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Bond Life Science Investigator honored with two distinctions

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Chris Pires in his greenhouse in the Bond Life Sciences Center.

By: Samantha Kummerer, Bond LSC

“If you told me when I was an undergrad at Berkley or when I was working at a consulting firm in San Francisco when I was 22 that I would be a professor in Missouri working on broccoli, I would have laughed my ass off,” Bond Life Sciences investigator Chris Pires admitted.

But that work on broccoli has taken him far.

Pires recently received the 2017 Chancellor’s Award for Outstanding Faculty Research and Creative Activity in Biological Sciences.

Pires was also elected as a Fellow of the American Association for the Advancement of Science. The honor places Pires alongside other AAAS fellows including Thomas Edison and Margaret Mead as well as some of the most productive faculty members at MU.

The awards add to a long list of honors received over the years ranging from Thomas Reuters’ Highly Cited Researcher to MU Outstanding Research Mentor.

Despite being no stranger to awards, his impact still surprises him.

“For me what’s nice is people who I’ve had some impact on in the past say things,” he said smiling.

Both recent distinctions cite his contributions to plant evolution and sequencing of genomes and their impact towards improving crops and understanding biodiversity.

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Chris Pires, a Bond Life Sciences Center researcher, accepts an award from MU Chancellor Alexander Cartwright. Pires won the 2017 Chancellor’s Award for Outstanding Faculty Research and Creative Activity in Biological Sciences. | Photo by Kate Anderson.

While his work on polyploidy and hybridization on plants is internationally renowned and even earned a shout out on the television show “The Big Bang Theory”, the findings go right over the average person’s head.

So, instead, he compares his research to dogs.

Golden Retrievers and Chihuahuas don’t look alike but both are dogs. This is the same for broccoli, kale and cabbage — they are all are apart of the same genus of plants, Brassica.

Pires said he started using that analogy after years of getting the conversation wrong.

One of Pire’s passions is communicating the research he does, including clearing up misconceptions surrounding scientists and professors.

Some days he compares his lab and 80-hour workweek to the life of a small business owner running a multi-million dollar business. Other days it’s a football coach.

“I do all those things, you just don’t know it. I train people, I hire people, I fire people, I do communication, I spend a lot of times applying for grants, I give talks,” he said comparing duties of a coach to his everyday life.

He is also a talent scout.

Pires travels the world and visits MU undergraduate research fairs searching for students passionate about making a difference and are able to answer a simple question: Why?

“They just have to have an answer,” he said. “What I don’t want is the students where it’s just the next step in life.”

The passionate and devoted teams he builds pays off.

He has put out more than 140 publications during his career, 11 in 2017.

His success he attributes back to team science.

“I’m being recognized for stuff my lab does and all the people I collaborate with, so I’m happy to be acknowledged for the achievements of our group,” Pires said.

As the researcher looks on to his future at the university he said he hopes to transition from mentoring undergraduates to mentoring faculty and post-doctoral students.

Pires also wants to be a part of helping to foster cross-discipline research teams both inside Bond LSC and across campus.

While it’s not where he expected to he’d be, it’s where he found his passion. Now he is committed to helping his students get their dream job even if it changes along the way.

“A good day is when I go into the lab and I feel like I’m impacting the six or seven people in my lab but when you realize your impact has maybe been bigger than you realize, that’s nice because you just don’t know,” Pires said.

Chris Pires is a Bond Life Sciences’ Investigator and Biological Sciences professor at the University of Missouri. He is also a member of the Interdisciplinary Plant Group and MU Informatics Institute. He received his bachelors in biology at the University of California, Berkeley and his Ph. D. in Botany from the University of Wisconsin.

Madeline McFarland #IAmScience

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Madeline McFarland, a senior biochemistry major, works in the Burke Lab in Bond LSC. | photo by Allison Scott, Bond LSC

Science isn’t limited to the lab. It’s more of a mindset than a discipline, and Madeline McFarland knows this all too well.

As a senior biochemistry major working in Donald Burke’s lab in Bond LSC, McFarland experiments with ribonucleic acid (RNA) to study the origin of life before DNA and protein served as genetic material and catalyst, respectively.

“I’m interested in the RNA World Hypothesis and how RNA may have played a role in getting life started on our planet,” McFarland said.

This hypothesis suggests early forms of life on Earth may have relied solely on RNA to store genetic information and to catalalyze, or spur, chemical reactions. The theory goes that DNA eventually evolved to take its place due to the instability and ineffectiveness of RNA.

