnos, which ultimately gave rise to some of the world’s most famous poisons, including strychnine and curare.

Poisons that would later find their way into blow-gun weapons, rat control, Sherlock Holmes stories and the movie “Psycho” appear to have had some of their ancestral and biological roots in the prehistoric jungles of what’s now the Dominican Republic, researchers say.

“The specimens are beautiful, perfectly preserved fossil flowers, which at one point in time were borne by plants that lived in a steamy tropical forest with both large and small trees, climbing vines, palms, grasses and other vegetation,” said George Poinar, Jr., a courtesy professor in the College of Science at Oregon State University, and one of the world’s experts on plant and animal life forms preserved in amber.

“Specimens such as this are what give us insights into the ecology of ecosystems in the distant past,” Poinar said.  “It shows that the asterids, which later gave humans all types of foods and other products, were already evolving many millions of years ago.”

Asterids, the researchers noted in this study, are among Earth’s most important and diverse plants, with 10 orders, 98 families, and about 80,000 species. They represent about one-third of all the Earth’s diversity of angiosperms, or flowering plants.

And one ancient genus, which has now been shown to be inherently toxic, existed for millions of years before humans appeared on the planet.

“Species of the genus Strychnos are almost all toxic in some way,” Poinar said. “Each plant has its own alkaloids with varying effects. Some are more toxic than others, and it may be that they were successful because their poisons offered some defense against herbivores.

“Today some of these toxins have been shown to possess useful and even medicinal properties.”

As natural poisons that humans came to understand and use, two extracts from plants in the Strychnos genus ultimately became famous – strychnine and curare.

Strychnine had practical uses for decades as a pesticide, and was often the deadly component of rat poison. But it also captured the imagination of writers, and was used by Norman Bates in the movie “Psycho” to kill his mother and her male companion. In small doses, it can increase mental and muscular activity.

Curare has an even stranger history. Sir Walter Raleigh may have first encountered it in 1596 when he observed poison arrows in South America, where natives also developed the poison in blow-gun darts to paralyze hunted prey. Curare was featured as the murder weapon in one Sherlock Holmes novel, and in lower doses it has been used as a muscle relaxant in surgery.

There are now about 200 species of Strychnos plants around the world, in forms ranging from shrubs to trees and woody climbing vines, mostly in the tropics. They are still being studied for medicinal properties, such as for the treatment of parasitic worm infections and even as drugs to treat malaria.

The discovery of these two fossil flowers, researchers said, suggests that many other related plant families could have evolved in the Late Cretaceous in tropical forests. Their fossil remains, however, still await discovery.

The co-author of this study, Lena Struwe, is an expert on plants in the strychnine family, Loganiaceae, and is a plant biologist at Rutgers University.

Multimedia Downloads

Ancient asterid

Asterid fossil

Asterid flower
Top of flower

Herpes outbreak, other marine viruses linked to coral bleaching event

CORVALLIS, Ore. – A study at Oregon State University has concluded that significant outbreaks of viruses may be associated with coral bleaching events, especially as a result of multiple environmental stresses.

One such event was documented even as it happened in a three-day period. It showed how an explosion of three viral groups, including a herpes-like virus, occurred just as corals were bleaching in one part of the Great Barrier Reef off the east coast of Australia.

The findings, reported in Frontiers in Microbiology, take on special significance as the world is now experiencing just the third incidence ever recorded of coral bleaching on a global scale, according to the National Oceanic and Atmospheric Administration, or NOAA.

Coral bleaching can occur when corals are exposed to stressful environmental conditions, such as warmer water, overfishing or pollution. This can cause them to expel symbiotic algae that live in their tissues and lose their color. The coral loses its major source of food and is more susceptible to disease. In severe or prolonged cases the bleaching can be lethal to the corals.

“People all over the world are concerned about long-term coral survival,” said Rebecca Vega-Thurber, an assistant professor of microbiology in the OSU College of Science and corresponding author on the study. “This research suggests that viral infection could be an important part of the problem that until now has been undocumented, and has received very little attention.”

In a natural experiment, an area of corals on the Great Barrier Reef was exposed to high levels of ultraviolet light at low tides during a period of heavy rain and high temperatures, all of which are sources of stress for the corals. At that time, viral loads in those corals exploded to levels 2-4 times higher than ever recorded in corals, and there was a significant bleaching event over just three days.

The viruses included retroviruses and megaviruses, and a type of herpes virus was particularly abundant. Herpes viruses are ancient and are found in a wide range of mammals, marine invertebrates, oysters, corals and other animals.

The findings, Vega-Thurber said, suggest that a range of stresses may have made the corals susceptible to viral attack, particularly high water temperatures such as those that can be caused by an El Nino event and global warming.

“This is bad news,” Vega-Thurber said. “This bleaching event occurred in a very short period on a pristine reef. It may recover, but incidents like this are now happening more widely all around the world.”

