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New research into the cell-damaging effects of Huntington’s disease suggests a new approach for identifying possible therapeutic targets for treating the nerve-destroying disorder.

Huntington’s disease causes the progressive breakdown of nerve cells in the brain and affects an individual’s movement, cognition and mental state. Genetically, the disease is associated with a mutation in the Huntingtin gene that causes the huntingtin protein to be produced with an extended region containing the amino acid glutamine.

The mechanisms that control the severity and onset of the disease are poorly understood, as individuals with the same amount of expansion in their huntingtin proteins experience differences in toxicity and onset of the disease.  

A new study led by Georgia Institute of Technology researchers suggests that the toxic effects of the huntingtin protein on cells may not be driven exclusively by the length of the protein’s expansion, but also by which other proteins are present in the cell.

The researchers placed human huntingtin protein with an expanded region, called a polyglutamine tract, into yeast cells and found toxicity differences that were based on the other protein aggregates -- called prions -- present in the cells.

“This study clarifies genetic and epigenetic mechanisms that modulate polyglutamine’s toxicity on cells and establishes a new approach for identifying potential therapeutic targets through characterization of pre-existing proteins in the cell,” said Yury Chernoff, a professor in the School of Biology at Georgia Tech. “While this study was conducted in yeast, it is possible that there are differences in aggregated proteins present in human cells as well, which are causing variation in huntingtin toxicity among individuals.”

The results of the study were published in the April 2012 issue of the journal PLoS Genetics. This work was supported by the National Institutes of Health and the Hereditary Disease Foundation.

Also contributing to this research were former Georgia Tech graduate student He Gong and postdoctoral fellow Nina Romanova, University of North Carolina at Chapel Hill School of Medicine research assistant professor Piotr Mieczkowski, and Boston University School of Medicine professor Michael Sherman.

Expanded huntingtin forms clumps in human cells that are typically transported and stored in an internal compartment called an aggresome until they can be removed from the body. While the compartment is thought to protect the contents of the cell from the toxic contents inside the aggresome, the current study shows that huntingtin molecules inside an aggresome can still be toxic to the cell.

In the study, aggresome formation in the cells containing the prion form of the Rnq1 protein reduced the toxicity of the huntingtin protein in Saccharomyces cerevisiae yeast cells, whereas the huntingtin protein’s toxicity remained in the presence of the prion form of translation release factor Sup35.

“It remains uncertain whether the toxicity was primarily driven by sequestration of Sup35 into the aggresome or by its sequestration into the smaller huntingtin protein aggregates that remained in the cytoplasm,” explained Chernoff, who is also director of the Center for Nanobiology of the Macromolecular Assembly Disorders (NanoMAD). “While Sup35 was detected in the aggresome, we don’t know if the functional fraction of Sup35 was sequestered there.”

In a follow-on experiment, the researchers increased the level of another release factor, Sup45, in the presence of Sup35 and found that this combination counteracted the toxicity.

“While the Rnq1 and Sup35 prions did not cause significant toxicity on their own, the results show that prion composition in the cell drove toxicity,” noted Chernoff. “Prions modulated which proteins were sequestered by the aggresome, as proteins associated with the pre-existing prions were more likely to be sequestered, such as Sup45 because of its association with Sup35.”

It remains unknown if polyglutamines can sequester the human versions of the Sup35 and Sup45 release factors, but this study shows the possibility that organisms may differ by the protein composition in their cells, and this in turn may influence their susceptibility to polyglutamine disorders such as Huntington’s disease.

Research reported in this publication was supported by the National Institute of General Medical Sciences of the National Institutes of Health (NIH) under award numbers GM058763, GM093294 and GM086890. The content is solely the responsibility of the principal investigators and does not necessarily represent the official views of the NIH.

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By Josh Fischman

The ecological effects of the 2010 Deepwater Horizon oil spill are still largely unknown. Senior writer Josh Fischman is on the research vessel Endeavor in the Gulf of Mexico with a team of university scientists seeking answers. He is filing reports from the ship.

One hundred and twenty miles south of the Mississippi Delta—The Endeavor is moving at 1 knot through a thin but wide slick of oil. The sheen glints in the water for a hundred yards or more around the ship. “It’s a little disturbing when you see fish swimming underneath it,” says Nigel D’Souza, a postdoctoral researcher at Lamont-Doherty Earth Observatory, part of Columbia University. “I was on deck earlier collecting some of the oil with a bucket, and some mahi-mahi swam by. It makes you wonder how much of this stuff is in the food chain, and in what form.”

