From time to time, living cells will accidently make an extra copy of a gene during the normal replication process. Throughout the history of life, evolution has molded some of these seemingly superfluous genes into a source of genetic novelty, adaptation and diversity. A new study shows one way that some duplicate genes could have long-ago escaped elimination from the genome, leading to the genetic innovation seen in modern life.
Researchers have shown that a process called DNA methylation can shield duplicate genes from being removed from the genome during natural selection. The redundant genes survive and are shaped by evolution over time, giving birth to new cellular functions.
“This is the first study to show explicitly how the processes of DNA methylation and duplicate gene evolution are related,” said Soojin Yi, an associate professor in the School of Biology and the Parker H. Petit Institute for Bioengineering and Bioscience at the Georgia Institute of Technology.
The study was sponsored by the National Science Foundation (NSF) and was scheduled to be published the week of April 7 in the Online Early Edition of the journal Proceedings of the National Academy of Sciences (PNAS).
At least half of the genes in the human genome are duplicates. Duplicate genes are not only redundant, but they can be bad for cells. Most duplicate genes accumulate mutations at high rates, which increases the chance that the extra gene copies will become inactive and lost over time due to natural selection.
The new study found that soon after some duplicate genes form, small hydrocarbons called methyl groups attach to a duplicate gene’s regulatory region and block the gene from turning on.
When a gene is methylated, it is shielded from natural selection, which allows the gene to hang around in the genome long enough for evolution to find a new use for it. Some young duplicate genes are silenced by methylation almost immediately after being formed, the study found.
“What we have done is the first step in the process to show that young gene duplicates seems to be heavily methylated,” Yi said.
The study showed that the average level of DNA methylation on the duplicate gene regulatory region is significantly negatively correlated with evolutionary time. So, younger duplicate genes have high levels of DNA methylation.
For about three-quarters of the duplicate gene pairs studied, the gene in a pair that was more methylated was always more methylated across all 10 human tissues studied, said Thomas Keller, a post-doctoral fellow at Georgia Tech and the study’s first author.
“For the tissues that we examined, there was remarkable consistency in methylation when we looked at duplicate gene pairs,” Keller said.
The computational study constructed a dataset of all human gene duplicates by comparing each sequence against every other sequence in the human genome. DNA methylation data was then obtained for the 10 different human tissues. The researchers used computer models to analyze the links between DNA methylation and gene duplication.
The human brain is one example of a tissue for which gene duplication has been particularly important for its evolution. In future studies, the researchers will examine the link between epigenetic evolution and human brain evolution.
This research is supported by the National Science Foundation (NSF) under award numbers BCS-1317195 and MCB-0950896. Any conclusions or opinions are those of the authors and do not necessarily represent the official views of the sponsoring agency.
CITATION: Thomas E. Keller, et al., “DNA Methylation and Evolution of Duplicate Genes.” (PNAS, April 2014). http://www.dx.doi.org/10.1073/pnas.1321420111
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Writer: Brett Israel
Populations of predators and their prey usually follow predictable cycles. When the number of prey increases, perhaps as their food supply becomes more abundant, predator populations also grow.
When the predator population becomes too large, however, the prey population often plummets, leaving too little food for the predators, whose population also then crashes. This canonical view of predator-prey relationships was first identified by mathematical biologists Alfred Lotka and Vito Volterra in the 1920s and 1930s.
But all bets are off if both the predator and prey species are evolving in even small ways, according to a new study published this week in the journal Proceedings of the National Academy of Sciences. When both species are evolving, the traditional cycle may reverse, allowing predator populations to peak before those of the prey. In fact, it may appear as if the prey are eating the predators.
Researchers at the Georgia Institute of Technology have proposed a theory to explain these co-evolutionary changes. And then, using data collected by other scientists on three predator-prey pairs – mink-muskrat, gyrfalcon-rock ptarmigan and phage-Vibrio cholerae – they show how their theory could explain unexpected population cycles.
The new theory and analysis of these co-evolution cycles could help epidemiologists predict cycles of disease and the virulence of infectious agents, and lead to a better understanding of how population cycles may affect ecosystems. The research was supported by the National Science Foundation and the Burroughs Wellcome Fund.
