Francesca Storici, associate professor in the School of Biological Sciences and a researcher in the Petit Institute for Bioengineering and Bioscience, has been named a Howard Hughes Medical Institute (HHMI) Faculty Scholar.
Storici is one of 84 scientists from 43 institutions across the U.S., in first cohort of researchers who are receiving this first-time award supported by HHMI, the Simons Foundation, and the Bill & Melinda Gates Foundation.
“This is an awesome grant, really, because the goal is to support creative researchers. It’s not about a specific project with specific aims,” says Storici. “The award has been possible thanks to the exceptional dedication and enthusiasm of all my group members at Georgia Tech.”
Storici’s lab will receive $1.5 million over five years. The awards target early career scientists who have great potential to make unique contributions to their field, according to HHMI, who joined forces with the Simons and Gates foundations to create the program in response to growing concern about the significant challenges that early-career scientists face.
The career trajectory for these researchers has become much less certain as competition for grant support intensifies. In the last two decades, the U.S. has witnessed a sharp decline in the success rate for National Institutes of Health (NIH) research awards, as well as a striking increase in the average age at which an investigator receives his or her first R01-equivalent grant.
“Support for outstanding early-career scientists is essential for continued progress in science in future years,” notes Marian Carlson, the Simons Foundation’s director of life sciences.
HHMI was concerned that the time-consuming (and often frustrating) quest for grant funding could sap the creativity and energy that researchers bring to starting their own labs. Within a few years of a new faculty appointment, a researcher's institutional start-up funds typically come to an end. Pressure to secure federal grant money may lead to “safe” grant proposals. As a result, creative and potentially transformative research projects may fall by the wayside.
“This program will provide these scientists with much needed flexible resources so they can follow their best research ideas,” says HHMI Vice President and Chief Scientific Officer David Clapham.
The Storici lab’s research focuses on ribonucleotides embedded in DNA; RNA-driven DNA repair and modification; mechanisms of genomic stability/instability; and gene targeting and genome editing.
The Storici lab’s research focuses on RNA-driven DNA repair and modification; function and consequences of ribonucleotides embedded in DNA; mechanisms of genomic stability/instability; and gene targeting and genome editing.
Storici is considered a pioneer in the emerging field of RNA-mediated genome stability and instability. Her research led to the discovery of transcript RNA-templated DNA repair and recombination. The Storici group also has developed new tools to better understand the genetic and epigenetic consequences of the presence of RNA in DNA.
The HHMI award is just the latest in a string of recent successes for Storici. In August came two major announcements: a three-year grant from the National Science Foundation to gain new insight into the impact or RNA on genome maintenance, and a five-year, $1.4 million grant from the NIH supporting a collaborative effort with the lab of fellow Petit Institute researcher Fred Vannberg (assistant professor in the School of Biological Sciences) as well as the University of Udine in Italy.
Early-career researchers (four to 10 years of faculty experience) were eligible to apply for this competition. Distinguished scientists reviewed and evaluated more than 1,400 applicants on their potential for significant research productivity and originality, as judged by their doctoral and postdoctoral work, results from their independent research program, and their future research plans.
Expenses covered by the grant will include partial salary for faculty, salary for lab personnel, equipment, supplies, travel and publications.
Emeritus Professor Gerald (Jerry) Pullman was awarded a lifetime achievement award for outstanding contributions in somatic embryogenesis and other vegetative propagation technologies by the Fourth International Conference of the International Union of Forest Research Organizations focused on Somatic Embryogenesis and Other Vegetative Propagation Technologies held in September 2016 in Buenos Aires, Argentina.
Dr. Gerald Pullman, Emeritus Professor in the School of Biology, was recognized for his outstanding contributions and scientific endeavors in the vegetative propagation of trees, especially somatic embryogenesis in conifer species. The lifetime achievement award was presented at the Fourth International Conference of the International Union of Forest Research Organizations (IUFRO Unit 2.09.02) held September 19-23 in La Plata, Buenos Aires, Argentina. The conference participants gathered to discuss “Development and application of vegetative propagation technologies in plantation forestry to cope with a changing climate and environment”. The membership of the unit currently includes 742 scientists from 341 affiliations and 65 countries.
As demands for forest products grow and the land base to produce trees shrinks, it will become necessary to produce trees that produce more wood and fiber per acre, with improved wood and fiber properties. Clonal propagation of trees with desired growth and processing characteristics will facilitate this goal.