In the lab, McFarland focuses on using a program called systematic evolution of ligands by exponential enrichment (SELEX), which filters the RNA so she can find which strands do what she’s looking for. Specifically, she’s trying to determine if the RNA can make a reaction happen. If McFarland can find this connection, scientists would see that as support for for the RNA World Hypothesis.

“I’m trying to see which RNAs can perform a catalytic function,” McFarland said. “By doing that, we can kind of start to think about how RNA used to function in early earth.”

Her typical day starts at 9 a.m. when she heads to Bond LSC to get her experiments set up for the day.

“I go to class while they’re incubating,” McFarland said. “My science allows me to set stuff up and have a break while it’s running. I’m usually running experiments four days a week.”

McFarland was inspired by the work being done in Bond LSC and the analytical way of thinking about experiments.

“[Research] is kind of nailed into you as soon as you step on campus,” McFarland said. “That was the motivating factor, but I came to love it for a lot of reasons. It’s really shaped the way I think about things.”

When she’s not wearing her lab coat and investigating the origins of life, McFarland spends her time working in environmental efforts at Mizzou.

“I’m really passionate about sustainability in all of its forms: environmental, economic and social,” McFarland said. “I lead the electronic waste drives around campus, and I’m co-directing sustainability week this year.”

McFarland is also a co-president of the biochemistry club.

“In our meetings, we bring in grad students and faculty to talk about career options, so everyone can ask questions,” McFarland said. “We also do fun events. Last night, we had a biochemistry-themed breakout room. They had to balance chemical equations and transcribe and translate a DNA sequence to spell out a word. We have a lot of fun with it.”

All of her work in the lab in combination with her research at Bond LSC has only strengthened her bid for her next endeavor: medical school.

“I’m passionate about communicating science, and I think medicine would allow me to do that,” McFarland said. “I like the idea of radiology because it allows you to look at an image, or data, then think through things on your own, which is a lot like research.”

If she doesn’t end up at medical school, McFarland would like to continue to pursue education. She could see herself attending graduate school.

“I’m interested in a master’s in public health,” McFarland said. “It would allow me to expand my knowledge of science and how it relates to health beyond the scope of the lab.”

Regardless of if she continues to learn through medical or graduate school, though, McFarland credits research for having an immense impact on her career.

“Research has really shaped the way I think about things,” McFarland said.

Inside agriculture’s hottest controversy: dicamba

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A soybean plant grows in the Bond Life Sciences Center’s greenhouse. | Photo by Samantha Kummerer, Bond LSC.

By Samantha Kummerer, Bond Life Sciences Center

Every summer, MU Bond Life scientists Gary and Bing Stacey plant soybeans. In the summer of 2016, they were testing mutant crops’ tolerance to different herbicides. Among the multiple weed killers tested was one called dicamba.

The researchers knew this particular chemical was tricky so they turned to an expert to apply it, MU herbicide researcher Kevin Bradley.

The next morning, a soybean breeder with a neighboring plot discovered his soybeans were damaged.

“These were plots where some of his graduate students experimented so they basically couldn’t use any of their data and we felt terrible, but we explained to them we took every precaution we could possibly take but it was this vaporization that took place,” Gary Stacey explained.

What Gary Stacey didn’t understand at the time was dicamba has an ability to travel even after it is sprayed. The herbicide doesn’t just kill weeds, it kills or damages everything not engineered to be resistant to it.

“So let’s say I spray it in this spot right here. You would think its localized but if the temperature and humidity conditions are right it will vaporize and come up and then go into the air,” Gary Stacey said.

Just how far it can travel and how much damage it can achieve was realized all too well by farmers throughout the country this year.

An estimated 3.5 million acres of soybeans were damaged this summer.

One obvious solution may be to simply stop using the weed killer. But the issue is not that simple.

“This is the hardest issue I can remember because there are good responsible farmers on either side of the issue,” said Missouri Farm Bureau president Blake Hurst.

With so much on the line for all sides, dicamba has tangled farmers, corporations and researchers together in a controversial issue.

Bradley is right in the middle. He’s received calls from farmers who just lost 10 percent of their income for nothing they did wrong.

He’s also received calls from people who are upset by any suggestion that anything about the chemical is wrong. These are the farmers who need dicamba to control weeds that are no longer responding to the traditional weed killer Roundup.

“I’ve had the farmers who planted the traits saying ‘These are my highest yields ever how can you say these things?’ And their neighbor across the road just lost 20 bushels an acre because of your highest yields ever. It’s just a very personal issue for each person involved,” Bradley explained.

