A hidden treasure on the University of Missouri’s campus is a living and breathing work of art.
In the Christopher S. Bond Life Sciences Center, a 20-foot plant wall stands as a towering tribute to the diversity of plant life and coexistence of species — a botanical landscape of more than 200 individual plants from 40 to 50 species including many ferns, vines, perennials, orchids and geraniums.
The display continues to be a visual reminder of the building’s interdisciplinary nature – much like the plants within the wall, the Bond Life Sciences Center facilitates the coexistence and collaboration between an array of researchers within its walls.
One plant cascades down the wall and stands out more than most — it looks more like a large insect than any type of plant typically seen in such displays.
Tillandsia is a genus of succulent plant native to Central America that can undergo long dry spells. The wiry plant thrives on the stone beside the plant wall without the help of a pot of soil, and is seemingly absent an essential, anatomical feature of most flora — roots.
They still have tiny root protrusions, but the mass is minuscule compared to the thick leaves, which take up and store water and nutrients, rather than the root system which handles that work in most plants.
Approximately 60 Tillandsias pepper the plant wall, including a few mounted directly onto the stone wall with a special kind of non-toxic rubber cement manufactured by Davis Farms based out of San Diego.
The strange plant was added to the green tapestry by Jason Fenton, an office support associate at the Bond Life Sciences Center. He first noticed the rootless plants in Belize while on a trip there in 2003 and had been growing them at his home.
“I think they’re really beautiful and distinctive,” Fenton said. “They help give variety to the wall.”
The rootless plants require special treatment — just a little extra attention from facilities manager, Jim Bixby, who waters the Tillandsias with a spray bottle once a week.
The wall started with a vision from Jack Schultz, director of the Bond Life Sciences Center. The execution and maintenance of the feature is credited to Bixby, who has honed the project since 2010.
After trying several watering systems, Bixby found one that worked. He hung rows of pots with modified flat sides and tailored a simple, drip irrigation system made for easy watering along a grid.
Within the diverse landscape and after additions of a variety of plants over the years, Bixby has seen competition between several of the species.
The wall favors the ferns, which have taken over much of the space, crowding out other plants for the eastern sunlight that flows through the windows, Bixby said.
Several long-stemmed species have found ways to cope, however; venturing out between the ferns’ curtain-like fronds to get their fair share of sunlight.
Simple actions like walking, swallowing and breathing are the result of a complex communication system between cells. When we touch something hot, our nerve cells tell us to take our hand off the object.
This happens in a matter of milliseconds.
This hyperspeed of communication is instrumental in maintaining proper muscle function. Many degenerative diseases affecting millions of people worldwide result from reduced signaling speed or other cellular miscommunications within this intricate network.
Michael Garcia, investigator at the Christopher S. Bond Life Sciences Center and associate professor of biology at the University of Missouri, conducts basic research to answer fundamental questions of nerve cell mechanics.
“In order to fix something, you need to first understand how it works,” Garcia said.
Garcia’s research illuminates relationships between nerve cells to find factors affecting function. His goal is to provide insight on fundamental cellular mechanisms that aren’t fully understood.
Garcia’s research has been funded partly by the National Science Foundation and National Institutes of Health.
Technological advancements have made it possible to better understand disease development in the human body to create more effective treatments. Alas, a scientist’s work is never finished— when the answer to one question is found, ten more crop up in its wake.
Garcia’s research, which appeared in several journals including Human Molecular Genetics andthe Journal of Neuroscience Research initially sought to shed light on the neuronal response to myelination, the development of an insulating border around a nerve cell, called a myelin sheath, which is critical in rapid communication between cells.
How it works: Rebuilding cell theory
Garcia’s early research disproved a long-standing hypothesis concerning this cellular feature.
Mammals’ nervous systems are uniquely equipped with myelination, which has been shown to increase conduction velocity, or the speed at which nerve cells pass signals. Low velocity is often associated with neurodegenerative diseases, so research exploring why could later have application in therapeutic technology.
In addition to myelination, cell size makes a big difference in conduction velocity — the bigger the nerve cells, the faster they can pass and receive signals. Garcia’s findings disproved a hypothesis that related myelination to this phenomenon.
The hypothesis, published in a 1992 edition of Cell, claimed that myelination causes a cellular process called phosphorylation which then causes an increase in the axonal diameter (width of the communicating part of a nerve cell), leading to faster nerve cell communication. Garcia found that myelination did cause an increase in axonal diameter, and myelination was required for phosphorylation, but that the two results were independent of one another.