“Our work shows that co-evolution can yield new and unique behavior at the population scale,” explained Joshua Weitz, an associate professor in the School of Biology at Georgia Tech. “When you include evolution, the classic prey-predator dynamics have a much greater range of possible outcomes. We are not replacing the original theory, but proposing a more general model that opens the door to these new phenomena.”
Evolution is often perceived as an historical event, noted Weitz, who also has a courtesy appointment in the Georgia Tech School of Physics. But organisms are evolving continuously, with certain phenotypes becoming dominant as environmental and other conditions favor them. In organisms such as birds or small mammals, those changes can be manifested in as few as ten generations. In microbial species with brief lifespans, evolutionary changes can happen within days or weeks.
Evolutionary changes can dramatically affect relationships between species, potentially making them more vulnerable or less vulnerable. For instance, if a mutation that confers viral resistance in a species of bacteria becomes dominant, that may change the predator-prey relationship by rendering the bacteria population safe from harm. More generally, co-evolutionary cycles can arise when predator offense is costly and prey defense is effective against low offense predators.
“With predator and prey co-evolution, you can see oscillations in which there are lots of prey around even when there are many predators, or lots of predators around even when there are very few prey,” noted Michael Cortez, a postdoctoral fellow in the Weitz lab and first author of the paper.
“When prey is abundant and there are few predators, it may be because there are many defended prey – prey that the predators can’t eat,” he added. “When there are lots of predators around and few prey, it’s because the prey are very good food sources and the predators are doing quite well.”
In their paper, Weitz and Cortez simulated models in which the evolutionary process was sped up to show how their theory of co-evolution would affect predator-prey population cycles. Speeding up the process allowed them to break the cycle up into smaller segments that could be analyzed in more detail. They then used the earlier observations of the changing abundances of the three pairs of predators and prey -- leveraging data sets collected by other scientists – to show how the models would apply.
“Although the structure of the cycles in these three systems had been noted as unusual by the authors who observed them, there had been, as yet, no unified theoretical framework from which to make sense of such as radical departure from the classic signature of predator-prey interactions,” Weitz said.
Scientists have long studied how the interaction between species affects overall populations in ecosystems. Weitz and Cortez believe their new model will give scientists a broader and more complete picture of the complex process.
“This study identifies how adaptation between two species and interactions between their numbers can result in something different from what you would get if you just had the interaction between the numbers,” said Cortez. “This is something that will show up across many ecological systems. We can now explain broad trends that occur in vastly different systems using a theoretical approach, and the fact that we can identify the mechanism responsible for it is unique to our study.”
This research was supported by the National Science Foundation under Award DMS-1204401, and by the Burroughs Wellcome Fund. Any conclusions or opinions expressed are those of the authors and do not necessarily represent the official views of the sponsoring agencies.
CITATION: Michael H. Cortez and Joshua S. Weitz, “Coevolution Can Reverse Predator-Prey Cycles,” (Proceedings of the National Academy of Sciences, 2014). www.pnas.org/cgi/doi/10.1073/pnas.1317693111
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Writer: John Toon
A study of 338 patients with coronary artery disease has identified a gene expression profile associated with an elevated risk of cardiovascular death. Used with other indicators such as biochemical markers and family history, the profile – based on a simple blood test – may help identify patients who could benefit from personalized treatment and counseling designed to address risk factors.
Researchers found the risk signature by comparing gene expression profiles in 31 study subjects who died of cardiovascular causes against the profiles of living members of the study group. Twenty-five of the 31 deaths occurred in the group with the high-risk profile, though coronary deaths were also recorded among the lower risk members of the study group. All of the patients studied had coronary artery disease (CAD), and about one in five had suffered a heart attack prior to the study.
Researchers from the Georgia Institute of Technology, Emory University and Princeton University participated in the study, which obtained gene expression profiles from blood samples taken from patients undergoing cardiac catheterization at Emory University clinics in Atlanta. The results were published in the open-access journal Genome Medicine on May 29, 2014.
“We envision that with our gene expression-based marker, plus some biochemical markers, genotype information and family history, we could produce a tiered evaluation of people’s risks of adverse coronary events,” said Gregory Gibson, director of the Center for Integrative Genomics at Georgia Tech and one of the study’s senior authors. “This could lead to a personalized medicine approach for people recovering from heart attack or coronary artery bypass grafting.”