Jerry’s research interests for the past 35 years have been in the areas of multiplication of high-value trees through somatic embryogenesis, understanding the fundamental physical and chemical factors driving natural plant embryo development, creation of tissue culture systems necessary for the genetic engineering of forest trees and methods to propagate and conserve rare and endangered Southeastern plants. Jerry has over 120 publications with 55 focused in the field of somatic embryogenesis and additional publications on understanding seed conditions occurring during natural embryo development, vegetative propagation of forest trees, and conservation of endangered species through tissue culture and cryogenic storage.
Jerry continues to lead a small tissue culture program at the Georgia Tech Renewable Bioproducts Institute focused on conifer somatic embryogenesis and conservation of rare and endangered species in the Southeast. The research on rare and endangered plants is in partnership with the Atlanta Botanical Garden and often works with School of Biology undergraduate students.
Editor's Note: This item was originally published as a blog post in the Amplifier.
A recent study published in the Proceedings of the National Academy of Sciences analyzed the viral content of the human gut (Manrique et al., PNAS, 2016). The research focused on a particular kind of virus called bacteriophage, which only infect bacterial cells and do not infect human cells. Manrique and colleagues found that healthy individuals had a “core” group of bacteriophage. In addition, they found that these core bacteriophage were less frequently found in individuals with gastrointestinal disease. This novel finding reveals a potential link between the viruses in our gut and our health.
Joshua Weitz, a professor in the School of Biological Sciences explains the findings:
Yogurt is a breakfast staple. In my family, we pack single-serve yogurt containers with our kids’ lunches and eat “stinky” cheese. In doing so we are also serving our children bacteria. Intentionally. Yogurt and cheese are examples of “living” food. The living component are cultures of bacteria.
As any shopper knows, the marketing of yogurt is tied not just to its taste but to its health benefits. The active bacteria in yogurt differ among company and brands. Irrespective of the brand-name, the active bacteria are nearly all close relatives of “lactic acid bacteria”. Lactic acid bacteria take the sugars in milk, break them down, and release lactic acid. That lactic acid and other byproducts give yogurt its distinctly sour taste.
The idea that eating more bacteria could be good for you reflects a paradigm shift in the scientific attitude towards microbes and health. Bacteria can make us sick. But, many bacteria keep us healthy. We could not go about our daily routine without them. These bacteria constitute part of our “microbiome” – that is the world of bacteria that lives in and on us. Yet, despite the changing attitudes towards bacteria, there has not been a similar paradigm shift with respect to viruses. I have yet to see a yogurt offered with extra viruses. I would imagine it would not be a sales hit… Or would it?
The study of Manrique and colleagues identified a core “virome” correlated to human health. But we still do not know if there is a causative link between the two, e.g., do bacteriophage in the human virome infect components of the healthy human microbiome and/or do they infect otherwise harmful pathogens? Future research will be needed to tease apart these relationships. But one thing is clear: consumers may eventually need to consider the health benefits of viruses and bacteria when thinking about maintaining or improving their health.
EDITOR’S NOTE: This item first appeared as a blog post in the Amplifier.
Oceanic dead zones are natural laboratories for exploring biological diversity. In a study published this year in the journal Nature, scientists at Georgia Tech discovered new species of the world's most abundant organism group, a bacterial clade called SAR11, which have adapted to life in dead zones by acquiring genes necessary to breath the chemical nitrate. Other work by Tech scientists shows that dead zones in the Pacific, which contain the largest pools of the greenhouse gas methane (CH4) in the open ocean, support microbes adapted to consume methane, potentially through a process that requires these microbes to make their own oxygen. Research on dead zones is challenging scientists to devise new tools to collect and manipulate ocean microbes while maintaining the exact environmental conditions the cells experience in nature. Frank Stewart, of the School of Biological Sciences, explains:
The oceans are losing oxygen. A poignant example is the "dead zone" that forms each summer in the Gulf of Mexico. Each spring, fertilizers from farms and lawns wash into the rivers feeding the Gulf. This influx of nutrients, primarily nitrogen and phosphorus from the Mississippi River, fuels expansive blooms of photosynthetic algae near the river mouths. When these algae die, they are eaten by single-celled microbes (bacteria) that consume oxygen during growth. If oxygen removal exceeds replenishment, as occurs in the Gulf during high microbial growth in the calm of summer, seawater oxygen levels can fall nearly to zero, creating a "dead zone" devoid of larger marine life. Dead zones like those in the Gulf can span thousands of square miles and, by altering the distributions of animals such as shrimp and fish, compromise the health of the ocean's most productive and biodiverse ecosystems.
