It’s been almost a week since the 2016 MU Life Sciences and Society Program Symposium, “Confronting Climate Change” wrapped up. If you missed the event, check out our Flickr gallery to see a little bit of the excitement.
We also had the chance to chat a few minutes with most of the LSSP speakers who graciously shared their insight on climate change in our lives. Check out these conversations on our YouTube page from the link at the top of the page.
Last but not least, we put together a radio piece for KBIA giving some speaker highlights. Visit our SoundCloud to see more.
Naomi Oreskes is a professor of the history of science at Harvard University and a geologist by training.
At a time when global warming was framed by the media as a debate, her 2004 paper in the journal Science showed that climate change was a settled fact among climate scientists. Of the 928 papers she sampled in her literature search, not a single author denied the reality of climate change. Digging further, Oreskes explored in her book, Merchants of Doubt, co-authored with Eric Conway, the people, organizations, and motivations behind climate science misinformation. From cigarettes and acid rain to global warming and the ozone hole, Oreskes and Conway uncovered how industries such as Big Tobacco and Big Oil employed a core group of ideologically-motivated scientists to fabricate doubt and stymie government regulations.
Naomi Oreskes speaks on Saturday,3:30 pm as part of the LSSP Symposium, “Combatting Climate Change,” held at the Bond Life Sciences Center.
What has been the response of people who, through reading Merchants of Doubt or watching the documentary, have changed their minds about climate change?
Many people have written to me and Erik Conway to thank us for writing the book. I’d say the most common response was that the book helped them to understand why there was so much opposition to accepting the scientific evidence. I can’t say that I know for sure that thousands of people changed their minds after reading the book, but I do know that among those who did, the link to the tobacco industry was most compelling. Our research showed that the opposition was not rooted in problems with or deficiencies in the science.
You said in an interview with Mongabay, “In our society, knowledge resides in one place, and for the most part, power resides somewhere else.” How can we hold accountable oil and gas companies which have quietly known since the early 1980s that burning fossil fuels contributes to global warming, but used their power to impede actions that would combat climate change?
I’m not a lawyer, so I cannot answer the legal aspects of this question, but state attorneys around the country are now looking into that question. As a citizen and a consumer, I can say this: One way we can hold companies accountable by not investing in them, and this is why I support the divestment movement. We can also boycott their products. In the current world, that is very difficult to do, but we can make a start. I installed an 8-watt solar PV system in my house, and we are now just about net-zero for electricity.
Is it possible to make up for 30 years of squandered time?
No of course not. Lost time is lost time. But knowing how much time has been lost, we should have a sense of urgency now, try not to lose any more.
Which strategies are being proposed for immediate climate action? Are environmental scientists and economists in agreement over which courses of action make the most sense?
Yes I think so. Nearly everyone who has studied the issue agrees that the most effective immediate action that is available to us is to put a price on carbon. This will immediately make renewables and energy efficiency more economically attractive, and it will send a signal to investors that fossil fuels will no longer be given a free pass for their external costs. This means that future returns will be greater in the non-carbon based energy sector. Anyone interested in this should read Nicolas Stern’s very informative book, Why are we Waiting?
How might the nomination of Merrick Garland to the Supreme Court and the results of the 2016 presidential elections affect the role that the US will play in combating climate change? Best case and worse case scenarios.
Best case: Republicans in Congress come to their senses, and listen to fellow Republicans like Bob Inglis, Hank Paulson, and George Schultz who have made the conservative case for putting a price on carbon. They can do this pretty much any way they want— through a tax, thru tradeable permits, or whatever. it’s clear Democrats would support either, and we know from experience that either approach can work, so long as the price is real (i.e., not just symbolic.) Right now Alberta is talking about $20—that is probably a bit low. BC is at $30
Of all the important issues out there, what motivates you to devote your time and energy to fighting climate change?
Oh that’s a good question. I didn’t decide to work on climate change, I fell into it when Erik Conway and I tripped over the merchants of Doubt story. Then, as I learned more and more about the issue, I came to appreciate scientists’ sense of urgency about it.
The 12th annual Life Sciences & Society Program symposium — with events from March 17 to 19 — will tackle one of the most pressing issues facing the world today. Titled “Combating Climate Change,” speakers will address topics such as using technology to help curb global warming, how rising temperatures and more extreme weather will impact human health, the role of government in taking action to combat man-made climate change, and how to effectively communicate climate change.