To narrow in on the processes affecting axonal diameter, Garcia identified the protein responsible for growth.
Garcia followed earlier work, showing that one subunit controls whether there is growth at all with myelination, by identifying the domain of this protein that determines how much growth.
After clarifying this part of the process, a question still remains: If not to control myelination, why does phosphorylation happen?
Jeffrey Dale, a recent PhD graduate from Garcia’s lab, said current research is in part geared toward finding a connection between phosphorylation and a process called remyelination.
Remyelination could be key to new therapeutic approaches. When a cell is damaged (as in neurodegenerative disease) the myelin sheath can be stripped away. Remyelination is the process a cell goes through to replace the myelin.
Imagine you have a new wooden toy boat, painted and smooth. If you take a knife and whittle away all the paint and then repaint it—even exactly how it was painted before—the boat is not going to be as shiny and smooth as it was before. This is how remyelination works (or rather, doesn’t). When nerve cells are damaged, the myelin sheath is stripped away and even after the cell rebuilds it, the cell can’t conduct signals at the same speed it was able to before.
“If you can learn what controls myelination, maybe you can improve effectiveness of remyelination,” Dale said.
Garcia said it is possible that revealing the mechanics involved in phosphorylation could lead to better treatments. In context of neurodegenerative diseases, the question why don’t axons function properly might be wrapped up in Garcia’s question: In healthy cells, why do they?
The most puzzling scientific mysteries may be solved at the same machine you’re likely reading this sentence.
In the era of “Big Data” many significant scientific discoveries — the development of new drugs to fight diseases, strategies of agricultural breeding to solve world-hunger problems and figuring out why the world exists — are being made without ever stepping foot in a lab.
Developed by researchers at the Bond Life Sciences Center, SoyKB.org allows international researchers, scientists and farmers to chart the unknown territory of soybean genomics together — sometimes continents away from one another — through that data.
Digital solutions to real-world questions
As part of the Obama Administration’s $200 million “Big Data” Initiative, SoyKB (Soy Knowledge Base) was born.
The digital infrastructure changes the way researchers conduct their experiments dramatically, according to plant scientists like Gary Stacey, Bond LSC researcher, endowed professor of soybean biotechnology and professor of plant sciences and biochemistry.
“It’s very powerful,” Stacey said. “Humans can only look at so many lines in an excel spreadsheet — then it just kind of blurs. So we need these kinds of tools to be able to deal with this high-throughput data.”
The website, managed by Trupti Joshi, an assistant research professor in computer science at MU’s College of Engineering, enables researchers to develop important scientific questions and theories.
“There are people that during their entire career, don’t do any bench work or wet science, they just look at the data,” Stacey said.
The Gene Pathway Viewer available on SoyKB, shows different signaling pathways and points to the function of specific genes so that researchers can develop improvements for badly performing soybean lines.
“It’s much easier to grasp this whole data and narrow it down to basically what you want to focus on,” Joshi said.
A 3D-protein modeling tool lends itself especially to drug design. A pharmaceutical company could test the hypothesis and in some situations, the proposed drug turns out to yield the expected results — formulated solely by data analysis.
The Big Data initiative drives a blending of “wet science” — conducting experiments in the lab and gathering original data — and “dry science” — using computational methods.
Testament of the times?
“Oh, absolutely,” Joshi said.
Collaboration between the “wet” and “dry” sciences
Before SoyKB, data from numerous experiments would be gathered and disregarded, with only the desired results analyzed. The website makes it easy to dump all of the data gathered to then be repurposed by other researchers.
“With these kinds of databases now, all the data is put there so something that’s not valuable to me may be valuable to somebody else,” Stacey said,
Joshi said infrastructure like SoyKB is becoming more necessary in all realms of scientific discovery.
“(SoyKB) has turned out to be a very good public resource for the soybean community to cross reference that and check the details of their findings,” she said.
Computer science prevents researchers having to reinvent the wheel with their own digital platforms. SoyKB has a translational infrastructure with computational methods and tools that can be used for many disciplines like health sciences, animal sciences, physics and genetic research.
“I think there’s more and more need for these types of collaborations,” Joshi said. “It can be really difficult for biologists to handle the large scope of data by themselves and you really don’t want to spend time just dealing with files — You want to focus more on the biology, so these types of collaborations work really well.
It’s a win-win situation for everyone,” she said.
The success of SoyKB was perhaps catalyzed by Joshi. She adopted the website and the compilation of data in its infant stages as her PhD dissertation.