But not all life deplores a dead zone. Indeed, thousands of microbial species thrive under the low-oxygen conditions of the dead zone, occurring at densities of millions of cells per milliliter (~1/5 of a teaspoon). These microbes employ a wide spectrum of biochemical solutions to life without oxygen, many of which remain poorly understood but are critical for ocean processes. For example, many of the microbes responsible for controlling the bioavailability of nitrogen, an essential component of proteins and DNA, grow only under low-oxygen conditions by using nitrogen-containing compounds, such as nitrite (NO2-), in place of oxygen. In metabolizing such compounds, these microbes produce nitrogen-containing gases, including the potent greenhouse gas nitrous oxide (N2O).
Studies of dead zone microbes are transforming our knowledge of ocean ecosystems. By collecting water at different depths through a dead zone, researchers can sample microbes exposed to vastly different oxygen and chemical conditions, thereby testing predictions of how ecosystem-level processes, such as the cycling of nutrients or greenhouse gases, may change as human activities influence ocean parameters.
Dead zones, in addition to exerting critical effects on the function of marine ecosystems, are breathing life into a broader understanding of microbes in the oceans.
Joshua Weitz, professor in the School of Biological Sciences, discusses his study on selfishness with Georgia Public Broadcasting presenters.
Ever think about discovering artifacts à la Indiana Jones? You have one final chance to be a fossil hunter this semester: on Wednesday, Nov. 30, 2016, when Jenny L. McGuire opens her lab to all comers to search for fossils in rock samples.
Although you will not have to flee from massive boulders or fight off Nazis, you can still become an explorer of the past. At 3-5 PM, amid the electronic white noise that washes over Georgia Tech, you will be transported to a faraway dig site and engage in simple but enthralling discovery.
An independent research scientist in the School of Biological Sciences, McGuire has hosted Fossil Wednesdays all semester. To see what goes on, I visited the lab and got my hands dirty. I grabbed a pair of tweezers, scooped a pile of light-colored gravel, and searched for fossils.
Fortunately for amateurs, the fossils were distinctly darker than gravel, and I could see bone fragments. Some were easy to identify: Vertebrae were pointy; intact lizard bones looked like they fell out of a game of Operation. Others were bone shards, unidentifiable bits and bobs.
During the two hours, people popped in, sifted through a few handfuls of gravel, and grabbed a snack on the way out. Small conversations bubbled throughout the room, but most of the fossil hunters were quietly focused on the work as McGuire helped participants identify specimens.
In attendance that week was School of Biological Sciences Associate Professor Sam Brown. He came with his daughters Chloe, 8, and Lily, 5. The two showed remarkable flair for finding fossils, some of which were so small they looked like specks of dust unless viewed under a microscope. “They loved the whole adventure and keep asking me when we can come back” Brown said.
“I told my class that I found an arm bone and a spine bone,” Lily said.
“It was really cool to look through the microscope and see all the details, like the teeth in the jaw of a lizard,” Chloe said. “There were some super tiny bones that were hard to find, but it was cool when you found them.”
As a child, McGuire loved rock collecting. While pursuing this interest in college, she landed in South Africa looking for human or human-like fossils. The field study yielded lots of fossils from other animals, which got McGuire, as she said, “really excited about the idea of change through time, about morphological microevolution and what that can tell us about how species change through time.”
McGuire collected the material for Fossil Wednesdays from Natural Trap Cave, in Wyoming. The site is exquisite, she said: “Inside the cave, it’s 40 degrees year-round, so everything preserves beautifully; it’s a refrigerator.” Because the cave has layers of fossils that span from 30,000 years old to 4,000 years old, McGuire can look at how a community changes across a vast time period.
The McGuire lab is asking what types of species filled ecological niches after extinction events and how long it took population structures to normalize after a major transition. Similar extinctions of large mammals are occurring today in Africa and South Asia, she said. McGuire is using the data to determine what to expect not only from specific extinctions, but also from major ecological disruptions occurring worldwide.
This miniature fossil hunt is both relaxing and engaging, a puzzle with a higher purpose. If you’re around this Wednesday and want to have a unique science experience, head to the Cherry Emerson Building, room 326, and get digging for some bones.
College of Sciences
Prions are notorious for causing devastating neurodegenerative diseases, such as mad cow disease. How these infectious self-perpetuating protein aggregates propagate—by getting other protein molecules of the same sequence to join the pile—is hands down insidious.
Yet prion formation could represent a protective response to stress, according to research from Emory University School of Medicine, Georgia Tech School of Biological Sciences, and St. Petersburg State University, in Russia. The results were published in the Jan. 17, 2017, issue of Cell Reports.
The scientists show that the yeast protein called Lsb2 forms a “metastable” prion in response to high temperature. The Lsb2 prion can persist for a number generations after the heat stress and can convert other proteins into prions, says Yury O. Chernoff, a professor in the Georgia Tech School of Biological Sciences.