Coronary artery disease is the leading cause of death for both men and women in the United States. Manifested in the narrowing of blood vessels through the buildup of plaque, CAD sets the stage for heart attacks and long-term heart failure.
As many as half of Americans over the age of 50 suffer from CAD to some extent, so the researchers wondered if they could single out those with the highest risk of death. From a cohort of more than 3,000 persons known as the Emory Cardiovascular Biobank (EmCD), they selected two groups of patients for extensive gene expression analysis based on blood samples.
After following the patients for as long as five years, the researchers examined gene expression patterns in a total of 31 persons from the study group who had suffered coronary deaths. Comparing these patterns against those of other study subjects revealed a pattern in which genes affecting inflammation were up-regulated, while genes affecting T-lymphocytes were down-regulated.
The patients studied ranged in age from 51 to 73, were mostly Caucasian, and 65 percent male. Seventy percent of the subjects had significant CAD, and 18 percent were experiencing an acute myocardial infarction when blood samples were taken. Gene expression was analyzed using microarrays and two different normalization procedures to control for technical and biological covariates. Whole genome genotyping was used to support comparative genome-wide association studies of gene expression. Two phases of the study were conducted independently with the two different groups, and produced similar results.
“What’s new in this research is the recognition that this risk pathway exists and that it relates to particular aspects of immune system functions that include T-cell signaling,” said Gibson, who is also a professor in Georgia Tech’s School of Biology. “We went beyond the signature of coronary artery disease to really provide a signature for adverse outcomes in that high-risk population.”
The pattern, said Gibson, doesn’t indicate the causes of the disease. The researchers would now like to expand the study to include a larger group of patients and learn more about what causes the disease. They’d also like to know whether the risks can be reversed through diet, exercise or drug therapy.
Cardiologist Arshed Quyyumi, the paper’s other senior author, directs Emory University’s Clinical Cardiovascular Research Center and created the Biobank five years ago to facilitate cardiovascular research. He says that identifying patients at highest risk could help encourage their compliance with treatment programs, and prioritize introduction of newer therapeutics, such as cholesterol lowering medications like PCSK9 inhibitors.
“A number of patients with CAD are currently not maximally treated,” said Quyyumi, who is a professor in Emory’s School of Medicine. “In those that appear to have been prescribed adequate medication, a significant proportion of subjects are non-compliant with their medications. Thus, knowledge of a high risk genetic profile in a patient can prompt both the patient and physician to maximize currently available medications and improve patient compliance.”
Approximately 15,000 genes are expressed in human blood, but analyzing them is not as daunting as it sounds. Most of the gene expression is correlated, so there may be only a few dozen independent measurements that can be related to disease states, Gibson said. In the study, researchers identified nine “axes” that represented specific biological pathways to disease. Two of them were relevant to the high-risk profile.
Gibson believes identifying the high-risk signatures in CAD patients may lead to opportunities for improving their health.
“Our dream would be a hand-held device that would allow patients to take a droplet of blood, much like diabetics do today, and obtain an evaluation of these transcripts that they could track at home,” he said. “If we can use this information to help people adopt healthier behaviors, it will be very positive.”
In addition to those already mentioned, the co-authors include Jinhee Kim, from the Georgia Tech School of Biology; Nima Ghasemzadeh and Danny Eapen from the Emory University School of Medicine, and John Storey and Neo Christopher Chung from the Lewis-Sigler Institute at Princeton University.
CITATION: Jinhee Kim, Nima Ghasemzadeh, Danny J. Eapen, Neo Christopher Chung, John D. Storey, Arshed A. Quyyumi and Greg Gibson, “Gene expression profiles associated with acute myocardial infarction and risk of cardiovascular death.” (Genome Medicine 2014). http://genomemedicine.com/content/6/5/40.
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Writer: John Toon
New research reveals how the algae behind red tide thoroughly disables – but doesn’t kill – other species of algae. The study shows how chemical signaling between algae can trigger big changes in the marine ecosystem.
Marine algae fight other species of algae for nutrients and light, and, ultimately, survival. The algae that cause red tides, the algal blooms that color blue ocean waters red, carry an arsenal of molecules that disable some other algae. The incapacitated algae don’t necessarily die, but their growth grinds to a halt. This could explain part of why blooms can be maintained despite the presence of competitors.