Joshi is unique because she has both a biology degree and a computer science background. Stacey said Joshi, who has “had a foot in each camp,” serves as an irreplaceable translator.
Most recently, the progress of SoyKB as part of the Big Data Initiative was presented at the International Conference on Bioinformatics and Biomedicine Dec. 2013 in Shanghai. The ongoing project is funded by NSF grants.
Here’s a scenario: You are trying to find a lost section of string in the world’s most massively tangled spool of yarn. Then try cutting that section of yarn that’s deeply embedded in the mess without inadvertently cutting another or losing track of the piece you’re after.
For researchers, this problem is not unlike something they encounter in the study of genetic information in the tangled spool that is DNA.
A new tool will help scientists straighten things out.
The tool, developed by University of Missouri Bond Life Sciences Center investigators helps researchers effectively screen cell behavior by limiting epigenetic silencing, which occurs when a cell packages and stows away important genetic information, much like an accountant puts a client’s information away in a filing cabinet.
The cell can go digging to find that information when it absolutely needs it, but otherwise that information is tucked away and inactive.
Professors of biochemistry Mark Hannink, Tom Mawhinney and research assistant professor Valeri V. Mossine used insulators to develop the piggyBac transposon plus insulators, a better reporter of signaling between cells that makes improved screening possible.
This simple addition to an existing screening tool used in laboratories will help streamline research and contribute to screening products like vitamins and supplements and medicines for authenticity, Hannink said.
This is why the insulator addition to the piggyBac reporter assay by MU researchers is a game changer in the scientific world.
How it works
DNA stretches out to nearly 10 feet when it’s uncoiled. That’s 10 feet of your body’s deepest secrets coiled into a microscopic package and tucked away into each and every one of your cells. The human body, by the way, holds an estimated 10 trillion cells. An inconceivable number, right?
Let’s go back to our yarn analogy. You’re trying to find one specific piece to cut but it’s deeply tangled in the mass of yarn. You need to find the piece that you really care about and clamp your fingers onto the yarn to reduce the slack — straighten it out — so you can cut it easily.
Think of your fingers as the insulators.
The insulators of the new piggyBac transposon tool perform the same task of stretching out the DNA so certain expressions through signaling pathways are held open, enabling the investigation of specific genetic material.
Hannink hypothesizes this new reporter could provide answers to questions like: Does an anti-migraine medicine have the component that will relieve that ailment? Does a multi-vitamin deliver all of the nutrients on its label?
“A lot of botanicals are said to have anti-inflammatory benefits,” Hannink said. “By using an assay like this, we can easily determine if they actually do and if so, what molecules in these complex mixtures are in fact the cause of the punitive inflammatory activity.”
Replication is a critical part of verifying scientific discovery and epigenetic silencing is a big headache for investigators trying to reproduce results.
Scientists studying genetic material can open certain expressions with other reporter tools but often, the cell will turn expressions off and block signaling pathways, causing an expected result to fail because of epigenetic silencing.
The new assay preserves conditions of an experiment so the same results can be reached. Cell behavior under the same conditions and expressions that were switched on during the experiment will be expressed.
The new version of the reporter assay is being used at the MU Center for Botanical Interaction Studies to understand how botanical compounds affect the immune system and in other research on the central nervous system and on the development of prostate cancer.
This research appeared in the Dec. 20, 2013 edition of PLoS ONE. It was funded by the University of Missouri Agriculture Experiment Station Laboratories and grants from the National Center for Complementary and Alternative Medicines, Office of Dietary Supplements and the National Cancer Institute.
Over the weekend, Bond LSC HIV researchers Stefan Sarafianos, Marc Johnson and Donald Burke-Aguero joined Trail to a Cure, Inc., a Columbia nonprofit organization that helped fund important HIV research.
Since 2008, the organization has raised $74,000 for HIV/AIDS research, with some of that funding going directly to the Bond LSC providing additional hours of lab research. The 2014 online fundraising is still open and donations can be made to Trail to a Cure, Inc. until the end of the month.
The funding from Trail to a Cure helps Bond LSC researchers train future scientists and physicians in labs and in some cases, training them on the development of next generation therapies, Johnson said.
A princess kisses a frog and it turns into a prince, but when a scientist uses a frog to find out more information about a grapevine disease, it turns into the perfect tool narrowing in on the cause of crop loss of Vitis vinifera, the world’s favorite connoisseur wine-producing varietal.