One case got so personal that a farmer in Arkansas allegedly shot his neighbor.

“I’ve been here for 14 years and I’ve been doing this kind of work for 20, never seen anything like this is agriculture. Period. Never seen this level of controversy between farmer to farmer and farmer to company or between company and university people. I’ve never seen anything like this,” Bradley said.

Dicamba is not a new formulation, but its use is. Monsanto developed genetically modified soybeans and cotton seeds that are resistant to dicamba. One of the problems farmers are pointing to is that Monsanto released the new seeds while still in the process of developing a better formula of dicamba. The new formula aimed to reduce volatilization, a tendency to vaporize after being sprayed on fields and then drift to neighboring areas. Monsanto claims the new formula reduces volatility by 90 percent, but Bradley said 90 percent is not 100 percent.

Bradley’s work has been consumed by this single herbicide as he tries to find the truth of what aspect of dicamba is causing the damage.

In Bradley’s eyes, there are four factors contributing to the widespread damage: physical drift mistakes (spraying with the wind, nozzle not attached correctly), tank contamination, temperature inversion, and volatility.

These factors are recognized by other researchers and Monsanto. The disagreement is over which factor is most at fault.

“Monsanto has a pretty high number for the farmer fault percentage,” Bradley said explaining the blame game. “ I don’t know when they’ll ever really say, ‘yeah, volatility could be contributing to this problem, too’ and that’s the difference between university weed science.”

This contributes to the confusion among users.

“You don’t know who to believe,” Gary Stacey said.

But Gary Stacey thinks this is where researchers are able to help. By acting as an objective third party, scientists can sort the fact from the fiction.

“We’re just trying to get out the truth and what science says, that’s my job,” Bradley explained. “I don’t care necessarily what amount of money a company has invested in something. Our job is to call it like we see it and show the science.”

With a controversial issue like this, sometimes the truth comes with some risk.

MU has been conducting experiments that test the air for the volatility of the chemical. The research is detecting dicamba in the air up to four days after initial application of the chemical. Bradley explained this is not something the companies want to be made public and there’s been considerable pushback.

In addition to research, Bradley is working with the Missouri Department of Agriculture to create training courses for farmers wanting to use the chemical next season.

Despite millions of damaged acres, dicamba is not going away anytime soon.

Gary and Bing Stacey haven’t used dicamba again, but many farmers making their money off crops have no choice. Bradley said Monsanto is planning on doubling the amount of dicamba-resistant soybeans in 2018 and many of the farmers who have been continuously hit by their neighbors’ chemical plan to plant the new seeds.

Bradley said part of the issue is soybeans are not a crop people directly consume. In general, soybeans yields were considerably high this year, so the damaged acres didn’t make as big of an impact on overall production.

“I think the only thing that is going to make a difference next year is if we have an off-target movement that is hitting more high-value crops, more high-value plant species throughout a wider geography,” Bradley said.

If this same type of damage was affecting produce people directly consume or trees, Bradley thinks dicamba would have been off the market by now.

EPA will reevaluate the use of the herbicide next November. This is one of the first times Bradley can remember that the industry granted only a two-year registration.

“I am absolutely convinced that if we have a summer in 2018 like we had in 2017, it will not be renewed,” Hurst said.

Bradley is not so certain. He said he has heard mixed reviews about how the future of this controversial weed killer could go.

“It is an unique situation for sure, hopefully it ends soon,” Bradley said.

German heart and lung researcher speaks at Bond LSC

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Scientist Thomas Braun speaks at Bond LSC about skeletal muscle regeneration. Braun is the director of the Max-Planck Institute that studies the heart,lungs and blood vessels.| Photo by Samantha Kummerer, Bond LSC

By: Samantha Kummerer, Bond LSC

Thomas Braun, a researcher with the German-based Max Planck Institute for Heart and Lung Research, visited MU for a Bond Life Sciences and Mizzou Advantage seminar.

The Max Planck Institute aims to find treatment for heart and lung disease. Part of its research focuses on stem cells and how they can decrease damage done to patients’ tissues who suffer from heart or lung disease.

Many components can interfere with effective muscle regeneration and a lot of those this components are connected to cell death.

Braun’s talk focused on the epigenetic and transcriptional control involved in skeletal muscle regeneration. His research explores cell death’s effect on muscle regeneration. They initially hypothesized that cell death would interfere with regeneration.

Muscle regeneration requires satellite cells. Satellite cells, aptly named for being located near muscle and nerve cells, help skeletal muscle fibers grow, repair and regenerate.

