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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.

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.

 

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.

Dr. Burke wins Distinguished Professor Award

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Donald Burke-Agüero stands in his office in Bond LSC, holding a model of an RNA protein structure. Burke-Agüero studies the bio-chemical functions of RNA, and how those functions might be able to be artificially designed or replicated. | Phillip Sitter, Bond LSC

By Samantha Kummerer, Bond LSC

“He’s a triple threat in science,” Bond Life Sciences researcher David Pintel said.

Donald Burke’s combination of scientific excellence, caring mentorship and devotion to the University of Missouri led Pintel to nominate Burke for the 2017 William H. Byler Distinguished Professor Award.

The university agreed, awarding him the honor in October.

The University-wide accolade recognizes a faculty member for their “outstanding abilities, performance, and character.” When Pintel read this description he said he instantly thought of Burke.

This is the first time a faculty member from Bond LSC has won the award. Pintel said the award shows the quality of people here and the department is proud of him for receiving it.

Burke is a Molecular Microbiology & Immunology professor. His lab in Bond LSC studies RNA, the molecule used to help cells copy genetic information from DNA.

For Burke, the award is an honor.

“You always try to do everything you can to contribute to making the place great and you don’t do it for the purpose of being recognized, yet when the recognition happens, it’s nice,” he said.

Burke’s lab hosts students from the high-school to post-doctoral level. For each member, Burke said he tries to figure out their motivation. He starts by just asking questions and is able to align their goals and his.

“You can’t just say ‘This is what we do in my lab, deal with it.’ You can’t do that,” Burke elaborated, “Yes, it’s a lot of work and a lot of effort, but it has ceased being a burden for me. Now, I think of it as a new fun challenge.”

He said that challenge has paid off because every student that has gone through his lab has taken his science in new directions.

Pintel said this connection Burke has with his students is easy to see.

“People in his lab love him and, to me, that’s always a good sign,” Pintel said. “When I see people in a lab like that, I know it’s a good environment. That always means something good is going on.”

During their time in his lab, Burke tries to teach his students the importance of working as a team as well as learning understand the research process.

“Some of the things I’m most proud of aren’t necessarily the most impactful research, but the things where I know the struggle that went into solving the puzzle that was in front of us,” he explained. “The thrill of the chase may not be as interesting to the rest of the world but you know how hard that person worked and how many false leads there were.”

Recently, Burke has expanded his passion for motivating others to a new area. In July, Burke became the Interim Chair of Molecular Microbiology & Immunology.

“Now that he’s the interim chair he is trying to provide the same kind of supportive environment for the department that he’s been doing for his lab,” Pintel said.

Burk said he wants to help other faculty members achieve their goals and prioritize tasks. He is also involved in a new faculty search where he works to ensure the applicant pool reflects those that might be wanting to apply by removing language that may prevent people from applying.

“Again, I want to help find what obstacles can be in their way and get rid of those before it slows them down,” Burke said restating his passion for helping others achieve excellence.

Donald Burke-Aguero is an MU professor in the Department of Molecular Microbiology & Immunology. He received his bachelors’ degree from the University of Kansas and his Ph.D. from the University of California, Berkeley. Burke joined the MU community in 2005.

The Truth Behind BPA- Free Labels

Cheryl Rosenfeld

Cheryl Rosenfeld, a Bond Life Sciences Center investigator and professor of biomedical sciences at the University of Missouri. | photo by Jinghong Chen, Bond LSC

What companies aren’t telling you about their merchandise

By: Samantha Kummerer, Bond LSC

Bisphenol A, otherwise known as BPA, is used to make plastic containers, coats the inside your metal food cans, and leaches into your food and water.

BPA has concerned scientists, health practitioners and the general public for many years because of its potential to mimic hormones and disrupt the developmental stages in animals.

Opposition to the chemical has led to certain manufacture’s marketing their items, such as food containers and water bottles, as“BPA–Free” and a global push to reduce the usage of BPA in commonly used household-items.

However, new evidence suggests consumers may not be as ‘free’ from harm as they think.

Bond Life Sciences Center researcher Cheryl Rosenfeld suggested that many consumers might not be aware of how these alternatives are made. BPA-substitutes — bisphenol S (BPS), bisphenol F (BPF) and bisphenol AF (BPAF) — aren’t too different from BPA chemically.