Last year, NOAA declared that the world was now experiencing its third global coral bleaching event, the last two being in 1998 and again in 2010. The current event began in the northern Pacific Ocean in 2014, moved south during 2015, and may continue into this year, NOAA officials said.

NOAA estimated that by the end of last year, almost 95 percent of U.S. coral reefs were exposed to ocean conditions that can cause corals to bleach.  If corals die, there will be less shoreline protection from storms, and fewer habitats for fish and other marine life.

Viruses are abundant, normal and diverse residents of stony coral colonies, the researchers noted in their study. Viruses may become a serious threat only when their numbers reach extremely high levels, which in this case was associated with other stressful environmental conditions, scientists said.

This work was supported by the National Science Foundation.

Story By: 

Rebecca Vega-Thurber, 541-737-1851

Multimedia Downloads

Bleached coral
Coral bleaching

New therapy halts progression of Lou Gehrig’s disease in mice

CORVALLIS, Ore. – Researchers at Oregon State University announced today that they have essentially stopped the progression of amyotrophic lateral sclerosis (ALS), or Lou Gehrig’s disease, for nearly two years in one type of mouse model used to study the disease – allowing the mice to approach their normal lifespan.

The findings, scientists indicate, are some of the most compelling ever produced in the search for a therapy for ALS, a debilitating and fatal disease, and were just published in Neurobiology of Disease.

“We are shocked at how well this treatment can stop the progression of ALS,” said Joseph Beckman, lead author on this study, a distinguished professor of biochemistry and biophysics in the College of Science at Oregon State University, and principal investigator and holder of the Burgess and Elizabeth Jamieson Chair in OSU’s Linus Pauling Institute.

In decades of work, no treatment has been discovered for ALS that can do anything but prolong human survival less than a month. The mouse model used in this study is one that scientists believe may more closely resemble the human reaction to this treatment, which consists of a compound called copper-ATSM.

It’s not yet known if humans will have the same response, but researchers are moving as quickly as possible toward human clinical trials, testing first for safety and then efficacy of the new approach.

ALS was identified as a progressive and fatal neurodegenerative disease in the late 1800s, and gained international recognition in 1939 when it was diagnosed in American baseball legend Lou Gehrig. It’s known to be caused by the death and deterioration of motor neurons in the spinal cord, which in turn has been linked to mutations in copper, zinc superoxide dismutase.

Copper-ATSM is a known compound that helps deliver copper specifically to cells with damaged mitochondria, and reaches the spinal cord where it’s needed to treat ALS. This compound has low toxicity, easily penetrates the blood-brain barrier, is already used in human medicine at much lower doses for some purposes, and is well tolerated in laboratory animals at far higher levels. Any copper not needed after use of copper-ATSM is quickly flushed out of the body.

Experts caution, however, that this approach is not as simple as taking a nutritional supplement of copper, which can be toxic at even moderate doses. Such supplements would be of no value to people with ALS, they said.

The new findings were reported by scientists from OSU; the University of Melbourne in Australia; University of Texas Southwestern; University of Central Florida; and the Pasteur Institute of Montevideo in Uruguay. The study is available as open access in Neurobiology of Disease.

Using the new treatment, researchers were able to stop the progression of ALS in one type of transgenic mouse model, which ordinarily would die within two weeks without treatment. Some of these mice have survived for more than 650 days, 500 days longer than any previous research has been able to achieve.

In some experiments, the treatment was begun, and then withheld. In this circumstance the mice began to show ALS symptoms within two months after treatment was stopped, and would die within another month. But if treatment was resumed, the mice gained weight, progression of the disease once again was stopped, and the mice lived another 6-12 months.

In 2012, Beckman was recognized as the leading medical researcher in Oregon, with the Discovery Award from the Medical Research Foundation of Oregon. He is also director of OSU’s Environmental Health Sciences Center, funded by the National Institutes of Health to support research on the role of the environment in causing disease.

“We have a solid understanding of why the treatment works in the mice, and we predict it should work in both familial and possibly sporadic human patients,” Beckman said. “But we won’t know until we try.”

Familial ALS patients are those with more of a family history of the disease, while sporadic patients reflect the larger general population.

“We want people to understand that we are moving to human trials as quickly as we can,” Beckman said. “In humans who develop ALS, the average time from onset to death is only three to four years.”

The advances are based on substantial scientific progress in understanding the disease processes of ALS and basic research in biochemistry. The transgenic mice used in these studies have been engineered to carry the human gene for “copper chaperone for superoxide dismutase,” or CCS gene. CCS inserts copper into superoxide dismustase, or SOD, and transgenic mice carrying these human genes die rapidly without treatment.

After years of research, scientists have developed an approach to treating ALS that’s based on bringing copper into specific cells in the spinal cord and mitochondria weakened by copper deficiency. Copper is a metal that helps to stabilize SOD, an antioxidant protein whose proper function is essential to life. But when it lacks its metal co-factors, SOD can “unfold” and become toxic, leading to the death of motor neurons.