When cells become obsolete they activate a cell program to commit suicide. This cell death comes in the form of apoptosis — normal programmed cell death triggered to eliminate old, unnecessary or unhealthy cells — and necroptosis that is a death by inflammation to counter viruses and other disease.

Braun said when muscle fibers break down there is lots of killing of cells.

“We wanted to see if we take the muscle stem cells out of the tissue and put them into a dish whether they would still maintain this increased function to undergo program cell death and quite interestingly this enhanced tendency to go into cell death is actually maintained even after a few different transitions in vitro,” Braun said describing a particular experiment.

This increase cell death, Braun hypothesized, is caused by changes in the chromatin, a complex of DNA and protein.

To better understand exactly which cell death program was responsible for this increase, Braun’s team repeated the experiment but block certain components. This led them to discover the increased cell death correlates with an increase in necrosis.

Braun also believes there are some epigenetic mechanisms involved. Epigenetic involves biological mechanisms that switch genes on and off.

CDH4 is a component of a complex within this epigenetic function. The larger complex is a repressor and keeps the chromatin together. The researchers thought CHD4 might be what is acting on the pathways

“This actually goes along with a massive increase in cell death so this lack of proliferation of the fiber is simply dependent or caused by the cell death of these satellite cells. They undergo cell death and therefore cannot proliferate,” Braun explained.

Braun said his team landed on the conclusion that normally CDH4 represses the expression of

RIBK3, a protein-coding gene, and thus prevents necrosis cell death. But without CHH4, necrosis begins, cells die.

There are still many questions and experiments that lie ahead to figure out the details involved.

Braun’s talk was made possible by the support of Mizzou Advantage and Bond LSC.

 

Makenzie Mabry #IAmScience

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Makenzie Mabry, a Ph.D. candidate, works in the Pires Lab in Bond LSC. | photo by Allison Scott, Bond LSC

For Makenzie Mabry, every day is a new puzzle when it comes to science.

That desire to solve new problems led her from wanting to be a veterinarian to considering much less cuddly focus in plants.

“I think the beautiful thing about research is that it evolves itself,” Mabry said.

Although she had an acceptance letter to vet school in tow, she altered her career path to work with a new passion: plants. That led her from California to the lab of Chris Pires at Bond LSC.

“I did all of my undergraduate studies [at San Diego State University] with a vet school plan,” Mabry said. “I took a class my senior year talking about plants — Taxonomy of California Plants — with a great professor [Dr. Michael Simpson], and he really sold me on how unique plants are. They break all the rules.”

With vet school no longer in her plans, Mabry volunteered to work with Dr. Simpson and learn as much about plants as she could.

“I was all ready for vet school and I emailed him a week after I was supposed to start to volunteer,” Mabry said.

After two years of volunteering, Mabry began working toward a master’s degree. During that time, she studied a plant native to her home state of California, Cryptantha. She also studied those which occur in Chile and Argentina by visiting both countries.

“That fueled my passion for research,” Mabry said.

However, it wasn’t until five years ago that Mabry met Chris Pires at a conference in Columbus, Ohio.

“He was very energetic and I had just started learning about polyploidy [which Pires studies]. Three years later, he somehow convinced me to move from California to Missouri,” Mabry said. “I really enjoy the work I’m doing here, and it was a good decision.”

Now as a third year in Pires’ lab at Bond LSC, Mabry uses Brassicales — a family of plants that range from papaya to Brussel sprouts — to explore the multiple genomes of plants. She enjoys her lab work, analyzing data and getting to know the plants.

“Learning the subtle differences between them — whether branches are really close together or their leaves are clustered — is key,” Mabry said. “Being able to account for those differences might mean a lot for being able to find genes that are responsible for them. You have to know what those differences are to know what genes are responsible for it.”

Specifically, Mabry tries to understand how polyploidy — when an organism duplicates their genome to end up with two or more sets of chromosomes — comes about and what impact it has on plant species.

“We want to prove that polyploidy can lead to adaptive variation,” Mabry said. “It can be two different species forming a hybrid, and they keep all of their chromosomes, or a single species that doesn’t go through reduction. That’s the major question our lab is focusing on.”

These extra chromosomes can potentially give a plant new traits that help them react better to the environment or reproduce better without compromising essential plant functions. There are complexities to polyploidy that make deciphering its existence difficult, though. For instance, they’re trying to uncover why certain genes are kept and others aren’t.

“There’s evidence that there’s one genome that’s dominant to the other,” Mabry said. “Polyploids have a larger gene size, so that helps them accommodate.”