“They’re just playing with various synthetic structures is what many industrials groups are doing,” she said.

BPA is made up of two chemical compound groups called phenols. Picture two rings with different elements connected. In BPF, BPS and BPAF all those same parts are still present, and the only change is that the rings are rotated differently and contain various branching chemicals .

Since these alternate chemicals are structurally similar to BPA, they still bind to estrogen receptors, receptors to which the natural hormone estrogen binds and activates, which results in up- or down-regulation in the expression of various genes.

“The worst problem is that humans and animals are unknowingly serving as test subjects. Industrial companies are not required to show definitive evidence that these alternatives to BPA are safe. They can cite their own limited studies, but currently, no rigorous testing is required for these BPA-alternative chemicals that are being to flood the market. There is no requirement for the products that contain these chemicals to state as such. Thus, consumers cannot make educated decisions when purchasing various food and beverage products,” Rosenfeld said speaking of the industry.

Substitutes aren’t always better

Rosenfeld recently published a literature review exploring the use of the BPA-alternatives and their potential risk. She began the work out of curiosity since her Bond LSC lab studies the harmful effects of BPA.

After putting the puzzle pieces together, the big picture began to emerge that exposure of rodent models to these substitute chemicals exert analogous effects as BPA — depressive behaviors, increased anxiety, decrease in social behavior and decreased maternal/paternal care. In some cases, the alternatives have an even greater effect, according to Rosenfeld.

Understanding BPA

Production of the industrial chemical, BPA, began in the mid 1900’s to make plastics. Today, it can be found in everything from water bottles to storage containers and even food. With this increase exposure comes an increased risk to consumers.

Past studies linked exposure to the chemical with health effects on the brain and behavior and many other widespread effects.

When BPA enters the body, the can at least partially metabolize and break down the chemical via enzymes, which is then removed from the body. But there is a limited supply of such metabolizing enzymes used and those consuming BPA daily will end up overwhelming their body’s ability to metabolize and eliminate it with the net effect that BPA can accumulate over time and continue to exert potential harmful effects.

The most serious effect of BPA and now the substitutes happens during development. Fetuses have poorability to break down the chemical. Evidence links BPA exposure during development with neurological disorders like autism spectrum disorders (ASD) and attention deficit hyperactivity disorder (ADHD).

Most studies have examined the effects of BPA alternatives in rodents and zebrafish. While numerous factors prevent scientists from establishing causation in humans, Rosenfeld suggested it is time to at least start correlating early life exposure to BPA alternatives and risk of neurobehavioral disorders, including ASD, ADHD, and other neurodegenerative disorders.

“What’s worrisome is the women who are seeking to become pregnant or are currently pregnant, they are under the impression that they are making positive choices for their sons and daughters by using BPA-free products, but such products likely contain these BPA-substitute chemicals that can result in equal and possibly even greater negative consequences for their unborn offspring. Ultimately, the question is then what sort of products should be using?” Rosenfeld explained.

Humans aren’t alone in the impact. Rosenfeld explained these chemicals don’t break down in the environment and could play a part in the decline of certain animals. Previous studies by Rosenfeld’s lab and others at MU revealed BPA has the ability to feminize what should otherwise be male turtles.

“I just wish we could stop and pause and think about the havoc we are wrecking on our own environment and ourselves,” she said.

Without definitive results, a lot of unanswered questions remain. Future studies will likely explore the full range of effects caused by the BPA alternatives. Rosenfeld is calling for researchers to begin to treat these alternatives like BPA and put them through rigorous studies. These studies, however, come with a cost.

Rosenfeld’s lab is funded for BPA research. To add these additional chemicals to her current studies, the cost would double and triple due to the increased amount of animal test subjects that would be required.

“They keep upping the bar of how many replicas we have to test. If you want to show effects, if you want us to believe your results, we have to test 12-15 animals, well then you need to test another 12-15 animals in these groups and then your research dollars are all-of-a-sudden gone,” Rosenfeld said.

Research costs are going up and in the meantime BPA is still being produced in high quantities, so the industry as a whole has to decide where to allocate its funds.