Marcia McNutt–editor-in-chief of the leading journal, Science, and a geophysicist by training—will talk about the “promise and peril” of climate interventions such as carbon dioxide removal (CDR) and albedo modification, a process that involves spraying particles into the atmosphere to reflect more sunlight back into space to cool the earth.
There has been “significant advancement” in technologies such as carbon capture and storage, McNutt wrote by email, but these technologies have not moved beyond the research stages for economic reasons.
She pointed out that most climate interventions act slowly and take time to implement.
Albedo modification is the exception, McNutt said, but while quite a bit of work has been done to model its effects, the risks are high.
Few scientists believe we know enough about albedo modification to seriously consider it, she said.
“There is no silver bullet that is a magical antidote to climate change,” McNutt said.
The full line-up of speakers for this year’s symposium includes:
Andrew Revkin, environmental journalist and author, who proposed the term “anthrocene” to describe “a geological age of our own making” in his 1992 book, Global Warming: Understanding the Forecast. (Paul Crutzen, an atmospheric chemist who won a Nobel prize for studying ozone layer depletion , popularized the more familiar term, ”Anthropocene,” in 2000.)
Wes Jackson, founder and president of The Land Institute, a non-profit organization dedicated to sustainable agriculture
Marshall Shepherd, professor of geography and director of the atmospheric science program at the University of Georgia
George Luber, an epidemiologist at the Center for Disease Control and the associate director for climate change in the division of environmental hazards and health effects
Naomi Oreskes, professor of the history of science at Harvard University. Her book co-written with Erik M. Conway, Merchants of Doubt, showed how rich and powerful industries retained a core group of scientists who used their expertise to create doubt and protect industry interests
To see the schedule of this week’s events and register for the symposium, visit the MU LSSP website.
How unruly data led MU scientists to discover a new microbiome By Roger Meissen | MU Bond Life Sciences Center
This seminal vesicle contains a newly-discovered microbiome in mice. Some of its bacteria, like P. acnes, could lead to higher occurrences of prostate cancer. | contributed by Cheryl Rosenfeld
It’s a strange place to call home, but seminal fluid offers the perfect environment for particular types of bacteria.
Researchers at MU’s Bond Life Sciences Center recently identified new bacteria that thrive here.
“It’s a new microbiome that hasn’t been looked at before,” said Cheryl Rosenfeld, a Bond LSC investigator and corresponding author on the study. “Resident bacteria can help us or be harmful, but one we found called P. acnes is a very important from the standpoint of men. It can cause chronic prostatitis that results in prostate cancer. We’re speculating that the seminal vesicles could be a reservoir for this bacteria and when it spreads it can cause disease.”
Experiments published in Scientific Reports — a journal published by Nature — indicate these bacteria may start disease leading to prostate cancer in mice and could pass from father to offspring.
A place to call home
From the gut to the skin and everywhere in between, bacterial colonies can both help and hurt the animals or humans they live in.
Seminal fluid offers an attractive microbiome — a niche environment where specific bacteria flourish and impact their hosts. Not only is this component of semen chockfull of sugars that bacteria eat, it offers a warm, protected atmosphere.
“Imagine a pond where bacteria live — it’s wet it’s warm and there’s food there — that’s what this is, except it’s inside your body,” said Rosenfeld. “Depending on where they live, these bacteria can influence our cells, produce hormones that replicate our own hormones, but can also consume our sugars and metabolize them or even cause disease.”
Rosenfeld’s team wasn’t trying to find the perfect vacation spot for a family of bacteria. They initially wanted to know what bacteria in seminal fluid might mean for offspring of the mice they studied.
“We were looking at the epigenetic effects — the impact the father has on the offspring’s disease risk — but what we saw in the data led us to focus more on the effects this bacterium, P. acnes, has on the male itself,” Rosenfeld said. “We were thinking more about effect on offspring and female reproduction — we weren’t even considering the effect the bacteria that live in this fluid could have on the male — but this could be one of the more fascinating findings.”
But, how do you figure out what might live in this unique ecosystem and whether it’s harmful?
First, her team found a way to extract seminal fluid without contamination from potential bacteria in the urinary tract.