And, as a result, Mabry’s research requires coding skills.

“If you want to be successful you need to know how to code. You at least need to know what data is put in and what comes out,” Mabry said. “In the next 10 years, I think it’s going to be even more of a part of the undergraduate curriculum – it’s going to have to be.”

Luckily, Mabry doesn’t work alone.

“I’m really grateful because I have four amazing undergrad students who work with me,” Mabry said. “I could not do it without them. They all have individual projects that they are responsible for and it is very rewarding to watch them succeed in writing grants, presenting their work, and getting results.”

Ultimately, though, the undergraduates she works with are a big reason why she envisions herself in academia.

“Mentoring — that’s what keeps me going every day,” Mabry said.

Celebrating a mystery solved

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Roberts honored for breakthrough discovery in reproductive biology 30 years ago
By Eleanor C. Hasenbeck | Bond Life Sciences Center

In 1987, Michael Roberts published a groundbreaking discovery that changed the world of reproductive biology research.

Roberts and members of his lab discovered that a type of protein, an interferon, impacted how the bodies of animals such as sheep, goats and cows, recognized an embryo early in pregnancy. Previously thought to only be a part of a cell’s immune system response, this new signaling role changed the field.

In honor of his lab’s groundbreaking discovery, Roberts recently curated a section of six reviews examining the history of the discovery and current research that has built on it for the November issue of the journal Reproduction.

The discovery revealed an unknown in the reproductive systems of the ruminant family of animals, including sheep, goats, cows and deer. When an embryo first begins developing, before it’s placenta even attaches to the uterus, it releases interferons. Only present for a few days, these proteins signal to the mother’s body that the embryo is there. It triggers the response that keeps the animal from going into heat, basically shifting the animal’s hormones from breeding mode to pregnancy mode.

If the embryo doesn’t release interferons, the mother miscarries. Placing interferons in sheep that were not pregnant made the animals pseudopregnant, a false pregnancy in which no fetus is present.

Scientists at the time knew something made the mother’s body recognize the embryo, but they were not sure what. The discovery of interferon-tau was a mystery solved. That this ‘something’ was an interferon was also a surprise. Before Roberts and his co-discoverer, Fuller Bazer, found interferon-tau, researchers thought that interferons only function was in the immune system. Other interferons help the body recover from viral infections, like cold and influenza, Roberts said. The discovery that the protein also played a role in pregnancy caused some hubbub. It even caught the attention of The New York Times, Roberts said.

“It opened up a whole new area,” he said. “We all the sudden understood how these animals got pregnant, so people went off in all sorts of directions with it.”

The discovery of interferon-tau created opportunities for more research in how ruminant’s unique reproductive systems evolved. Other studies focused on using interferon-tau to improve livestock fertility, but ultimately this interest fizzled out as researchers found fertility treatments for cows were cost-ineffective for producers and unappealing to the public.

The discovery of interferon-tau earned Roberts and his co-discoverer the Wolf Prize in agriculture in 2002. Some consider the prize an equivalent to the Nobel Prize since the Nobel prize does not regularly honor agriculturalists.

After the discovery of interferon tau, Roberts found another protein that impacts pregnancy, which formed the basis of a pregnancy test for cows. Roberts said it’s now a multi-million dollar product in the cattle industry.

Today, Roberts’ lab has moved to other developmental research. He started studying human placentas. His work focuses on preeclampsia, a condition which impacts 5-10 percent of all pregnancies and is caused by the placenta. Roberts’s lab has also developed new lines of pluripotent pig stem cells which are helping scientists learn how to regenerate eye and heart tissue. At age 77, he is still funded and active.

Roberts was featured as a guest editor in the November 2017 issue of Reproduction. He also wrote an editorial introducing the topic and summarizing each review, “30 years on from the molecular cloning of interferon-tau.”

Engineering the Immune System

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Chemical engineering students Caitlin Leeper and Rui Zhang work in Bret Ulery lab. The lab conducts innovative research combining chemical engineering with immunology.| Photo by Samantha Kummerer, Bond LSC.

 

Saturday Morning Science talks engineering our next defense

By: Samantha Kummerer, Bond LSC

Saturday Morning Science brings science to the people, bagels included. In an effort to highlight this outreach effort, we’re profiling a recent SMS speaker who talked about … well, read for yourself below.

Inside your body is a complex network of interlocking biological pieces. Tissues, cells and organs are consistently working together to defend against an outside attack. This is the immune system, the body’s natural defense mechanism, which is incredibly important to keeping us healthy but are we currently using it to its full advantage?