MU researchers recently published a study that uncovered a specific gene in the Vitis vinifera varietal Cabernet Sauvingon, that contributes to its susceptibility to a widespread plant disease, powdery mildew. They studied the biological role of the gene by “incubating” it in unfertilized frog eggs.
The study, funded by USDA National Institute of Food and Agriculture grants, was lead by Walter Gassmann, an investigator at the Bond Life Sciences Center and University of Missouri professor in the division of plant sciences.
The findings show one way that Vitis vinifera is genetically unable to combat the pathogen that causes powdery mildew.
Gassmann said isolating the genes that determine susceptibility could lead to developing immunities for different varietals and other crop plants and contribute to general scientific knowledge of grapevine, which has not been studied on the molecular level to the extent of many other plants.
The grapevine genome is largely unknown.
“Not much is known about the way grapevine supports the growth of the powdery mildew disease, but what we’ve provided is a reasonable hypothesis for what’s going on here and why Cabernet Sauvingon could be susceptible to this pathogen,” Gassmann said.
The research opens the door for discussion on genetically modifying grapevine varietals.
Theoretically, Gassmann said, the grapevine could be modified to prevent susceptibility and would keep the character of the wine intact — a benefit of genetic modification over crossbreeding, which increases immunity over a lengthy process but can diminish character and affect taste of the wine.
Grapevine under attack
Gassmann’s recent research found a link between nitrate transporters and susceptibility through a genetic process going on in grapevine infected with the powdery mildew disease.
Infected grapevine expressed an upregulation of a gene that encodes a nitrate transporter, a protein that regulates the makes it possible for the protein to enter the plant cell.
Once the pathogen is attracted to this varietal of grapevine, it tricks grapevine into providing nutrients, allowing the mildew to grow and devastate the plant.
As leaves mature, they go through a transition where they’re no longer taking a lot of nutrients for themselves. Instead, they become “sources” and send nutrients to new “sink” leaves and tissues. The exchange enables plants to grow.
The powdery mildew pathogen, which requires a living host, tricks the grapevine into using its nutrient transfer against itself. Leaves turn into a “sink” for the pathogens, and nutrients that would have gone to new leaves, go instead, to the pathogen, Gassmann said.
“We think that what this fungus has to do is make this leaf a sink for nitrate so that nitrate goes to the pathogen instead of going to the rest of the plant,” Gassmann said.
According to a report by the USDA, powdery mildew can cause “major yield losses if infection occurs early in the crop cycle and conditions remain favorable for development.”
Powdery mildew appears as white to pale gray “fuzzy” blotches on the upper surfaces of leaves and thrives in “cool, humid and semiarid areas,” according to the report.
Gassmann said powdery mildew affects grapevine leaves, stems and berries and contributes to significant crop loss of the Vitas vinifera, which is cultivated for most commercial wine varietals.
“The leaves that are attacked lose their chlorophyll and they can’t produce much sugar,” Gassmann said. “Plus the grape berries get infected directly, so quality and yield are reduced in multiple ways.”
Pinpointing a cause
Solutions to problems start with finding the reason why something is happening, so Gassmann and his team looked at a list of genes activated by the pathogen to find transporters that allowed compounds like peptides, amino acids, and nitrate to pass.
Genes for nitrate transporters, Gassmann said, pointed to a cause for vulnerability to the mildew pathogen.
Over-fertilization of nitrate increases the severity of mildew in many crop plants, according to previous studies sited in Gassmann’s article in the journal of Plant Cell Physiology.
The testing system for isolating and analyzing the genes began with female frogs.
Gassmann used frog oocytes (unfertilized eggs), to verify the similar functions of nitrate transporters in Arabidopsis thaliana, a plant used as a baseline for comparison.
A nitrate transporter, he hypothesized, would increase the grapevine’s susceptibility to mildew.
“The genes that were upregulated in grapevine showed similarity to genes in Arabidopsis that are known to transport nitrate,” Gassmann said. “We felt the first thing we had to do was verify that what we have in grapevine actually does that.”
The eggs are very large relative to other testing systems and act as “an incubating system” for developing a protein. Gassmann and his team of researchers injected the oocyte with RNA, a messenger molecule that contains the information from a gene to produce a protein. The egg thinks it’s being fertilized and protein reproduces and is studied.
“The oocyte is like a machine to crank out protein,” Gassmann said. “We use that technique to establish what we have is actually a nitrate transporter.”
The system confirmed that the gene isolated from grapevine encodes a nitrate transporter.