“We gowned up just like for surgery and we had to extract the fluid directly from the seminal vesicles to avoid contamination,” said Angela Javurek, primary author on the study and recent MU graduate. “You only have a certain amount of time to collect the fluid because it hardens like glue.”
Once they obtained these samples, they turned to a DNA approach, sequencing it using MU’s Genomics Technology Core.
They compared it to bacteria in fecal samples of the same mice to see if bacteria in seminal fluid were unique. They also compared samples from normal mice and ones where estrogen receptor genes were removed.
The difference in the data
It sounds daunting to sort and compare millions of DNA sequences, right? But, the right approach can make all the difference.
“A lot of it looks pretty boring, but bioinformatics allow us to decipher large amounts of data that can otherwise be almost incomprehensible,” said Scott Givan, the associate director of the Informatics Research Core Facility (IRCF) that specializes in complicated analysis of data. “Here we compared seminal fluid bacterial DNA samples to publicly available databases that come from other large experiments and found a few sequences that no one else has discovered or at least characterized, so we’re in completely new territory.”
The seminal microbiome continued to stand out when compared to mouse poop, revealing 593 unique bacteria.
One of the most important was P. acnes, a bacteria known to cause chronic prostatitis that can lead to prostate cancer in man and mouse. It was abundant in the seminal fluid, and even more so when estrogen receptor genes were present.
“We’re essentially doing a lot of counting, especially across treatments to see if particular bacteria species are more common than others,” said Bill Spollen, a lead bioinformatics analyst at the IRCF. “The premise is that the more abundant a species is, the more often we’ll see its DNA sequence and we can start making some inferences to how it could be influencing its environment.”
Although this discovery excites Rosenfeld, much is unknown about how this new microbiome might affect males and their offspring.
“We do have this bacteria that can affect the male mouse’s health, that of his partner and his offspring,” Rosenfeld said. “But we’ve been studying microbiology for a long time and we still find bacteria within our own bodies that nobody has seen before. That blows my mind.”
How food cravings and eating affects the brain By Jennifer Lu | MU Bond Life Sciences Center
When it comes to cookie dough, we’re not the only ones who can’t control our cravings. Kyle Parker’s rats couldn’t resist, either, thanks to a tweak in their brain chemistry.
Matthew Will, associate professor of psychological sciences at the Bond Life Sciences Center, studies the neuroscience of behaviors such as over-eating and addiction | photo by Jennifer Lu, Bond LSC
Parker studies the neuroscience of food-based rewards.
“It’s like when I eat dessert after I’ve eaten an entire meal,” said Parker, a former grad student from the lab of Bond LSC’s Matthew Will. “I know that I’m not hungry, but this stuff is so good so I’m going to eat it. We’re looking at what neural circuitry is involved in driving that behavior.”
Behavior scientists view non-homeostatic eating — that’s noshing when you’re not hungry — as a two-step process.
“I always think of the neon sign for Krispy Kreme donuts.” Will said, by way of example.
“The logo and the aroma of warm glazed donuts are the environmental cues that kick-start the craving, or appetitive, phase that gets you into the store. The consummatory phase is when you “have that donut in your hand and you eat it.”
Parker activated a “hotspot” in the brains of rats called the nucleus accumbens, which processes and reinforces messages related to reward and pleasure.
He then fed the rats a tasty diet similar to cookie dough, full of fat and sugar, to exaggerate their feeding behaviors. Rats with activated nucleus accumbens ate twice as much as usual.
But when he simultaneously inactivated another part of the brain called the basolateral amygdala, the rats stopped binge eating. They consumed a normal amount, but kept returning to their baskets in search for more food.
“It looked like they still craved it,” Will said. “I mean, why would a rat keep going back for food but not eat? We thought we found something interesting. We interrupted a circuit that’s specific to the feeding part — the actual eating — but not the craving. We’ve left that craving intact.”
To find out what was happening in the brain during cravings, Parker set up a spin-off experiment. Like before, he switched on the region of the brain associated with reward and pleasure and then inactivated the basolateral amygdala in one group of rats but not the other.
This time, however, he restricted the amount of the tasty, high-fat diet rats had access to so that both groups ate the same amount.