Chemical engineering Professor Bret Ulery feels we have gotten a good start, but overall the answer is still a resounding no.

“We have this unique opportunity to leverage the things that are going on to make a difference in the immune system,” said Ulery, the Assistant Professor of Chemical Engineering and Courtesy Assistant Professor of Bioengineering.

Ulery runs a lab within Lafferre Hall centered on creating designer biomaterials.

He describes biomaterials as any substance that carries out a biological function which are commonly created to avoid interfering with the immune system. They can be used to replace a knee joint, a heart valve, or even contact lenses to correct vision.

“That’s been very successful for a long time in certain areas but what if we want to tackle some grand challenges?” Ulery said. “We may want to rethink what we’re doing with biomaterials and how we design them.”

To take on these bigger problems, his lab leverages the chemical and physical properties of materials to facilitate unique biological functions in regenerative medicine and immunology.

Vaccines seemed a logical place to start. A vaccine introduces a portion of a pathogen to a patient so they can be exposed to just enough to create an immune response without developing the actual disease. Ulery explained a person does not get sick from a vaccine because it is designed to target both the innate and adaptive immune responses without having the capacity to induce illness.

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Traditionally, there are just a few ways to create a vaccine. First, scientists use heat or radiation to inactivate a pathogen. It is killed so the patient will not be exposed to the full disease but the immune response will still be triggered. While this type of vaccine is safe and easy to transport, the immune response it induces is weak and thus requires a great number and more frequent immunizations to be effective.

Another method is to keep the pathogen alive but to knock out its disease activity like what is done with the flu shot. Scientists take out part of the virus but keep it alive. This way the virus can still grow but won’t create the same degree of damage as the normal pathogen. Here, the immune response is stronger but not always equally effective in everyone due to differences in viral strains that have mutated to get around certain immune defenses.

Ulery wants to engineer more effective vaccines by only exposing the patient to the components absolutely necessary.

“We wouldn’t have to worry about any of this other bacterial gunk that would be with it. However, the problem there is the immune response is very weak because all that other junk actually plays a role in inducing the immune response, but it’s a lot safer, we can make it cheaper, make it easier to transport,” Ulery said. “We can do a lot of manipulation.”immune_system2

This manipulation involves taking a portion of a protein called a peptide and tethering a fat to it. This new molecule called a peptide amphiphile folds in water in unique ways to create interesting nanostructures called micelles.

“Instead of having some sacrificial material where we load our drug or vaccine into the core, this is actually a nanoparticle that is made almost entirely from the vaccine itself, so we get really high concentrations of the peptide and the vaccine,” he said, explaining the benefits.

By adding different peptides, the lab is able to create a vaccine that works for multiple types of infections. Ulery said his team is working towards applying these techniques to combat diseases such as Lyme disease, influenza and even cancer.

Current methods of targeting cancer are tricky because of the similarity between cancer cells and healthy cells. Ulery said it’s difficult to make a vaccine that just kills the unwanted cells.

Despite the challenge, Ulery and other researchers at MU think they found a molecule that is good at killing cancer cells without hurting healthy cells. Initial tests revealed engineered micelles can be used to deliver a peptide drug to allow patients to receive smaller doses because the treatment kills more cancer cells in a targeted area. Ulery explained the exciting part of this is the method does not require changing the immune response.

But what if the team did use the immune system to improve treatments?

The chemical engineer explained there are immune cells within a cancerous tumor. However, the tumor’s environment prevents the immune system from doing its job. Ulery believes it might be possible to retrain the immune system to kill cancer.

That method would be similar to how vaccines are created. Instead of modifying portions of a protein, scientists could modify tumor cells so the immune system could process them easier. That’s one possibility but an even better option would be making a vaccine specific to a patient. Ulery said this would be the third generation of immunotherapy where different therapies work for different areas.

Much of Ulery’s work at MU is just starting to touch the surface of its potential, but the lab continues to challenge traditional immunology notions as it aims to create better solutions.

Ulery’s spoke Sept. 30 as part of Saturday Morning Science. The series invites speakers in all types of science to speak every Saturday at 10:30 a.m. This outreach effort is free and open to the public. Find its schedule speakers at bondlsc.missouri.edu/saturday-morning-science/schedule.

Kris Budd #IAmScience

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Kris Budd, a Ph.D. candidate in Lori Eggert’s lab, works with Bond LSC to track elephant DNA in Southeast Asia. | photo by Allison Scott, Bond LSC

“#IAmScience because I have the ability to transform the fate of endangered species.”