In the new study, scientists used cutting-edge tools in an attempt to solve an old ecological mystery: Why do some algae boom and some algae bust? The research team used cultured strains of the algae that cause red tide, exposed competitor algae to its exuded chemicals, and then took a molecular inventory of the competitor algae’s growth and metabolism pathways. Red tide exposure significantly slowed the competitor algae’s growth and compromised its ability to maintain healthy cell membranes.
“Our study describes the physiological responses of competitors exposed to red tide compounds, and indicates why certain competitor species may be sensitive to these compounds while other species remain relatively resistant,” said Kelsey Poulson-Ellestad, a former graduate student at the Georgia Institute of Technology, now at Woods Hole Oceanographic Institution, and the study’s co-first author, along with Christina Jones, a Georgia Tech graduate student. “This can help us determine mechanisms that influence species composition in planktonic communities exposed to red tides, and suggests that these chemical cues could alter large-scale ecosystem phenomena, such as the funneling of material and energy through marine food webs.”
The study was sponsored by the National Science Foundation and was published June 2 in the Online Early Edition of the journal Proceedings of the National Academy of Sciences (PNAS). The work was a collaboration between Georgia Tech, the University of Washington, and the University of Birmingham in the United Kingdom.
The algae that form red tide in the Gulf of Mexico are dinoflagellates called Karenia brevis, or just Karenia by scientists. Karenia makes neurotoxins that are toxic to humans and fish. Karenia also makes small molecules that are toxic to other marine algae, which is what the new study analyzed.
“In this study we employed a global look at the metabolism of these competitors to take an unbiased approach to ask how are they being affected by these non-lethal, subtle chemicals that are released by Karenia,” said Julia Kubanek, Poulson-Ellestad’s graduate mentor and a professor in the School of Biology and the School of Chemistry and Biochemistry at Georgia Tech. “By studying both the proteins and metabolites, which interact to form metabolic pathways, we put together a picture of what’s happening inside the competitor algal cells when they’re extremely stressed.”
The research team used a combination of mass spectrometry and nuclear magnetic resonance spectroscopy to form a holistic picture of what’s happening inside the competitor algae. The study is the first time that metabolites and proteins were measured simultaneously to study ecological competition.
"A key aspect of this study was the use of high-resolution metabolomic tools based on mass spectrometry," said Facundo M. Fernández, a professor in the School of Chemistry and Biochemistry, whose lab ran the mass spectrometry analysis. "This allowed us to detect and identify metabolites affected by exposure to red tide microorganisms.”
Mass spectrometry was also used for analysis of proteins, an approach called proteomics, led by Brook Nunn at the University of Washington.
The research team discovered that red tide disrupts multiple physiological pathways in the competitor diatom Thalassiosira pseudonana. Red tide disrupted the energy metabolism and cellular protection mechanisms, inhibited their ability to regulate fluids and increased oxidative stress. T. pseudonana exposed to red tide toxins grew 85 percent slower than unexposed algae.
“This competitor that’s being affected by red tide is suffering a globally upset state,” Kubanek said. “It’s nothing like what it would be in a healthy, normal cell.”
The work shows that chemical cues in the plankton have the potential to alter large-scale ecosystem processes including primary production and nutrient cycling in the ocean.
The research team found that another competitor diatom, Asterionellopsis glacialis, which frequently co-occurs with Karenia red tides, was partially resistant to red tide, suggesting that co-occurring species may have evolved partial resistance to red tide via robust metabolic pathways.
Other work in Kubanek’s lab is examining red tide and its competition in the field to see how these interactions unfold in the wild.
“Karenia is a big mystery. It has these periodic blooms that happen most years now, but what’s shaping that cycle is unclear,” Kubanek said. “The role of competitive chemical cues in these interactions is also not well understood.”
This research is supported by the National Science Foundation under award number OCE-1060300. Any conclusions or opinions are those of the authors and do not necessarily represent the official views of the sponsoring agency.