This way, both groups of rats outwardly displayed the same feeding behaviors. They ate similar portions and kept searching for more food.
But inside the brain, Parker saw clear differences. Rats with activated nucleus accumbens showed increased dopamine production in the brain, which is associated with reward, motivation and drug addiction. Whether the basolateral amygdala was on or off had no effect on dopamine levels.
However, in a region of the brain called the hypothalamus, Parker saw elevated levels of orexin-A, a molecule associated with appetite, only when the basolateral amygdala was activated.
“We showed that what could be blocking the consumption behavior is this block of the orexin behavior,” Parker said.
The results reinforced the idea that dopamine is involved in the approach — or the craving phase — and orexin-A in the consumption, Will said.
Their next steps are to see whether this dissociation in neural activity between cravings and consumption exists for other types of diets.
Will also plans to manipulate dopamine and orexin-A signaling in rats to see whether they have direct effects on feeding.
“Right now, we know these behaviors are just associated with these neural circuits, but not if they’re causal.”
Scientists explore genetic similarities between plants and mice
University of Missouri PhD Candidate Daniel L. Leuchtman peers through an Arabidopsis plant. Leuchtman has been experimenting with replacing a gene in the plants immune system with a similar gene from mice. | Photograph by Justin L. Stewart/MU Bond Life Sciences Center
By Justin L. Stewart | MU Bond Life Sciences Center
Almost two-thirds of what makes a human a human and a fly a fly are the same, according to the NIH genome research institute.
If recent research at the University of Missouri’s Bond Life Sciences Center is verified, we’ll soon see that plants and mice aren’t all that different, either.
Dan Leuchtman studies a gene in Arabidopsis plants called SRFR1, or “Surfer One.” SRFR1 regulates plant immune systems and tell them when they are infected with diseases or illnesses. Leuchtman studies this model plant as a Ph.D. candidate at MU, splitting time between the labs of Walter Gassmann and Mannie Liscum.
His research involves breeding Arabidopsis plants missing the SRFR1 gene and then replacing it with the MmSRFR1 gene.
A series of Arabidopsis plants show the differences between the plants, from left, without SRFR1, with MmSRFR1 and with SRFR1. | Photograph by Justin L. Stewart/MU Bond Life Sciences Center
So, what is MmSRFR1? Leuchtman and company believe it’s the animal equivalent of SRFR1, though they aren’t fully aware of all of its’ functions.
“We’re actually one of the first groups to characterize it,” Leuchtman said.
Arabidopsis plants missing the SRFR1 gene struggle to grow at all, appearing vastly different from normal plants. Leuchtman says that a plant missing the SRFR1 gene is a mangled little ball of leaves curled in on itself. “It’s really strange looking.”
While his experiments haven’t created statuesque plants equal to those with natural SRFR1 genes present, the Arabidopsis plants with MmSRFR1 show a notable difference from those completely lacking SRFR1. Leuchtman says the plants with MmSRFR1 lie somewhere in between a normal plant and one lacking SRFR1.
University of Missouri PhD Candidate Daniel L. Leuchtman poses for a portrait in a Bond Life Sciences Center greenhouse. Leuchtman has been experimenting with replacing a gene in Arabidopsis plants immune system with a similar gene from mice. | Photograph by Justin L. Stewart/MU Bond Life Sciences Center
“At its’ core, it’s more understanding fundamental biology. How do we work? How do organisms tick? How do you go from DNA in a little bag of salts to a walking, talking organism?” Leuchtman said. “The more you know about how an organism functions, the more opportunities you have to find something that makes an impact.”
Bond LSC is now producing monthly segments for KBIA, Columbia’s NPR station at 91.3 FM.
This month highlights the work of Melissa Mitchum, a molecular plant nematologist at Bond LSC and an associate professor of Plant Sciences in the College of Agriculture, Food and Natural Resources.
She studies nematodes, a pest that cost soybean farmers billions of dollars each year. Her lab recently helped discover that this tiny parasite produces molecules that mimic plant hormones in order to siphon nutrients from soybean roots.
Tune in at 12:30 to hear her profile or visit the Soundcloud link above to hear the segment.
You can imagine it’s hard to distinguish yourself from the crowd when it comes to scientific papers.