Because high temperature causes proteins to misfold, the scientists propose, prion formation could be an attempt by cells to impose order upon a chaotic jumble of misfolded proteins, which would harm the cell. If so, the prion forms are protective—even if as the “lesser of two evils,” as Chernoff puts it—and prion formation under heat stress could be an adaptive response.
“It’s fascinating that stress triggers a cascade of prion-like changes in Lsb2 and that a memory of stress may persist for a number of cell generations,” Chernoff says. “It would be interesting to see whether other proteins can respond to environmental stresses in the same way the Lsb2 does.”
"What we found suggests that Lsb2 could be the regulator of a broader prion-forming response to stress," Wilkinson says.
Other investigators studying yeast prions have been finding examples of how they may help cells adapt to a changing environment. The new findings are consistent with this idea, Chernova says. Moreover, the evolutionary history of the yeast genome indicates that increased heat tolerance coincides with an amino acid substitution that enables Lsb2 to transform into a prion.
Understanding how and why prions form could illuminate Alzheimer’s disease research, because the behavior of the toxic protein fragment beta-amyloid, central in Alzheimer’s, strongly resembles some features of prions. The Cell Reports authors note that the yeast protein Lsb2 has some sequence similarity to a human protein called Grb2, known to interact with APP, the precursor of amyloid-beta.
This research was supported by the National Institutes of Health (GM093294), the National Science Foundation (MCB 1516872), and the Russian Science Foundation (RSF 14-50-00069).
You never know when a frog playing an electronic game will lead to an experiment on the physics of saliva....Alexis C. Noel, a Ph.D. student in mechanical engineering at Georgia Tech, and her supervisor, David L. Hu, were watching a viral YouTube video in which a frog is attacking the screen of a smartphone running an ant-smashing game. It appears to be winning. They started wondering how — in reality — frog tongues stick to insects so quickly when they shoot out to grab them, and decided it was a phenomenon worth studying. David Hu is an associate professor of mechanical engineering and of biology, as well as an adjunct associate professor of physics, at Georgia Tech.
By Alexis Noel and David Hu
Note: This article was first published in The Conversation on Jan. 31, 2017. It is republished here under the Creative Commons License.
How does one get stuck studying frog tongues? Our study into the sticky, slimy world of frogs all began with a humorous video of a real African bullfrog lunging at fake insects in a mobile game. This frog was clearly an expert at gaming; the speed and accuracy of its tongue could rival the thumbs of texting teenagers.
The versatile frog tongue can grab wet, hairy and slippery surfaces with equal ease. It does a lot better than our engineered adhesives – not even household tapes can firmly stick to wet or dusty surfaces. What makes this tongue even more impressive is its speed: Over 4,000 species of frog and toad snag prey faster than a human can blink. What makes the frog tongue so uniquely sticky? Our group aimed to find out.
Baseline Frog Tongue Knowledge
Early modern scientific attention to frog tongues came in 1849, when biologist Augustus Waller published the first documented frog tongue study on nerves and papillae – the surface microstructures found on the tongue. Waller was fascinated with the soft, sticky nature of the frog tongue and what he called:
“the peculiar advantages possessed by the tongue of the living frog…the extreme elasticity and transparency of this organ induced me to submit it to the microscope.”
Fast-forward 165 years, when biomechanics researchers Kleinteich and Gorb were the first to measure tongue forces in the horned frogCeratophrys cranwelli. They found in 2014 that frog adhesion forces can reach up to 1.4 times the body weight. That means the sticky frog tongue is strong enough to lift nearly twice its own weight. They postulated that the tongue acts like sticky tape or a pressure-sensitive adhesive – a permanently tacky surface that adheres to substrates under light pressure.
To begin our own study on sticky frog tongues, we filmed various frogs and toads eating insects using high-speed videography. We found that the frog’s tongue is able to capture an insect in under 0.07 seconds, five times faster than a human eye blink. In addition, insect acceleration toward the frog’s mouth during capture can reach 12 times the acceleration of gravity. For comparison, astronauts normally experience around three times the acceleration of gravity during a rocket launch.
On To The Materials Testing
Thoroughly intrigued, we wanted to understand how the sticky tongue holds onto prey so well at high accelerations. We first had to gather some frog tongues. Here at Georgia Tech, we tracked down an on-campus biology dissection class, who used northern leopard frogs on a regular basis.
The plan was this: Poke the tongue tissue to determine softness, and spin the frog saliva between two plates to determine viscosity. Softness and viscosity are common metrics for comparing solid and fluid materials, respectively. Softness describes tongue deformation when a stretching force is applied, and viscosity describes saliva’s resistance to movement.