When I pointed out that he was on the ship to help answer that question, he said, “Yes, well, this makes it seem more urgent.”

Urgency is never lacking on the Endeavor, where science is a mixture of precision and controlled frenzy. Ship time is staggeringly expensive, so the 17 scientists and technicians on board have crammed round-the-clock experiments and sample-collecting into fewer than 10 days at sea. On July 5 they are off the ship because other researchers are waiting to use it.

But the rush to get everything done doesn’t negate the need to get it right. Sampling bottles are sent 1,200 meters down to the bottom of the gulf, and temperature, oxygen levels, and the pigment chlorophyll (derived from phytoplankton) are measured every moment. The bottles are opened remotely at very specific depths. Back on the surface, in the ship’s main lab, recovered water is filtered for gases like methane and the chemicals that reveal the presence of microorganisms. A highly specialized instrument called a flow cytometer can count the number of single-celled creatures in a droplet of water. All of this, and more, is done over and over again, to compare different locations at different depths at different times of day.

“We have to push pretty hard,” says Chief Scientist Joseph Montoya, a biogeochemist from the Georgia Institute of Technology. Every day, Montoya figures out how many nets, drift traps, sampling bottles, and bottom-sediment cores can be taken from each site, and posts a plan that has scientists and crew members lowering equipment over the side and recovering it at all hours of the day and night. He and I share a cabin, and I’m sure he slept for five hours at a stretch—once. “If you snap a picture of Joe cat-napping,” says one of his students in the science contingent, “you win a prize.”

Everyone was awake as last Monday night ticked into Tuesday morning and the Endeavor arrived at the Deepwater Horizon site. The ruined wellhead that blew apart in April 2010 was some 1,600 meters below us. From the starboard side of the boat, as Captain John Wilder held the 185-foot ship steady in the currents and wind, scientists paid out a wire that held a cluster of sampling bottles called a CTD. Then Montoya and Patrick Quigley, the botswain, headed for the fantail, at the back of the ship, crowded with so much scientific equipment it was hard to walk. As Quigley attached shackles and lines and directed hydraulic hoists and heavy-powered winches, two sediment traps went over the side and down to the bottom, where they will collect samples for a year, anchored by big iron train wheels. An underwater camera went over next, followed by a “robotic” CTD that dives and samples free of the ship; we will collect it—if its radio beacon works—on our way back to port.

“Look at all this room!” called Quigley, standing in the middle of the now-empty fantail.

The Endeavor then turned southwest and farther into the Gulf, toward the site the scientists called GC 600, where oil and methane seep from the ocean bottom naturally—a good comparison with the unnatural Deepwater Horizon. The ship arrived at 10:30 Tuesday evening and the routine began again.

Well, it was the routine plus, which meant minus more sleep. Melitza Crespo-Medina, a microbiologist, postdoctoral researcher, and leader of what has been dubbed “the mud people” from the University of Georgia, had to find active gas or oil plumes on the sea floor, so Montoya and the other scientists would know where to focus their sampling. That meant a fine-grained sonar survey starting at 4 in the morning; the sound waves can reveal streams of bubbles from mud that’s more than 1,000 meters below the ship. That evening, Crespo-Medina sent a device to the bottom to bring back tubes of mud and sediment. These meter-long cores need to be extracted from the machine, cut into sections, and looked at for hydrocarbon content and signs of bacterial activity. Crespo-Medina was up for 24 hours straight, slept for three hours, then went at it again.

Thursday began with a problem. The sonar survey hadn’t homed in on a plume, and then Joy Battles, a graduate student who works with Crespo-Medina, announced that levels of methane in the water were on the low side. Seeps flow irregularly, and we seem to have caught this one napping. Bad news for a project aimed at measuring the effects of natural seeps. Montoya is worried that further experiments where we’ve been working are a waste of time.

And we’ve been working that area, around the edges of GC 600, because the middle—which had been bubbling nicely on previous visits—is now in a “no go” zone, a box on the map indicating we can’t sample there. Another scientist has a package of instruments at the bottom, and is afraid our coring might disturb it.