But, publishing quality work in a well-known journal adds value to the whole scientific world by assisting others and inspiring new science. Three Bond LSC researchers recently were recognized for doing just that.
Bond Life Sciences Center scientists Chris Pires, Shuqun Zhang and Yidong Liu are among five University of Missouri System researchers named in the 2015 Thomson Reuters’ Highly Cited Researchers list.
This list spotlights the top 1 percent of papers published from nearly 9 million scientists and scholars. The Highly Cited Researchers 2015 list represents the world’s most influential scientific minds from 21 scientific fields. The rankings are based on how often scientific papers published in the last decade get cited in newly published research, according to Essential Science Indicators (ESI), a component of the Web of Science.
Chris Pires, associate professor of Biological Sciences, studies the evolution of plants by looking at changes in their genetics over millions of years. Pires published work in 2015 looking at how plant defenses evolved in tandem with the defenses of caterpillars that feed on them.
Shuqun Zhang is a Distinguished Researcher from the MU College of Agriculture, Food and Natural Resources and a professor of Biochemistry. His research seeks to improve plants’ response to adverse environmental conditions. By identifying molecular targets that aid in protecting crops from disease, his research aims to help create healthier, more productive agricultural products. In particular, he focuses on a family of enzymes called mitogen-activated protein kinases (MAPKs) that are involved in plant cell-to-cell communication and plant interaction with its environment.
Yidong Liu is a senior research specialist from MU’s Department of Biochemistry that manages Shuqun Zhang’s lab. She also works on MAPKs and their role in plant defense responses such as pathogen-induced ethylene biosynthesis and phytoalexin induction.
The Bond Life Sciences Center is an interdisciplinary research center at the University of Missouri exploring problems in human and animal health, the environment and agriculture since 2004. Learn more about our research by visiting bondlsc.missouri.edu.
Marc Johnson, associate professor of molecular microbiology and immunology at the Bond Life Sciences Center, studies viruses such as HIV. | photo by Jennifer Lu, Bond LSC
Nineteen colorful foam flowers decorate the walls of Marc Johnson’s office, a memento from his lab members when they “redecorated” while he was out of town.
Each flower is labeled in bold Sharpie with the names of viruses and viral proteins that his lab studies—MLV, RSV, Gag, Pol, to name a few.
One flower stands out, marked in capital letters: H-I-V.
Johnson, an associate professor of molecular microbiology and immunology, is one of four researchers at Bond LSC who studies HIV, the virus that leads to AIDS. His research focuses on understanding how HIV assembles copies of itself with help from the cells it infects.
Like most viruses, HIV hijacks cellular functions for its own purposes.
“It has this tiny itty bitty little genome and yet it can infect 30 million people,” Johnson said. “It doesn’t do it by itself.”
To understand how viruses reprogram the proteins in our bodies to work against us, he said, you have to understand the cells they infect. If cells were a chamber, then viruses are the keyhole.
For example, cells use a protein called TSG101 to dispose of unwanted surface macromolecules by bending a patch of cellular membrane around the macromolecule until it is surrounded inside a membrane bubble. The process, like trapping a bug inside a sheet of tissue paper, is called budding.
The cell sweeps all the pinched-off bubbles into a larger receptacle, or multivesicular body. These bodies, Johnson said, act as the cell’s garbage collection system. To dispose of the trash, the compartments become acidic enough to disintegrate everything inside or fuse with the cell membrane so that the trash gets dumped outside the cell.
It’s like in the second Star Wars movie, “The Empire Strikes Back,” Johnson said. “They just drop all their garbage before they go into hyperspace, and that’s how the Millennium Falcon got out.”
HIV uses the same housekeeping mechanism to break out of infected cells and infect more cells, but it remains unclear which other host proteins HIV commandeers.
“It’s all part of the puzzle,” Johnson said.
THE GAME CHANGER
On his desk, Johnson keeps a white legal pad with a list of 16 projects written in blue ink.
Marc Johnson observes cells modified with CRISPR under the microscope. | photo by Jennifer Lu, Bond LSC
“Things make it off the list or they’ll get added,” Johnson said. “Or they’ll spend years on the back burner. I have a lot of projects.”
One of the biggest projects involves using CRISPR/Cas9 — a precision gene-editing tool — to identify genes that make a cell resistant to viral infections.