“We contributed to the general knowledge of the nitrate transporter family,” Gassmann said. “It turned out to be the first member of one branch of nitrate transporters that, even in Arabidopsis haven’t been characterized before.”
The mounting knowledge of Vitis vinifera genes could make genetically modifying the strain to prevent the susceptibility easier.
“Resistance is determined sometimes by a single gene,” Gassmann said. “Until people are willing to have the conversation of genetic modification, the only way to save your grapevines is to be spraying a lot.”
Sharon Pike, Gassmann, other investigators from the MU Christopher S. Bond Life Sciences Center and post-doctoral student, Min Jung Kim from Daniel Schachtman’s lab at the Donald Danforth Plant Science Center in Saint Louis, Mo. contributed to the report.
The article was accepted November 2013 into the Plant Cell Physiology journal.
Recently, one of our investigators, J. Chris Pires traveled to Fudan University in Shanghai and the Wuhan Vegetable Research Institute for the 19th annual Crucifer Genetic Workshop and Brassica 2014 Conference in Wuhan, China.
Pires was invited to the esteemed event as the keynote speaker of the Brassica Conference. He led workshops as part of the three-day conference March 30 through April 2 and also visited Fudan University in Shanghai during the trip.
Pires is an associate professor in biological sciences and focuses much of his research on the evolution of plants. His talk at Fudan University discussed his research on whole genome duplications and the origins of novelty in plants.
Every year the College of Agriculture, Food and Natural Resources puts on a Float Your Boat for the Food Bank Race. All proceeds go to the Columbia Food Bank and last year, with 45 participants, more than $17,000 was donated. All participants craft their own boat and obey one golden rule: cardboard only.
The Bond LSC crew are returning to the race, this year on April 12, with a Popeye themed boat they say will win it all. Cash donations are being accepted until the race day by Maureen Kemp in 106 at the Bond Life Sciences Center. The People’s Choice Award is given to the boat with the team that raised the most money for the Food Bank.
The difference between walking and being paralyzed could be as simple as turning a light switch on and off, a culmination of years of research shows.
Recently, University of Missouri Assistant Professor of biology Samuel T. Waters isolated a coding gene that he found has profound effects on locomotion and central nervous system development.
Waters’ work with gene expression in embryonic mouse tissue could shed light on paralysis and stroke and other disorders of the central nervous system, like Alzheimer’s disease.
Waters works extensively with two coding genes called “Gbx1” and “Gbx2”. These genes — exist in the body with approximately 20,000 other protein-coding genes — are essential for development in the central nervous system.
“To understand what’s going wrong, it’s critical that we know that’s right,” Waters said.
Coding genes essentially assign functions for the body. They tell your fingernail to grow a certain way, help develop motor control responsible for chewing and, as shown in Waters’ research, help your legs work with your spinal cord to facilitate movement.
Waters and his researchers, including graduate student Desiré Buckley, investigated the function of the Gbx1 by deactivating it in mouse embryos and observing their development over a 18.5-day gestation period — the time it takes a mouse to form.
The technology could eventually contribute to developing gene therapies for paralysis that happens at birth or from a direct result of blunt trauma, like a car accident.
“Understanding what allows us to walk normally and have motor control, allows us to have better insight for developing strategies for repairing neural circuits and therapies,” Waters said.
Technology for isolating genes and their functions
Waters studies embryonic mouse development. To understand certain gene functions, he inactivates different genes using a technology called “Cre-loxP.”
Genes can be isolated, then inactivated throughout embryonic tissue. Many of Waters’s studies inactivate genes to harness a better understanding of which genes are responsible for what.
“The relevance of it to the well-being of humans, is apparently relevant to development and more importantly to the development of the central nervous system,” Waters said. “Now it’s taking me to the point where we’re getting a bird’s eye view of what’s actually regulating our ability to have locomotive control.”
No Gbx1, no regular locomotion
Mice that Waters uses in his lab, “display a gross locomotive defect that specifically affects hind-limb gait,” according to their article published in Plos One, February, 2013.
In contrast to its family member Gbx2, when Gbx1 is inactivated, Waters concluded, the anterior hindbrain and cerebellum appear to develop normally. But neural circuit development in the spinal cord —- what allows us to walk normally —- is compromised, he said. According to an article published by
Waters, November 2013, in Methods in Molecular Biology, this occurs despite an increase in the expression level of its family member, Gbx2, in the spinal cord.