If someone had told Kris Budd that she’d be investigating elephant feces on daily basis in her Ph.D. program, she wouldn’t have bought it. If they’d said she’d realize it’s a passion of hers, she would’ve been in shock.

As a third year Ph.D. candidate in Lori Eggert’s lab, Budd is able to do meaningful work that is helping endangered elephants through feces.

“I always wanted to work with an endangered species,” Budd said. “I’ve always been excited about this, and the more you find out about elephants, the more you love them.”

Budd receives samples of elephant dung from Southeast Asia, and singles out the elephant DNA from the other species present in the sample — most commonly microbes and insects, but sometimes even goats and humans.

“You have to be aware that there can be DNA from anything that walked by that day,” Budd said. “We have to use specific tools to make sure we just get the elephant DNA.”

“After processing, we use the DNA Core Facility in Bond LSC, which isn’t an easy task since we typically run hundreds of samples several times for a single study.” Budd said. “But they always do it with grace.”

Budd then uncovers the genetic makeup with the help of the Informatics Research Core Facility (IRCF) and meetings with members of Chris Pires’ lab in Bond LSC.

From there, Budd is able to input the DNA into a system and keep track of the elephants overseas. They, however, become way more than numbers to her.

“They might just be a sample in your data, but you get to know the elephants,” Budd said. “Elephants are so much more. There are so many different elements to them — genetics, behavior, and ecology. Their evolutionary history and family structure tells a story, all seen through feces.”

Her work is about to get a lot more hands-on next semester, as Budd will be traveling overseas to collect samples herself.

“We’re going in the spring and we’ll teach local technicians how to go about collecting samples,” Budd said. “We’ll collect a lot of samples of our own while we’re there, too.”

Budd will be able to determine what is happening with the elephant populations in Southeast Asia more closely then.

“There’s a big push with critically endangered species to translate data into something that can help them,” Budd said. “The samples I’m working on from Myanmar are actually an extinct population, but we want to re-wild similar elephants in the same location.”

Essentially, that would require Budd to find a genetically similar elephant population that would be most likely to thrive in the same environment.

While actually implementing the re-wild process won’t happen for a while, Budd is certain about the influence of Bond LSC in the elephant re-wilding’s future success.

“My work wouldn’t be possible without the people who work at Bond LSC,” Budd said.

A zebrafish’s empty stomach can help scientists understand brain function

A new test can show how much a zebrafish larva has eaten. This basic information could be crucial to upcoming discoveries.

A zebrafish swims in its tank. Understanding how zebrafish move  can give researchers insight into how certain diseases impact human motion.  Photo courtesy National Institute of Child Health and Human Development.

A zebrafish swims in its tank. Understanding how zebrafish move can give researchers insight into how certain diseases impact human motion. Photo courtesy National Institute of Child Health and Human Development.

By Eleanor C. Hasenbeck | Bond Life Sciences

Until now, it was hard to know when a zebrafish larva had a full stomach.

Researchers in Anand Chandrasekhar’s Lab at the Bond Life Sciences Center are studying the networks of neurons that control the zebrafish’s jaw, but to do that, they first had to figure out just how much these fish larvae eat.

They didn’t just need to understand it, they had to be able to test it. The successful development of a test that measures how well a zebrafish larva can eat has already lead to more discoveries.

To develop this test, researchers fed the larvae fluorescent fish food for three hours at a time. That’s just long enough for them to eat it, and just before their intestine starts to push it out. Their tiny, fluorescent bellies were examined under a microscope and scored. A zero meant that there was no food in the larva’s stomach, while a three meant the stomach was completely full.

With this feeding test under their belts, researchers are now able to form and test more research questions. The Chandrasekhar Lab used it to better understand networks of branchiomotor neurons, the circuitry that controls jaw movement. These neurons also control the gill muscles that move in automatic movements, such as breathing, just as neurons in the human brainstem allow us to breathe without thinking. Researchers look at the zebrafish’s very basic motor neurons to understand how these nerves develop, heal and control simple tasks.

One experiment tested how fewer branchiomotor neurons affect the action of eating. They destroyed 50-80 percent of the larvae’s branchiomotor neurons using a chemical-genetic method. The fish with fewer branchiomotor neurons also ate less food. They tried a similar experiment, but this time using lasers to remove only a select portion of branchiomotor neurons that controls a set of jaw muscles. Again, they found that the larvae that went under the laser were not able to eat as much food as the normal larvae. Finally, they conducted the food-intake test with mutant larvae that did not have any cranial motor neurons. As the researchers predicted, the mutants were not able to eat.