The solution is, of course, more work and less sleep. Getting permission to edge into the “no go” box, the scientists begin redoing surveys done yesterday. Crespo-Medina does another painstaking sonar pass over the bottom, and Battles combs new water samples for signs of gas. Another cost of doing this extra work is the team gives up a planned trip to a nearby site that could hold a new seep. But better the devil you know is the consensus aboard ship.

The gamble pays off. Just after midnight Thursday, as the ship was completing another 1,200-meter surface-to-bottom probe, Battles bursts into the main lab to announce methane levels at the new target shot way up. They were, in fact, about 15 times higher than the levels we were seeing yesterday. And oil slicks began drifting by. Montoya put down his laptop and clapped.

This was not a medical miracle, no cure for cancer, but it meant the central premise of the project, comparing the natural to the unnatural, would work. A delicately placed core even returned some oil-impregnated mud from the bottom, droplets that winked back at Crespo-Medina as she illuminated them with a flashlight.

“I found the methane,” she sang softly and repeatedly, as she worked on deck drawing water from the sample bottles her colleagues had sent into the deep.

IPST faculty member Jerry Pullman, Ph.D., a Georgia Tech Biology professor, has partnered with the Atlanta Botanical Garden to help save some of the South’s rarest plants. Jerry uses the knowledge and skills he has gained over decades of developing cloning technology for high-value pines and Douglas fir to help multiply and preserve Georgia’s rare and critically endangered species. In the process, he has created some life-changing experiences for his students.

Over one-fifth of the world’s plants are becoming rare and endangered due to loss of habitat, over-collection, diseases, competition from exotic and invasive species, and global warming. Jerry strives to help save these species for the future by preserving them in seed banks, at safekeeping sites like botanical gardens, and by multiplying the rarest plants using plant tissue culture techniques.

One of his projects involves an ancient evergreen tree—Torreya taxifolia—of which fewer than 1,000 are known to remain. Jerry and his staff have worked out methods of somatic  embryogenesis to keep natural multiplication processes going in culture, resulting in multiple plant copies. The multiplying embryos can often be stored for the long term at ultra-low temperatures in liquid nitrogen (cryogenic storage) and retrieved when needed.

Several years ago, during a construction project at the Atlanta Botanical Garden, Conservatory Director Ron Determann arranged to store some rare seeds at normal freezer temperatures in a federal government installation at Fort Collins, CO. When the seeds were retrieved about six years later, 98% of them were no longer viable. Jerry’s work with the Atlanta Botanical Garden and his students at Georgia Tech has developed improved, species-specific methods of propagation and long-term storage to address this problem.

In vitro germination and micropropagation experiments with the threatened Georgia aster (Symphyotrichum georgianum) produced methods to store and retrieve seeds after cryopreservation and 300 viable plants that were recently installed at the Chattahoochee River National Recreation Area. With ongoing interest in Georgia’s natural heritage, there is talk of the threatened aster replacing the Cherokee rose as the Georgia state flower.

This work captures the imagination of many undergraduate students. One student, who wanted to culture a seaweed, explored a Fijian Sea alga with cancer-fighting properties. Another student, who was interested in shark biology, was put to work cloning the carnivorous pitcher plant (Sarracenia oreophila) and returning the plants to the field. Some of the students come back after graduating to help complete the research. Several students have wound up as authors on publications. One student even continued her education in forest policy and is now employed by the US Fish and Wildlife Service.

Georgia Tech and members of the botanical community have created a stronger bond through these research projects saving plants. Those interested in supporting the work can contact Jerry at jerry.pullman@ipst.gatech.edu. References to some recent papers on the work are found at this link http://www.biology.gatech.edu/people/jerry-pullman.

“I am proud to work with undergraduate students teaching them how to conduct research while at the same time helping to save endangered plants,” says Jerry. “And this is my way of making the world a little better place.”

Dr. Brian Hammer (Assistant Professor, School of Biology), was recently honored with an award from the Faculty Career Development (CAREER) Program at the National Science Foundation.   The CAREER award supports junior faculty who exemplify the role of teacher-scholars through effective integration of outstanding research and excellent education.  Hammer was chosen for this highly competitive award from among the very best young scientists in the United States. The award provides $900,000 over five years to support his research project in molecular microbiology. 