There’s some evidence that this approach, which works in part by improving mitochondrial function, may also have value in Parkinson’s disease and other conditions, researchers said. Research is progressing on those topics as well. 

The treatment is unlikely to allow significant recovery from neuronal loss already caused by ALS, the scientists said, but could slow further disease progression when started after diagnosis. It could also potentially treat carriers of SOD mutant genes that cause ALS.

This work has been supported by the Department of Defense Congressionally Directed Medical Research Program, the U.S. National Institutes of Health, the Amyotrophic Lateral Sclerosis Association, the Australian National Health and Medical Research Association, and gifts by Michael Camillo and Burgess and Elizabeth Jamieson to the Linus Pauling Institute.

Story By: 

Joseph Beckman, 541-737-8867

Multimedia Downloads

Copper, zinc superoxide dismutase
Copper, zinc superoxide dismutase

Research identifies key genetic link in the biology of aging

CORVALLIS, Ore. – New research at Oregon State University suggests it may be possible to slow age-related disease with new types of treatments.

Scientists have tracked the syndromes associated with aging to their biochemical roots, and identified a breakdown in genetic communication as part of the problem. The findings imply that aging happens for a reason, and that while aspects of it may be inevitable, there could be ways to slow down disease development.

The newest study relate to a protein, Nrf2, that helps regulate gene expression and the body’s reaction to various types of stressors. The research was published in Free Radical Biology and Medicine, in work supported by the National Institutes of Health and the Medical Research Foundation of Oregon.

“We’re very excited about the potential of this area of research,” said Tory Hagen, corresponding author on this study, and the Helen P. Rumbel Professor for Health Aging Research in the Linus Pauling Institute and the OSU Department of Biochemistry and Biophysics in the College of Science.

“At least one important part of what we call aging appears to be a breakdown in genetic communication, in which a regulator of stress resistance declines with age,” Hagen said. “As people age and their metabolic problems increase, the levels of this regulator, Nrf2, should be increasing, but in fact they are declining.”

Nrf2 is both a monitor and a messenger, OSU researchers say. It’s constantly on the lookout for problems with cells that may be caused by the many metabolic insults of life – oxidative stress, toxins, pollutants, and other metabolic dysfunction.

When it finds a problem, Nrf2 essentially goes back to the cellular nucleus and rings the alarm bell, where it can “turn on” up to 200 genes that are responsible for cell repair, detoxification of carcinogens, protein and lipid metabolism, antioxidant protection and other actions. In their report, the scientists called it a “longevity-assurance” factor.

Nrf2 is so important that it’s found in many life forms, not just humans, and it’s constantly manufactured by cells throughout the body. About half of it is used up every 20 minutes as it performs its life-protective functions. Metabolic insults routinely increase with age, and if things were working properly, the amount of Nrf2 that goes back into the nucleus should also increase to help deal with those insults.

Instead, the level of nuclear Nrf2 declines, and the OSU scientists say they have discovered why.

“The levels of Nrf2, and the functions associated with it, are routinely about 30-40 percent lower in older laboratory animals,” said Kate Shay, director of the Healthy Aging Core Laboratory at OSU and co-author on this study. “We’ve been able to show for the first time what we believe is the cause.”

The reason for this decline, the scientists said, is increasing levels of a micro-RNA called miRNA-146a.

Micro-RNAs have been one of the most profound scientific discoveries of the past 20 years. They were once thought to be “junk DNA” because researchers could see them but they had no apparent biological role. They are now understood to be anything but junk – they help play a major role in genetic signaling, controlling what genes are “expressed,” or turned on and off to perform their function.

In humans, miRNA-146a plays a significant role. It can turn on the inflammation processes that, in something like a wound, help prevent infection and begin the healing process. But with aging, this study now shows that miRNA-146a expression doesn’t shut down properly, and it can significantly reduce the levels of Nrf2.

This can cause part of the chronic, low-grade inflammation that is associated with the degenerative diseases that now kill most people in the developed world, including heart disease, cancer, diabetes and neurological disease.

“The action of miRNA-146a in older people appears to turn from a good to a bad influence,” Shay said. “It may be causing our detoxification processes to decline just when we need them the most.”

Some of the things found to be healthy for individuals, in diet or lifestyle, may be so because they help to conserve the proper balance between the actions of miRNA-146a and Nrf2, the OSU researchers said. Alternatively, it may be possible to reduce excessive levels of miRNA-146a with compounds that interfere with its function. There may also be other micro-RNAs associated with this process, they said, that need further research.

“Overall, these results provide novel insights for the age-related decline in Nrf2 and identify new targets to maintain Nrf2-dependent detoxification with age,” the researchers wrote in their conclusion.

Story By: 

Tory Hagen, 541-737-5083