Now, they want to test how these animals eat when these neurons develop differently. While the first tests essentially smashed nearly all of the zebrafish’s branchiomotor neuron circuitry, their upcoming research will examine what happens when these circuits are wired in a different way, with neurons in the wrong spots. They’ll be looking at much subtler changes, Chandrasekhar said.

“If they don’t eat properly, do they move their jaw properly? That’s the next question that I want to answer,” said Emilia Asante, a doctoral candidate in the lab. “Are the axons not going to the right position? Are their neuromuscular junctions not properly positioned? Are there fewer of them in the mutant? There are all these questions that these assays are actually critical in answering.”

Asante is also working to make the feeding test more quantitative and less labor intensive. In its current form, someone has to look at each larva and judge if the food in its stomach makes it a zero, one, two or three. They want to be able to measure more accurately how much food is in the fish’s belly. If they were able to develop a faster and more accurate test, researchers would be able to rapidly measure food intake in a greater number of fish and to test the effects of many different chemical and environmental factors.

Zebrafish are a unique lab animal model used in research for a number of reasons. They’re easy to observe because the embryo develops quickly in an egg outside of the mother. They’re transparent, so researchers can make certain cells visible using florescence and observe them in a developing animal without killing it. Their genome is fully sequenced, so researchers can easily create mutations in specific genes using CRISPR technology.

“Many of the same circuitry that you find in humans are also there in more primitive organisms, and one of them happens to be the zebrafish,” Chandrasekhar said. “It has got some of the same types of neurons and the same types of circuits that you can find in humans.”

Research into the zebrafish’s neural networks can help researchers understand diseases like Amyotrophic Lateral Sclerosis, better known as Lou Gehrig’s disease, which causes a loss of function in a human’s motor abilities, including those of the branchiomotor neurons.

This study “Role of branchiomotor neurons in controlling food intake of zebrafish larvae” was recently published in the Journal of Neurogenetics.

Lisa Caesar #IAmScience

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Lisa Caesar is a biological sciences Ph.D. candidate who works in Laura Schulz’s lab. | photo by Allison Scott, Bond LSC

“#IAmScience because education and my pursuit of learning became my ticket out of poverty and a way that I can really help others.”

“Mother knows best” rings true for Gerialisa Caesar. In her family, the career options were either to be a lawyer, engineer or doctor.

But with little interest in law and a greater love for science than math, Caesar decided to pursue her doctorate.

“I graduated high school at 16 fully equipped to enter the work force,” Caesar said. “I went back to school to study science because my mom basically told me I had to, but biology fit me really well, so it worked out.”

Initially, Caesar was hesitant that she could even become a scientist.

“I had an idea of what a scientist was, and it wasn’t me,” Caesar said. “After I immigrated from Guyana, my undergraduate advisors, Drs. Carroll and Catapane, explained the opportunities I had to study biology. It opened the world of possibilities for me to pursue science.”

Now, as a biological sciences Ph.D. candidate in Laura Schulz’s lab, Caesar focuses on women’s health and reproductive biology.

“My research is to understand how a mother’s nutrition prior to and during pregnancy affects the baby’s development,” Caesar said. “This is important as several studies link maternal diet during pregnancy to an increase in susceptibility of the offspring developing diseases such as obesity, diabetes and hypertension in adulthood.”

That includes connecting how mother’s diets cause fetal health issues, which is a highly debated topic.

“For example, a lot of women are told to take folic acid pills during pregnancy,” Caesar said. “Doing that has been tied to help with neural development concerns — things like spina bifada [a birth defect that affects developing babies’ spinal cords]. Understanding the mechanisms that make that occur would aid in developing better interventions to prevent such occurrences.”

As a result, Caesar’s research has the ability to help the world’s greatest health concerns in an impactful way.

“My work is directly contributing to prevent health issues that exist for future generations,” Caesar said. “Knowing that is motivating.”

After she earns her Ph.D., Caesar would love to work for the Center for Disease Control and Prevention.

“The CDC has immediate response teams that react to major disease concerns. Being a part of that would be incredible,” Caesar said. “There’s something about working for the CDC and being able to have a meaningful impact within the community that calls me.”

Caesar plans to channel that passion regardless of where she ends up, though.

“Biology is literally the study of life,” Caesar said. “As much as I thought science was challenging, I am able to see how it affects everyday life. I have a purpose, and I know what I do is going to make a difference.”