CITATION: Kelsey L. Poulson-Ellestad, et al., “Metabolomics and proteomics reveal impacts of chemically mediated competition on marine plankton.” (June, PNAS) www.pnas.org/cgi/doi/10.1073/pnas.1402130111
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Writer: Brett Israel
To test whether the presence of RNA in DNA duplexes could alter the elasticity and structure of DNA, a group of researchers at Georgia Tech and Georgia State University, inspired by Francesca Storici, and including the labs of Elisa Riedo, Angelo Bongiorno and Markus Germann conducted a multidisciplinary study at the interface of physics, chemistry and molecular biology. The group employed atomic force microscopy (AFM)-based single molecule force-measurements of short rNMP(s)-containing oligonucleotides in combination with molecular dynamics (MD) simulations and nuclear magnetic resonance (NMR).
Ribonucleotides (rNMPs), the units of RNA, are the most abundant non-canonical nucleotides found in genomic DNA. rNMPs, either not removed from Okazaki fragments during DNA replication or incorporated and scattered throughout the genome, pose a perturbation to the structure and a threat to the integrity of DNA. The instability of DNA is mainly due to the extra 2’-hydroxyl (OH) group of rNMPs which gives rise to local structural effects that may disturb various molecular interactions in cells. As a result of these structural perturbations by rNMPs, the elastic properties of DNA may also be affected.
DNA has unique mechanical properties that are crucial in many natural biochemical processes and play an important role in DNA-based nanotechnology applications. Despite demonstrations of their abundance and importance, no data exist in literature regarding elastic measurements and sequence-dependent structural distortions of DNA with isolated single rNMP intrusions. With the goal to bring insights on how rNMPs change elastic properties of DNA and its structure, the Georgia Tech team with Hsiang-Chih Chiu and Kyung Duk Koh, a postdoctoral fellow at the time in the lab of Elisa Riedo in the School of Physics, and a PhD candidate in the lab of Francesca Storici from the School of Biology, respectively, together with the graduate student Annie Lesiak from Angelo Bongiorno lab in the School of Physics and School of Chemistry and Biochemistry, and in collaboration with Markus Germann and his graduate student Marina Evich from the Department of Chemistry at Georgia State University, conducted an innovative, experimental and theoretical study utilizing two short DNA molecules containing isolated rNMP intrusions. Storici said: <<We examined and identified how the elasticity and structure of DNA are altered by the rNMP intrusions in the studied DNA sequences>>. AFM-based single molecule force spectroscopy demonstrated that rNMP intrusions in short DNA duplexes can decrease – by 32% – or slightly increase the stretch modulus of DNA depending on specific sequence contexts next to the rNMPs. In addition, MD simulations and NMR experiments indicated that rNMP inclusions locally change the torsional distortion of the sugar-phosphate backbone in DNA only when the rNMPs are in specific locations in the DNA sequence. Riedo concluded: <<Our work opens up the route to use AFM single molecules measurements to understand how defects and the base sequence can affect the elasticity of short DNA molecules>>.
The demonstrated ability of rNMPs to locally change DNA mechanical properties and structure may find applications in structural DNA nanotechnology and help understanding how such intrusions impact DNA biological functions. Overall, these findings open a new route for understanding how rNMPs may influence DNA structure, chemistry, and biology.
The study is just published as an article in the journal Nanoscale (accepted, 2014):
Chiu HC*, Koh KD*, Evich M, Lesiak AL, Germann MW, Bongiorno A, Riedo E, Storici F (2014)
RNA intrusions change DNA elastic properties and structure. Nanoscale, DOI: 10.1039/C4NR01794C; *equal contribution.
This project was supported by the Office of Basic Energy Sciences of the US Department of Energy (DE-FG02-06ER46293), the National Science Foundation (NSF)(CMMI-1100290 and DMR-0820382), the Samsung Advanced Institute of Technology and the NSF grant CHE-0946869, the Integrative Biosystems Institute grant IBSI-4, the Georgia Research Alliance grant R9028 and the NSF grant MCB-1021763.
Sir Isaac Newton probably wasn’t thinking about how animals urinate when he was developing his laws of gravity. But they are connected – by the urethra, to be specific.
A new Georgia Institute of Technology study investigated how quickly 32 animals urinate. It turns out that it’s all about the same. Even though an elephant’s bladder is 3,600 times larger than a cat’s (18 liters vs. 5 milliliters), both animals relieve themselves in about 20 seconds. In fact, all animals that weigh more than 3 kilograms (6.6 pounds) urinate in that same time span.