A video recording from the research, which was funded by the National Science Foundation and start-up funds from MU, show the mouse with the Gbx1 held back, with an abnormal hind-limb-gait.
Mice with this inactivated gene were otherwise normal, Waters said.
“If they were sitting there without moving, you wouldn’t know anything was wrong with them,” Waters said.” They’re able to mate, eat and appear to function normally.”
No Gbx2, no jaw mobility
When Gbx2 function is impaired in the mouse, Waters observed that development of the anterior hindbrain, including the cerebellum, a region of the brain that plays an important role in motor control, didn’t form correctly.
The mice, as a result, cannot suckle, so they die at birth, Waters said.
“We’re getting a better insight into the requirements for suckling — another motor function required for our survival,” Waters said.
The research has paved the way for investigating other coding genes and their responsibilities and roles in development, Waters said.
“We have a lot to do still,” Waters said. “So, why am I so excited about it? That’s part of the reason.”
The bridge between public knowledge and the inner-workings of the science community is one that many are reluctant to cross. Sometimes riddled with confusing terms, the most exciting discoveries aren’t always approachable.
The 10th annual MU Life Sciences & Society Symposium began Monday evening with Rebecca Skloot as she spoke to a nearly full house at Jesse Auditorium Monday. Every year the symposium erases the line between community understanding and the discoveries of the scientific community.
Skloot, the New York Times bestselling author of The Immortal Life of Henrietta Lacks, spoke about the power of science writing in making science more approachable, gave advice to scientists on spreading the word about their discoveries and gave an insight into to the decade of reporting she did for her book. Skloot autographed copies of the book following the talk.
This year’s theme, Decoding Science, speaks to the issue of communicating scientific issues and discoveries with the general public. Skloot said scientists need to keep terms and technicalities basic and exciting.
Jesse Hall was filled with an eclectic mix of community, faculty and students from MU many of which lined up following the talk for nearly 30 minutes of questions.
Throughout the week, the gap between the science community and the public will be bridged with an impressive list of speakers.
The symposium, organized by the Bond Life Sciences Center which houses researchers that represent various schools at the University of Missouri, is a week-long event that features many speakers prevalent in scientific communications.
Other events to catch this week
Tuesday The “Thoughts of Plants” will be uncovered 6 p.m. at Broadway Brewery. The talk, as part of the Science Café speaker series, will be lead by Dr. Jack Shultz, director of the Bond Life Sciences Center.
Wednesday Superhero Science 11 a.m. until noon at the Colonnade in Ellis Library. Superhero submissions will be judged by the spring symposium’s own superhero: “The Antidote.” Dressed in a mask and cape, MU professor Tim Evans’ alter ego, has spicing up the field of toxicology at MU for 12 years.
Thursday James Surowiecki, a contributor to The New Yorker, will speak at 7 p.m. Thursday at Bush Auditorium, Cornell Hall. Free admission and no ticket or registration required.
Saturday All Saturday talks will be held at Jesse Hall.
10:00 a.m. Bill Nye at Jesse Auditorium, doors open at 9:00 a.m. with overflow seating available at the Monsanto Auditorium at the Bond Life Sciences Center. Tickets are sold out. Nye, most well-known for his 1990’s show Bill Nye The Science Guy, has immersed youth in “fun science” by educating in easy-to-understand terms. Nye is one of the pioneers of science communication, trying to make science more approachable by the general public.
12:30 – 1:15 p.m. Chris Mooney is a science journalist and author of Unscientific America, The Republican Brain: The Science of Why They Deny Science and Reality, and New York Times bestselling The Republican War on Science.
1:20 – 2:10 p.m. Dominique Brossard, professor and chair of the Department of Life Sciences Communication at the University of Wisconsin, Brossard studies strategic communication and public opinion in science and risk communication.
2:30 – 3:15 p.m. Liz Neeley, assistant director of Science Outreach for COMPASS, leads communications training for scientists, specializing in social media and multimedia outreach. She previously studied tropical fish evolution.
3:20 – 4:05 p.m. Barbara Kline Pope, the executive director for communications for the National Academy of Sciences, leads the Science & Entertainment Exchange, which connects top scientists with the entertainment industry for accurate science in film and TV programming.
4:10 – 5:00 p.m. A recovering marine biologist, Randy Olson is an independent filmmaker and author of Don’t Be Such a Scientist and Connection: Hollywood Storytelling Meets Critical Thinking. Olsen is a leading proponent of storytelling in science communication. His films include “Flock of Dodos” and “Sizzle,” about evolution and climate change, respectively.