“It’s a game changer. It really is,” Johnson said. “It’s so cool.”
The technology uses a missile-like strand of guide RNA to target specific sites in the genome for deletion. Before CRISPR, scientists had to suppress gene expression using methods that were neither permanent nor absolute.
But because CRISPR manipulates the genome itself, Johnson said, there’s less doubt about what is happening.
Using the CRISPR library, the Johnson lab can scan the effects of 20,000 unique gene deletions in a population of cells. When these cells, each of which contains a different deleted gene, are exposed to HIV, not all of them die. Those that survive can cue researchers in to which genes might be important for blocking HIV infection.
And if another researcher has doubts that a gene is truly knocked out, Johnson said, you can tell them, “I’ll just send you the cell line. You try it and see for yourself.”
A DAY IN THE LIFE
The Johnson lab is a tight-knit group that consists of a lab manager, two grad students, a postdoc and four undergrads.
Dan Cyburt — a third year grad student — studies molecules that interact with proteins that keep HIV from infecting the cell, such as TRIM5α. TRIM5α, a restriction factor, blocks replication of the viral genome.
Graduate student Yuleum Song prepares cells for viral infection in the BL-2 hood. | Image by Jennifer Lu, Bond LSC
Fourth year grad student Yuleum Song focuses on how the viral envelope protein, Env, is packaged into viruses before they break free from cells. While Env isn’t necessary for viral assembly and release, she said, it’s critical for the infection of new cells.
Undergrads work in a tag team, picking up where the other left off, to generate a collection of new viral clones.
And lab manager Terri Lyddon keeps day-to-day experiments on task.
Lyddon, who has been with the Johnson lab for ten years, spends much of her day working with cells inside the biosafety level 2 hood. The area is specifically designated for work with moderately hazardous biological agents such as the measles virus, Samonella bacteria, and a less potent version of HIV.
Normally, HIV contains instructions in its genome for making accessory proteins that help the virus replicate, but the HIV strains used in the Johnson lab lack the genes for some of these proteins. That means the handicapped viruses can infect exactly one round of cells and spread no further.
Lyddon also ensures quality control for the lab by making sure students’ work is reproducible.
As a pet project, Johnson also independently confirms new findings reported in academic journals about HIV. Sometimes, Johnson says, the phenotypes that get published are not wrong, but they tend to represent the best outcomes, which might only exist in very specific scenarios.
“They’re only right by the last light of Durin’s day,” Johnson said, making a Lord of the Rings reference to a phenomenon in The Hobbit that reveals the secret entrance to a dwarven kingdom only once a year.
Because scientists base their work on the research of other scientists, he said, it’s always important to check.
A RECONSIDERED POSITION
According to the World Health Organization, 37 million people worldwide in 2014 have HIV or AIDS. The virus infects approximately two million new individuals every year. Breakthroughs in treatment have turned the autoimmune disease from a highly feared death sentence into a chronic and manageable condition.
For the longest time, HIV researchers scrambled to find better therapies against HIV why trying to develop a vaccine that could prevent AIDS.
But in the past five years, Johnson says he’s noticed a shift: researchers are gaining confidence in the possibility of finding a cure, something he once thought was impossible.
“Now it’s been demonstrated that it’s possible to cure a person,” Johnson said, referring to the Berlin patient. “So it’s only going to get easier.”
However, Johnson pointed out, most people would never undergo the kind of high-risk treatment that Timothy Ray Brown, the Berlin patient, received. Brown underwent a bone marrow transplant to treat his leukemia, and his new bone marrow, which came from an HIV-resistant donor, cured him of AIDS.
A “full blown cure” will be hard to attain, but Johnson believes there may be ways for HIV patients to live their lives without having to constantly take medication.
As an example, he points to certain “elite controllers” who are HIV positive but never progress further to show symptoms of AIDS. If scientists can figure out what’s different about their immune systems, Johnson said, then researchers could train the immune response in AIDS patients to resist HIV or keep it in check.
That’s a project for the immunologists. As a basic scientist, Johnson says he adds to the knowledge of how HIV works.
“I am not thinking about a therapy,” Johnson said, “but I’m also acutely aware that some of the best solutions come from basic science. “
Even though scientists haven’t discovered all the mechanisms behind cellular and viral function yet, Johnson said, the rules do exist.