The overall goal of Dr. Hammer's research project is to understand the contribution of extracellular chemical signaling in the exchange of genetic material that accelerates bacterial adaptation. The process of natural transformation is one mechanism that bacteria use for such horizontal gene transfer. The bacterium Vibrio cholerae, a common marine inhabitant and causative agent of the fatal cholera disease, induces the uptake of extracellular DNA in response to two signaling pathways, a chitin utilization system and a bacterial cell-cell communication (or "quorum sensing") system. The project will identify novel genes, proteins, and regulatory connections of the natural transformation network in Vibrio cholerae to dissect the role that both habitat and genetics play in the evolution of this bacterial pathogen.

A major component of Dr. Hammer’s CAREER project includes activities that promote integration of academic community members with the broader society in the process of modern scientific discovery. Dr. Hammer hosts seventh grade science teacher, Mr. David Taube, and an undergraduate student to work in his lab each summer.  During the academic year this team engages ethnically diverse urban K-12 students in stimulating hands-on scientific activities, which will be shared with local educators that teach under-represented minority students in the metro-Atlanta area.

As the medical community continues to make positive strides in personalized cancer therapy, scientists know some dead ends are unavoidable. Drugs that target specific genes in cancerous cells are effective, but not all proteins are targetable. In fact, it has been estimated that as few as 10 to 15 percent of human proteins are potentially targetable by drugs. For this reason, Georgia Tech researchers are focusing on ways to fight cancer by attacking defective genes before they are able to make proteins.

Professor John McDonald is studying micro RNAs (miRNAs), a class of small RNAs that interact with messenger RNAs (mRNAs) that have been linked to a number of diseases, including cancer. McDonald’s lab placed two different miRNAs (MiR-7 and MiR-128) into ovarian cancer cells and watched how they affected the gene system. The findings are published in the current edition of the journal BMC Medical Genomics.

“Each inserted miRNA created hundreds of thousands of gene expression changes, but only about 20 percent of them were caused by direct interactions with mRNAs,” said McDonald. “The majority of the changes were indirect – they occurred downstream and were consequences of the initial reactions.”

McDonald initially wondered if those secondary interactions could be a setback for the potential use of miRNAs, because most of them changed the gene expressions of something other than the intended targets. However, McDonald noticed that most of what changed downstream was functionally coordinated.  

miR-7 transfection most significantly affected the pathways involved with cell adhesion, epithelial-mesenchymal transitions (EMT) and other processes linked with cancer metastasis. The pathways most often affected by miR-128 transfection were different. They were more related to cell cycle control and processes involved with cellular replication – another process that is overactive in cancer cells.

“miRNAs have evolved for millions of years in order to coordinately regulate hundreds to thousands of genes together on the cellular level,” said McDonald. “If we can understand which miRNAs affect which suites of genes and their coordinated functions, it could allow clinicians to attack cancer cells on a systems level, rather than going after genes individually.”

Clinical trials for miRNAs are just beginning to be explored, but definitive findings are likely still years away because there are hundreds of miRNAs whose cellular functions must be fully understood. Another challenge facing scientists is developing ways to effectively target therapeutic miRNAs to cancer cells, something McDonald and his Georgia Tech peers are also investigating.

McDonald is a professor in the School of Biology in Georgia Tech’s College of Sciences.

Ninety-six percent of a chimpanzee’s genome is the same as a human’s. It’s the other 4 percent, and the vast differences, that pique the interest of Georgia Tech’s Soojin Yi. For instance, why do humans have a high risk of cancer, even though chimps rarely develop the disease?

In research published in September’s American Journal of Human Genetics, Yi looked at brain samples of each species. She found that differences in certain DNA modifications, called methylation, may contribute to phenotypic changes. The results also hint that DNA methylation plays an important role for some disease-related phenotypes in humans, including cancer and autism.

“Our study indicates that certain human diseases may have evolutionary epigenetic origins,” says Yi, a faculty member in the School of Biology. “Such findings, in the long term, may help to develop better therapeutic targets or means for some human diseases. “

DNA methylation modifies gene expression but doesn’t change a cell’s genetic information. To understand how it differs between the two species, Yi and her research team generated genome-wide methylation maps of the prefrontal cortex of multiple humans and chimps. They found hundreds of genes that exhibit significantly lower levels of methylation in the human brain than in the chimpanzee brain. Most of them were promoters involved with protein binding and cellular metabolic processes.