“It’s a moving target. We’re trying to keep up and they keep synthesizing more and more chemicals everyday. The problem is we are completely outspent in terms of avaibable research dollars compared to the money industrial companies have on hand to fight tighter reguation. It’s not even a fair fight,” she said.

Rosenfeld hopes this new publication prompts scientists and the public to begin to question and call for more action on testing these pervasive BPA subsitutes. The silver lining is even though we can’t control our exposure to these chemicals, Rosenfeld hopes we might be able to find a way to combat our exposure.

Cheryl Rosenfeld is a Biomedical Sciences professor,a researcher in Bond Life Sciences Center, and research faculty member in the Thompson Center for Autism and Neurobehavioral Disorders. Rosenfeld specializes in how the early in utero environment can shape later offspring health, otherwise considered developmental origins of health and disease (DOHaD)She earned her bachelors and doctor of veterinary medicine degrees from the University of Illinois and her PhD from the University of Missouri.

In a viral game, the fight isn’t fair

Lab explores how parvo wins in tug of war with cells

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Kinjal Majumder and David Pintel examine the protein levels in mouse cells during MVM infection. Each black band represents the amount of viral protein in infected cells over time. | Photo by Samantha Kummerer, Bond LSC

By: Samantha Kummerer, Bond LSC

At the start of any tug of war game, the battle is even. But it doesn’t stay that way for long. After a back and forth, the inevitable happens — the stronger team gives the rope one last tug and send the losers toppling over, claiming their dominance.

This is a game cells and viruses know well. In their version of tug of war, the virus eventually overtakes the cell and not only topples it but causes a consequence far worse than a few scraped knees.

This is how post-doctoral fellow Kinjal Majumder thinks of the interaction between parvoviruses and the dividing cells it conquers.

Majumder and others in the lab of David Pintel at Bond Life Sciences Center recently gained insight into how the virus achieves victory over the cell. These findings could improve human therapies and even play a role in treating cancer.

Meet the Champion

Parvoviruses are some of the smallest, simplest viruses. With only two genes, it has fewer DNA base pairs than most other viruses, up to ten times smaller in some cases. The virus’ size and simplicity, however, do not make it any easier to understand.

Pintel’s lab works at the “nitty gritty” level of the virus to study its basic molecular mechanism.

The group understands a little about how the virus operates but is working on the why.

Like a sly culprit, the virus uses its tiny nature to sneak inside the cell. The cell recognizes the presence of the virus as a foreign piece of DNA and responds to try to remove it. Once the cell responds, the virus begins replicating inside until it overtakes the cell. But, the tug of war game ends up more one-sided, so perhaps viewing the virus as a ruthless conqueror would be more accurate.

Latest Developments

Majumder’s experiments specifically focus on DNA damage response, an intrinsic function of cells. The DNA damage response constantly works to protect us from cancer by continuously repairing broken DNA to prevent harmful mutations in cells . This response uses a network of cellular pathways to monitor and provide checkpoints in the cell cycle to prevent damage from being passed on to the next generation of cells. But parvoviruses also tricks cells to begin a DNA damage response, which they use to eventually take over the host cell.

In July, the lab published the latest finding from a series of papers exploring a type of these parvoviruses called minute virus of mice (MVM). The discovery began when the team found that the virus stops cells from dividing within infected cells.

To do this, MVM uses the DNA damage response to stop cells from dividing, but still allows virus replication to continue. The group developed a system to examine how the virus took over the cell. Further experiments revealed the virus transcriptionally regulates cell cycle genes.

The team used CRISPR to target a cellular gene that the virus must inactivate for it to replicate. Expression of this gene is required for the cell to divide. They discovered the virus actually blocks the transcription of this gene so it cannot make its protein. Blocking this function also prevents the cell from dividing. Without cell division, the virus is free to rapidly replicate inside the cell.

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Post-doctoral fellow, Kinjal Majumder, points to the results of a recent experiment. When MVM is mutated at particular sites, the protein levels produced by the virus decrease, but the virus continues to replicate efficiently. | Photo by Samantha Kummerer. Bond LSC

Majumder said parvo’s manipulation of infected cell cycles is different from other viruses because it can only replicate in cells that are actively synthesizing DNA. It eventually halts the process of cell division in infected cells by dysregulating transcription factors that regulate cell cycle gene expression. That’s what makes this discovery unique.