“The sculpture is already there in the stone,” he said.
Johnson’s job is to chip away at the marble until the rules are found.
MU freshman follows in aunt’s footsteps while exploring career options
Robert Schmidt poses with one of the cats that lives at Horton Animal Hospital, where he works part-time. Schmidt, a freshman studying biochemistry at the University of Missouri, is a member of the Discovery Fellows Program where he is learning about plant genetics by working with biologist Scott Peck in the Bond Life Sciences Center. Photo by Justin L. Stewart | MU Bond Life Sciences Center
By Justin L. Stewart | MU Bond Life Sciences Center
Sometimes it’s socks. Another time, it was a book cover.
Robert Schmidt has retrieved quite a few things from misguided pets’ digestive systems as an assistant at Horton Animal Hospital, where he’s worked with his aunt for the past three years.
While most of the time he helps with simpler things — such as feeding kenneled animals or spaying and neutering pets — he also has amputated a dog’s toe after it had a lawnmower mishap.
Schmidt says he’s kind of following in his aunt’s footsteps. She majored in biochemistry at the University of Missouri and studied at its veterinary school, too. That’s what Robert wants to do with his life.
Schmidt demonstrates to a pet owner how to apply ear medication to a nervous small dog at Horton Animal Hospital on Forum. Schmidt works at the animal hospital part-time with his aunt. Photo by Justin L. Stewart | MU Bond Life Sciences Center
Schmidt likes working with animals, but pets aren’t the only animals he’s interested in. An internship at the MU Animal Sciences Research Center two summers ago had Schmidt elbow deep in fistulated cows’ stomachs as he assisted in research that tested the affects of adding different metals in cows feed to help them better absorb protein.
“My family’s always had a dog, my sister has a cat and I work at a small animal clinic. For a while, I was just like, ‘I’m not going to work with cows. I didn’t grow up on a farm.’ But now, after the internship, I’m interested in getting some more experience.”
As a freshman in the Discovery Fellows Program, Schmidt now finds himself knuckle deep in dirt as he digs into plant genetics.
The Discovery Fellows Program pairs first-semester freshmen and sophomores with scientists in their chosen field, allowing them to get hands-on experience in research on campus while earning a $1,700 stipend.
That led Schmidt, an MU Honors College student, to the lab of biologist Scott Peck in the Bond Life Sciences Center.
Schmidt plants Arabidopsis seeds in a petri dish inside the Bond Life Sciences Center, where his fellowship work is. Photo by Justin L. Stewart | MU Bond Life Sciences Center
Peck studies how plants recognize and respond to infections, specifically focusing on three proteins that begin to chemically modify shortly after a plant is infected.
No one knows what these proteins actually do, Peck said, making the research that much more interesting.
Schmidt has been growing Arabidopsis seeds of three different types, each missing one of the three proteins. Once those seeds have fully grown, Schmidt said they will cross-pollinate the three variations to hopefully create a plant without any of those three proteins.
He hopes to have triple mutants by early next semester, so they can experiment with them to better understand the roles of the absent proteins.
While Schmidt came into Peck’s lab with more of an interest in animals, he sees how the skills translate.
“If I worked with animals, I’d want to do genetics and I’m doing genetics with plants right now. A lot of the lab techniques are transferable.”
Schmidt moves an Arabidopsis seedling from a petri dish to fresh soil with the rest of the grown seedlings. Arabidopsis can grow from seed to seedling with two weeks. It’s a favorite among scientist, according to the National Science Foundation. Photo by Justin L. Stewart | MU Bond Life Sciences Center
Like most freshman, the former Rockbridge Valedictorian is still figuring out his life plans. He’s considering a double major in math, a favorite subject of his, and now wonders whether he might attend graduate school instead of vet school.
“I really like learning, being in a classroom and being a student. I really enjoy that. I think research is almost like a career where you’re almost always a student. You’re just always learning.”
As for now, he’s just waiting for his first batch of Arabidopsis seeds to mature.
Chris Pires
Yidong Liu is a senior research specialist from MU’s Department of Biochemistry that manages Shuqun Zhang’s lab. She also works on MAPKs and their role in plant defense responses such as pathogen-induced ethylene biosynthesis and phytoalexin induction.