“It’s possible because larger animals have longer urethras,” said David Hu, the Georgia Tech assistant professor who led the study. “The weight of the fluid in the urethra is pushing the fluid out. And because the urethra is long, flow rate is increased.”
For example, an elephant’s urethra is one meter in length. The pressure of fluid in it is the same at the bottom of a swimming pool three feet deep. An elephant urinates four meters per second, or the same volume per second as five showerheads.
“If its urethra were shorter, the elephant would urinate for a longer time and be more susceptible to predators,” Hu explained.
The findings conflict with studies that indicate urinary flow is controlled on bladder pressure generated by muscular contraction. The study has just been published in the Proceedings of the National Academy of Sciences (PNAS).
Hu (George Woodruff School of Mechanical Engineering and School of Biology) and graduate student Patricia Yang noticed that gravity allows larger animals to empty their bladders in jets or sheets of urine. Gravity’s effect on small animals is minimal.
“They urinate in small drops because of high viscous and capillary forces. It’s like peeing in space,” said Yang, who is pursuing her doctoral degree in the School of Mechanical Engineering. “Mice and rats go in less than two seconds. Bats are done in a fraction of a second.”
The research team went to a zoo to watch 16 animals relieve themselves, then watched 28 YouTube videos. They saw cows, horses, dogs and more.
The more they watched, the more they realized their findings could help engineers.
“It turns out that you don’t need external pressure to get rid of fluids quickly,” said Hu. “Nature has designed a way to use gravity instead of wasting the animal’s energy.”
Hu envisions systems for water tanks, backpacks and fire hoses that can be built for more efficiency. As an example, he and his students have created a demonstration that empties a teacup, quart and gallon of water in the same duration using varying lengths of connected tubes. In a second experiment, the team fills three cups with the same amount of water, then watches them empty at differing rates. The longer the tube, the faster it empties.
“Nature has shown us that no matter how big the fire truck, water can still come out in the same time as a tiny truck,” Hu added.
The trick is gravity. Newton would be proud.
It’s 3:15 p.m. and the sun is setting at Anvers Island. Just off the Antarctic Peninsula, surrounded by 300-foot cliffs of ice, Jeannette Yen pauses outside Palmer Station to watch. The sun spills over the ice cliffs. The frozen landscape melts in a golden glow.
This is one of nature’s great laboratories. Yen and her team of scientists are conducting experiments here that are possible nowhere else. Outfitted in red parkas, they are not here to drill into frozen lakes or fly over thinning ice sheets. They spend what little daylight they have searching for tiny organisms in the frigid waters.
The scientists climb aboard the R/V Lawrence M Gould, a massive research vessel operated by the National Science Foundation (NSF). They cruise past giant icebergs and through rafts of loose ice to Palmer Deep, a location where the water is 2,000 feet (600 meters) deep. From the huge stern A-frame of the ship, they lower plankton nets into the zero-degree Celsius water and haul live animals aboard. In Antarctica, zero degrees Celsius is a pleasant day, but the recent bout of 80-knot wind gusts tells them the austral winter is on its way.
“The weather has been good,” Yen said. “We’ve gone out and have been collecting plankton all around.”
Yen, a professor of biology at the Georgia Institute of Technology in Atlanta, is on her second polar plunge. She’s an ecologist with an engineer’s eye. Her team of biologists and engineers haul each day’s catch back to the lab at Palmer Station, which provides no escape from the cold. There, the scientists study plankton swimming motion with video cameras in a room kept at zero degrees Celsius, to mimic the animals’ natural environment.
Plankton are the base of the food chain, but their environment is changing. Around the southern continent, the water temperature is stable at around zero degrees Celsius because of the Antarctic Circumpolar Current. Carbon dioxide, a potent greenhouse gas, easily dissolves in the cold water, acidifying the ocean. The acidifying oceans might be triggering a destructive chain of events underwater that could harm the food web around the world.
That’s why Yen and her team have come here, in search of a tiny organism that could be a canary in the coal mine of climate change.