Endless Possibilities

This discovery only scratches the surface.

Majumder said the lab constantly thinks of new experiments to explore parvovirus biology. The simplicity of its DNA expedites the process of culturing and growing the virus, leaving more time for what Majumder calls the “fun experiments.”

“We try to be thorough and confident of our findings, so we attack experiments from many different angles,” Majumder said.

Imagine viewing an object from multiple angles under varying light conditions. The change in perspective reveals something different about it with each new look. This approach expands their understanding of parvoviruses.

Majumder explained the lab makes use of everything from high-resolution imaging and CRISPR technology to proteomics and deep sequencing to study the tug-of-war between MVM and the DNA damage response.

“The thing about being a postdoc is you kind of have to be a jack of all trades,” Majumder said about his ability to conduct the range of experiments.

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Parv O’Lantern: A nucleus of an infected mouse cell is captured using a super-resolution GSD microscope. Parvovirus MVM creates replication centers within host cell nuclei. The viral DNA can be labeled with fluorescent probes for imaging. Viral genomes that haven’t made it inside are illuminated on the edge. The viral genomes that have entered made replication centers that resemble the face of a Jack O’Latern. | Photo by Kinjal Majumder and Alexander Jurkevich

Wider Implications

While parvoviruses are not a deadly threat to humans, understanding it has major implications for humans.

Parvoviruses are used to develop gene therapy tools to treat disorders like muscular dystrophy and spinal muscular atrophy. The Pintel lab collaborates with labs such as the Lorson and Sarafianos lab in Bond LSC, to explore its therapeutic potential.

Majumder explained the lab is also interested in understanding how the virus could improve cancer treatment. Parvo’s tendency to replicate in dividing cells links it to how cells divide uncontrollably in cancer. Majumder explained those scientists are trying to use that function of the virus to target cancer cells.

This makes work in the Pintel lab that much more important. But, before the virus can fully improve humans’ conditions, researchers better grasp its capabilities. And that means more of the daily experiments within the Pintel lab.

“What we learn from studying a simple virus can be expanded to more complicated viruses because there are some viruses that can make a dozen different proteins, so that’s a more complicated system,” Majumder said. “Before you can get to the more complicated systems, you need to be able to understand the one that makes just a few proteins.”

For now, scientists will play their own tug of war as they go back and forth in their findings and experiments to uncover the mystery surrounding this small, unique virus.

Expanding the limits of knowledge

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Purva Patel presents her research on iron in plants during the undergraduate research forum. Patel works in Dr. Mendoza’s lab in the Bond Life Sciences Center.

By: Samantha Kummerer, Bond LSC

Purva Patel grew up captivated by newspaper articles discussing a method to grow plants without soil called hydroponics.

Today, she is one of the scientists mixing the mineral and nutrient solutions to plant seeds in this rapidly growing soil-less method.

The University of Missouri senior spent the past year working in David Mendoza-Cózatl’s Bond Life Sciences lab. Her research, which started out as a capstone project, has now turned into a pastime.

“I learn something new every day,” she said. “I did not know much about plants before joining this lab, but now I just love how all this is working at the genomic level, and I’m really very interested in understanding at what’s happening at the core of the plant.”

Patel studies how plants accumulate iron in the model organism, Arabidopsis thaliana. Iron is an important metal that provides nutrients humans need to perform important cellular processes. Plants are the primary source of iron and other essential micronutrients for humans and livestock worldwide.

Plants receive iron from the soil and transporters distribute iron from the roots to the rest of the plant. Most of the transporters involved in keeping the levels of iron balanced are not known; that’s where Patel comes in.

She started with more than 20 different Arabidopsis seed lines. Each seed line disabled a different gene, causing a loss of function that might be responsible for the movement of the metal into and out of cells.

The seeds were placed in different dishes with artificial soil that emulated real soil conditions. Some had regular levels of iron while others had an excess or deficient amount. Next, it’s time for them to grow. After they grow, she measures the roots and shoots and compares them to the wild-type plants that signify normal growth.

She narrowed down the potential genes to three seed lines. Those three types of seed lines were selected because they grew different than the normal plants and showed consistency in displaying the same leaf color and lengths of the shoots and roots.