“This list of genes includes disproportionately high numbers of those related to diseases,” said Yi. “They are linked to autism, neural-tube defects and alcohol and other chemical dependencies. This suggests that methylation differences between the species might have significant functional consequences. They also might be linked to the evolution of our vulnerability to certain diseases, including cancer.” 

Yi, graduate student Jia Zeng and postdoctoral researcher Brendan Hunt worked with a team of researchers from Emory University and UCLA. The Yerkes National Primate Research Center provided the animal samples used in the study. It was also funded by the Georgia Tech Fund for Innovation in Research and Education (GT-FIRE) and National Science Foundation grants (MCB-0950896 and BCS-0751481). The content is solely the responsibility of the principal investigators and does not necessarily represent the official views of the NSF.

At the 2012 annual meeting of the International Society of Chemical Ecology in Vilnius, Lithuania, Professor Julia Kubanek delivered an invited lecture sponsored by the society. This award is made each year to a chemical ecologist whose recent work is at the forefront of the field, and is named after the late Milt Silverstein and John Simeone, pioneers of this field and co-founders of the Journal of Chemical Ecology.  Professor Kubanek presented "War in the Plankton: Sublethal and reciprocal impacts of red tide algae on competing phytoplankton", co-authored by Georgia Tech current and former students Kelsey Poulson-Ellestad, Jessie Roy, Robert Drew Sieg, Christina Jones, Emily Prince, Tracey Myers, as well as former GT postdoctoral researcher Clare Redshaw, and collaborators Facundo Fernandez (GT), Brook Nunn (University of Washington), Jerome Naar (University of North Carolina at Wilmington), and Mark Viant and Jon Byrne (University of Birmingham UK).  

Dr. Kubanek is a Professor in the School of Biology at Georgia Tech. Her invited lecture is described below:

War in the Plankton: Sublethal and reciprocal impacts of red tide algae on competing phytoplankton

How individual species come to be dominant members of marine planktonic communities is not deeply understood; however, it is thought that chemistry plays a substantial role.  For example, some red tide-forming dinoflagellates produce toxic secondary metabolites that are hypothesized to enhance dinoflagellate fitness by acting as grazer deterrents, allelopathic agents, or antimicrobial defenses.  In field and lab experiments we have shown that the red tide dinoflagellate Karenia brevis is allelopathic, inhibiting the growth of several co-occurring phytoplankton species, but that K. brevis natural products other than well-known brevetoxins are responsible for suppressing most of these species.  At least one phytoplankton competitor, Skeletonema costatum, retaliates against K. brevis, reducing its allelopathic effects and degrading waterborne brevetoxins.  Several other phytoplankton species also metabolize brevetoxins, removing these toxins from the water column and mitigating the negative effects on invertebrates.  Death is a rare outcome of K. brevis allelopathy, with more subtle responses predominating, such as reduced photosynthetic output and increased cell permeability.  These changes in cellular metabolism and physiology may be more readily characterized and measured by a systems biology approach than by growth or cell lysis assays.  NMR metabolomics has provided preliminary evidence for sub-lethal impacts of exposure to K. brevis allelopathy on the metabolism of neighboring phytoplankton.  Future work will expand upon these initial results with mass spectrometry-based metabolomics and proteomics methods, as well as experiments with other vulnerable competing phytoplankton species, with the goal of identifying cellular targets and understanding the molecular mechanisms of red tide allelopathy.  Our results indicate that chemically-mediated interactions are reciprocal, and that ecosystem-level consequences of red tides (such as fish kills caused by waterborne toxins) may depend upon which other phytoplankton species are present.

Dr. Joshua Weitz (Associate Professor, School of Biology) has been awarded a grant from the Program in Biological Oceanography on "Understanding the Effects of Complex Phage-Bacteria Infection Networks on Ocean Ecosystems". The award provides over $470,000 over 4 years to study the interaction between viruses and bacteria in ocean ecosystems.

Bacteria and their viruses (phages) make up two of the most abundant and genetically diverse groups of organisms in the oceans. The extent of this diversity has become increasingly apparent with the advent of environmental sequencing. However, the ongoing discovery of new taxonomic diversity has, thus far, out-paced gains in quantifying the function of and interactions among phages and bacteria. In this proposal, Weitz will develop a theoretical framework for characterizing the effect of complex phage-bacteria interactions on microbial ecosystem structure and function.