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A study published in Scienceby researchers from the U.S. Department of Energy’s Argonne National Laboratory and co-authored by Georgia Tech may dramatically shift our understanding of the complex dance of microbes and minerals that takes place in aquifers deep underground. This dance affects groundwater quality, the fate of contaminants in the ground and the emerging science of carbon sequestration.
Deep underground, microbes don’t have much access to oxygen. So they have evolved ways to breathe other elements, including solid minerals like iron and sulfur.
The part that interests scientists is that when the microbes breathe solid iron and sulfur, they transform them into highly reactive dissolved ions that are then much more likely to interact with other minerals and dissolved materials in the aquifer. This process can slowly but steadily make dramatic changes to the makeup of the rock, soil and water.
“That means that how these microbes breathe affects what happens to pollutants — whether they travel or stay put — as well as groundwater quality,” said Ted Flynn, a scientist from Argonne and the Computation Institute at the University of Chicago and the lead author of the study.
About a fifth of the world’s population relies on groundwater from aquifers for their drinking water supply, and many more depend on the crops watered by aquifers.
For decades, scientists thought that when iron was present in these types of deep aquifers, microbes who can breathe it would out-compete those who cannot. There’s an accepted hierarchy of what microbes prefer to breathe, according to how much energy each reaction can theoretically yield. (Oxygen is considered the best overall, but it is rarely found deep below the surface.)
According to these calculations, of the elements that do show up in these aquifers, breathing iron theoretically provides the most energy to microbes. And iron is frequently among the most abundant minerals in many aquifers, while solid sulfur is almost always absent.
But something didn’t add up right. A lot of the microorganisms had equipment to breathe both iron and sulfur. This requires two completely different enzymatic mechanisms, and it’s evolutionarily expensive for microbes to keep the genes necessary to carry out both processes. Why would they bother, if sulfur was so rarely involved?
The team decided to redo the energy calculations assuming an alkaline environment — “Older and deeper aquifers tend to be more alkaline than pH-neutral surface waters,” said Argonne coauthor Ken Kemner — and found that in alkaline environments, it gets harder and harder to get energy out of iron.
“Breathing sulfur, on the other hand, becomes even more favorable in alkaline conditions,” Flynn said.
The team reinforced this hypothesis in the lab with bacteria under simulated aquifer conditions. The bacteria, Shewanella oneidensis, can normally breathe both iron and sulfur. When the pH got as high as 9, however, it could breathe sulfur, but not iron.
There was still the question of where microorganisms like Shewanella could find sulfur in their native habitat, where it appeared to be scarce.
The answer came from another group of microorganisms that breathe a different, soluble form of sulfur called sulfate, which is commonly found in groundwater alongside iron minerals. These microbes exhale sulfide, which reacts with iron minerals to form solid sulfur and reactive iron. The team believes this sulfur is used up almost immediately by Shewanella and its relatives.
“This explains why we don’t see much sulfur at any fixed point in time, but the amount of energy cycling through it could be huge,” Kemner said.
Indeed, when the team put iron-breathing bacteria in a highly alkaline lab environment without any sulfur, the bacteria did not produce any reduced iron.
“This hypothesis runs counter to the prevailing theory, in which microorganisms compete, survival-of-the-fittest style, and one type of organism comes out dominant,” Flynn said. Rather, the iron-breathing and the sulfate-breathing microbes depend on each other to survive.
Understanding this complex interplay is particularly important for sequestering carbon. The idea is that in order to keep harmful carbon dioxide out of the atmosphere, we would compress and inject it into deep underground aquifers. In theory, the carbon would react with iron and other compounds, locking it into solid minerals that wouldn’t seep to the surface.
Iron is one of the major players in this scenario, and it must be in its reactive state for carbon to interact with it to form a solid mineral. Microorganisms are essential in making all that reactive iron. Therefore, understanding that sulfur—and the microbe junkies who depend on it—plays a role in this process is a significant chunk of the puzzle that has been missing until now.
The study, “Sulfur-Mediated Electron Shuttling During Bacterial Iron Reduction,” appeared online in the May 1 edition of Science Express and was published in Science earlier this summer. Other authors on the study were Argonne scientists Bhoopesh Mishra (also of the Illinois Institute of Technology) and Edward O’Loughlin and Georgia Tech scientist Thomas DiChristina.