Determining the softness of frog tongue tissue was no easy task. We had to create our own indentation tools since the tongue softness was beyond the capabilities of the traditional materials-testing equipment on campus. We decided to use an indentation machine, which pokes biological materials and measures forces. The force-displacement relationship can then describe softness based on the indentation head shape, such as a cylinder or sphere.
However, typical heads for indentation machines can cost US$500 or more. Not wanting to spend the money or wait on shipping, we decided to make our own spherical and flat-head indenters from stainless steel earrings. After our tests, we found frog tongues are about as soft as brain tissue and 10 times softer than the human tongue. Yes, we tested brain and human tongue tissue (post mortem) in the lab for comparison.
For testing saliva properties, we ran into a problem: The machine that would spin frog saliva required about one-fifth of a teaspoon of fluid to run the test. Sounds small, but not in the context of collecting frog spit. Amphibians are unique in that they secrete saliva through glands located on their tongue. So, one night we spent a few hours scraping 15 dead frog tongues to get a saliva sample large enough for the testing equipment.
How do you get saliva off a frog tongue? Easy. First, you pull the tongue out of the mouth. Second, you rub the tongue on a plastic sheet until a (tiny) saliva globule is formed. Globules form due to the long-chain mucus proteins that exist in the frog saliva, much like human saliva; these proteins tangle like pasta when swirled. Then you quickly grab the globule using tweezers and place it in an airtight container to reduce evaporation.
After testing, we were surprised to find that the saliva is a two-phase viscoelastic fluid. The two phases are dependent on how quickly the saliva is sheared, when resting between parallel plates. At low shear rates, the saliva is very thick and viscous; at high shear rates, the frog saliva becomes thin and liquidy. This is similar to paint, which is easily spread by a brush, yet remains firmly adhered on the wall. Its these two phases that give the saliva its reversibility in prey capture, for adhering and releasing an insect.
To Catch A Cricket
How does soft tissue and a two-phase saliva help the frog tongue stick to an insect? Let’s walk through a prey-capture scenario, which begins with a frog tongue zooming out of the mouth and slamming into an insect.
During this impact phase, the tongue deforms and wraps around the insect, increasing contact area. The saliva becomes liquidy, penetrating the insect cracks. As the frog pulls its tongue back into the mouth, the tissue stretches like a spring, reducing forces on the insect (similar to how a bungee cord reduces forces on your ankle). The saliva returns to its thick, viscous state, maintaining high grip on the insect. Once the insect is inside the mouth, the eyeballs push the insect down the throat, causing the saliva to once again become thin and liquidy.
It’s possible that untangling the adhesion secrets of frog tongues could have future applications for things like high-speed adhesive mechanisms for conveyor belts, or fast grabbing mechanisms in soft robotics.
Most importantly, this work provides valuable insight into the biology and function of amphibians – 40 percent of which are in catastrophic decline or already extinct. Working with conservation organization The Amphibian Foundation, we had access to live and preserved species of frog. The results of our research provide us with a greater understanding of this imperiled group. The knowledge gathered on unique functions of frog and toad species can inform conservation decisions for managing populations in dynamic and declining ecosystems.
While it’s not easy being green, a frog may find comfort in the fact that its tongue is one amazing adhesive.
Mark Mandica of The Amphibian Foundation collaborated on the research published in Journal of the Royal Society Interface and coauthored this article.
Alexis Noel is a Ph.D. student in Biomechanics at Georgia Institute of Technology.
David Hu is an associate professor of mechanical engineering and of biology and an adjunct associate professor of physics at Georgia Institute of Technology.
Over the past year, scientists have made great strides in the development of brain-machine interfaces (BMIs), wired external devices that are controlled solely by brain activity [see “Roadmapping the Adoption of Brain-Machine Interfaces”]. Last October, Nathan Copeland, a man who had been paralyzed from the chest down for more than 10 years, made headlines when he fist-bumped President Obama with a BMI-controlled robotic arm using only his thoughts. As BMI-related technologies and neuroprosthetics become more sophisticated, researchers are learning that these tools can make some fascinating changes to the brain, engaging its natural plasticity in sometimes unanticipated ways. Understanding those changes to underlying plasticity, some say, could offer clues to how to rewire and rehabilitate the damaged brain—perhaps even without the need of external hardware. Prosthetics, even without the addition of a BMI component, can alter the brain’s connections, says Lewis Wheaton, director of the Cognitive Motor Control Lab at the Georgia Institute of Technology says.