As part of this grant, Weitz will also help train quantitative biologists interested in microbial systems.  The training will include the development of a new course, opportunities for undergraduate research, and opportunities for hands-on laboratory experience for modelers in collaboration with the viral ecology laboratories of Matt Sullivan (U of Arizona) and Steven Wilhelm (UT-Knoxville).

New Georgia Tech research shows that cell stiffness could be a valuable clue for doctors as they search for and treat cancerous cells before they’re able to spread. The findings, which are published in the journal PLoS One, found that highly metastatic ovarian cancer cells are several times softer than less metastatic ovarian cancer cells.

Assistant Professor Todd Sulchek and Ph.D. student Wenwei Xu used a process called atomic force microscopy (AFM) to study the mechanical properties of various ovarian cell lines. A soft mechanical probe “tapped” healthy, malignant and metastatic ovarian cells to measure their stiffness.

“In order to spread, metastatic cells must push themselves into the bloodstream. As a result, they must be highly deformable and softer,” said Sulchek, a faculty member in the George W. Woodruff School of Mechanical Engineering. “Our results indicate that cell stiffness may be a useful biomarker to evaluate the relative metastatic potential of ovarian and perhaps other types of cancer cells.”

Just as previous studies on other types of epithelial cancers have indicated, Sulchek also found that cancerous ovarian cells are generally softer and display lower intrinsic variability in cell stiffnesss than non-malignant cells.

Sulchek’s lab partnered with the molecular cancer lab of Biology Professor John McDonald, who is also director of Georgia Tech’s newly established Integrated Cancer Research Center.

“This is a good example of the kinds of discoveries that only come about by integrating skills and knowledge from traditionally diverse fields such as molecular biology and bioengineering,” said McDonald. “Although there are a number of developing methodologies to identify circulating cancer cells in the blood and other body fluids, this technology offers the added potential to rapidly determine if these cells are highly metastatic or relatively benign.”

Sulchek and McDonald believe that, when further developed, this technology could offer a huge advantage to clinicians in the design of optimal chemotherapies, not only for ovarian cancer patients but also for patients of other types of cancer.

This project was supported in part by the National Science Foundation (NSF) (Award Number CBET-0932510). The content is solely the responsibility of the principal investigators and does not necessarily represent the official views of the NSF.

New Georgia Tech research shows that cell stiffness could be a valuable clue for doctors as they search for and treat cancerous cells before they’re able to spread. The findings, which are published in the journal PLoS One, found that highly metastatic ovarian cancer cells are several times softer than less metastatic ovarian cancer cells.

Assistant Professor Todd Sulchek and Ph.D. student Wenwei Xu used a process called atomic force microscopy (AFM) to study the mechanical properties of various ovarian cell lines. A soft mechanical probe “tapped” healthy, malignant and metastatic ovarian cells to measure their stiffness.

“In order to spread, metastatic cells must push themselves into the bloodstream. As a result, they must be highly deformable and softer,” said Sulchek, a faculty member in the George W. Woodruff School of Mechanical Engineering. “Our results indicate that cell stiffness may be a useful biomarker to evaluate the relative metastatic potential of ovarian and perhaps other types of cancer cells.”

Just as previous studies on other types of epithelial cancers have indicated, Sulchek also found that cancerous ovarian cells are generally softer and display lower intrinsic variability in cell stiffnesss than non-malignant cells.

Sulchek’s lab partnered with the molecular cancer lab of Biology Professor John McDonald, who is also director of Georgia Tech’s newly established Integrated Cancer Research Center.

“This is a good example of the kinds of discoveries that only come about by integrating skills and knowledge from traditionally diverse fields such as molecular biology and bioengineering,” said McDonald. “Although there are a number of developing methodologies to identify circulating cancer cells in the blood and other body fluids, this technology offers the added potential to rapidly determine if these cells are highly metastatic or relatively benign.”

Sulchek and McDonald believe that, when further developed, this technology could offer a huge advantage to clinicians in the design of optimal chemotherapies, not only for ovarian cancer patients but also for patients of other types of cancer.

This project was supported in part by the National Science Foundation (NSF) (Award Number CBET-0932510). The content is solely the responsibility of the principal investigators and does not necessarily represent the official views of the NSF.