“The exciting findings reported in our study were made possible by combining the microbiology expertise of my laboratory in the School of Biology at Georgia Tech with the geochemical expertise of the Molecular Environmental Sciences group led by Ken Kemner at Argonne National Laboratory,” said Professor DiChristina, “The biogeochemical link between bacterial iron- and sulfur-breathing bacteria is important for survival of microbial communities in modern subsurface environments, and also provides clues to the evolution of ancient metabolic processes on an early Earth that lacked oxygen but contained large amounts of iron and sulfur.”
Funding for the research was provided by the U.S. Department of Energy’s Office of Science. The Advanced Photon Source (APS) is also supported by the DOE’s Office of Science. The team conducted X-ray analysis at the APS GeoSoilEnviroCARS beamline 13-ID-E, which is operated by the University of Chicago and jointly supported by the National Science Foundation and the DOE’s Office of Science. Additional support came from the National Institutes of Health and the National Science Foundation.
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Congratulations to Dr. Greg Gibson for being awarded a T32 training grant from the National Institute of General Medical Science. Titled, "Computational Biology and Predictive Health”, the grant will bridge Biology, Biomedical Engineering, Industrial Systems Engineering and Computer Science through the support of 4 graduate students each year over the five funding period. The Executive Committee for the grant includes Greg Gibson, Melissa Kemp, King Jordan and Nicoleta Serban.
New study, published in Hepatology, shows the regenerative capacity of liver cells
Patients suffering from chronic liver disease often develop liver fibrosis (the accumulation of scar tissue), which frequently results in cirrhosis, which means a loss of liver function, which often comes with a choice between a liver transplant and certain death.
It’s a perfect storm of terrible things as sustained fibrosis dampens the regenerative capacity of hepatocytes, thwarting their ability to make a therapeutic response, resulting in a grim prognosis and high mortality. At its essence, this is a communication problem, based on a study by a team of researchers in the lab of Chong Hyun Shin at the Georgia Institute of Technology.
Their findings explain how signaling pathways and cell-cell communications direct the cellular response to fibrogenic stimuli. But they also identify some novel potential therapeutic strategies for chronic liver disease. Results of the study (funded by the National Institutes of Health, the Emory/Georgia Tech Regenerative Engineering and Medicine Center, and Georgia Tech’s School of Biology) were published recently in the journal Hepatology.
“We aim to understand the molecular and cellular mechanisms that mediate the effects of sustained fibrosis on hepatocyte regeneration, using the zebrafish as a model,” explains Shin, assistant professor in the School of Biology, with a lab in the Parker H. Petit Institute for Bioengineering and Bioscience. Her fellow authors are Frank Anania (Emory), Mianbo Huang, Angela Chang, Minna Choi and David Zhou.
In their fibrotic zebrafish model, they studied the effects that different levels of signaling have on the regeneration of liver cells (hepatocytes). Specifically, they took note of the relationship between ‘Wnt’ and ‘Notch’ (signaling pathways). They discovered that lower level Notch signaling promotes cell regeneration (the proliferation and differentiation of hepatic progenitor cells, or HPCs, into hepatocytes), while high levels suppressed it. And they discovered that antagonistic interaction between Wnt and Notch modulates regenerative capacity: Wnt signals can suppress Notch signals, or, in other words, when Wnt is up, Notch is down, and hepatocyte regeneration can happen.
The data, says Shin, “suggest an essential interplay between Wnt and Notch signaling during hepatocyte regeneration in the fibrotic liver, providing legitimate therapeutic strategies for chronic liver failure in vivo.”
Inducing tissue regeneration via stem or progenitor cells, while delaying fibrosis, has been on the rise as antifibrogenic strategies of great potential, according to Shin, whose studies offer a clue of how to guide the differentiation of HPCs into hepatocytes in patients suffering from chronic liver failure. “Overall,” she explains, “employing the in vivo-based hepatic regeneration strategy may allow us to complement fundamental drawbacks in stem cell therapy, opening up new avenues of endogenous cellular regeneration therapy.”
This research is supported by grant number K01DK081351 from the National Institutes of Health (NIH), the Regenerative Engineering and Medicine Research Center Pilot Award (GTEC 2731336), and the School of Biology, Georgia Institute of Technology.
Read Hepatology journal abstract here