For Patel, this step was the most exciting,

“Even in the absence of iron, the mutated plant has longer roots and the wild type does not, so I think the very visible difference between those would be the biggest thing I have come across.”

Now she wants to know the amount of other essential metals, like zinc and copper, that accumulate in plants’ tissues during various growing conditions with or without iron. For this, she uses a machine called ICP-OES (Inductively Coupled Plasma Optical Emission Spectrometry). The machine detects and measures metals in a plant sample. The results from ICP will help Patel determine how the mutants accumulate elements differently than the wild-type.

Patel explained her work is only one step in the process to understand the mechanism. She hopes her findings could produce more nutrient-rich crops someday.

“It can be nothing,” she admitted. “There is a chance, but I want it to be something.”

Whether she finds something substantial or not, Patel hopes to use her knowledge of genetics she gained in the lab to get a master’s degree in the biomedical field.

“It’s great that the science we learn in the classrooms is not only limited to there, but we get to apply it here and see the results and try to make the world a better place by using that knowledge for practical uses,” Patel explained.

The state of the American marriage

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Eli Finkel explains not all modern marriages are getting worse. Finkel spoke about his new book, “The All-Or-Nothing Marriage”. | Photo by Samantha Kummerer, Bond LSC

By: Samantha Kummerer, Bond LSC

“And they lived happily ever after. Like, what the hell?” Eli Finkel exclaimed. “That’s a foolish way of thinking. Really what you’re doing is stepping on the welcome mat of what’s actually going to be interesting, of what’s actually going to be challenging.”

Finkel set out to write a book about how the quality of American marriages have declined. But while the modern marriage is nowhere near a fairy-tale ending, it’s not as doomed as Finkel predicted.

“The initial version of the theory was the suffocation of marriage, that we’re suffocating this institution,” Finkel explained. “Now it’s a story about divergence.”

In fact, Finkel found the best marriages are getting better.

But he wasn’t completely wrong either; the average marriage is getting worse.

“We in America have changed marriage from something that can grow when neglected to something that requires constant care and affection, but if you get it right is pretty special,” the Northwestern psychology professor said.

This is the idea behind Finkel’s new book, “The All-or-Nothing Marriage: How the Best Marriages Work.”

A better marriage has always been correlated with a higher quality of life. What’s new is the effect of marriage on an individuals life is increasing in importance.

To explain this change, Finkel breaks up the evolution of marriage into three stages.

The first was the pragmatic era during the preindustrial times. Life was fragile and couples married to meet basic needs to survive.

Then around the 1850’s, industrialization allows young people to be economically and geographically free. Finkel said this freedom was used to seek marriages for personal fulfillment and love.

“This marriage has a particular structure that had been the fantasy of people for generations,” Finkel elaborated.

By the 1950’s this idea of the wife as the homemaker and husband as the breadwinner was fully established. For Finkel, this is problematic because it assumes that men and women are fundamentally different and restricts them to two different roles. Data proves both genders can be assertive and nurturing.

People begin to revolt against this idea around the 1960’s. This is the third and current stage of marriage. Finkel calls it the expressive model of marriage. Now, in addition to love and personal fulfillment, people want a spouse who will help them grow.

For Finkel, these stages are mirror Maslow’s hierarchy of needs. At the base of the pyramid are basic needs then the psychological needs of love and belonging are positioned in the middle. At the top of the pyramid are self-fulfillment needs, which is what he views American couples need in a marriage today.

“In my mind, the story of rising expectations is not one where we are expecting too much,” he said. “There’s something special about looking to your marriage to do things up there. There’s something special about saying ‘what if I had a marriage that was not only loving but really helped turned us into the ideal versions of ourselves.’”

Finkel continued that such lofty expectations from a marriage are hard to achieve. Thus, the all-or-nothing state.

So how can we make our marriage meet these higher demands?

The author laid out three options.

  • Going All In: This option involves going on date nights, but not just going on specific types of date nights. A study revealed while going on comfortable dates and exciting dates increase the quality of the relationships, only exciting dates increase sexual desire.
  • Love Hacking: This technique doesn’t involve making a relationship better, but is about changing how you think about a relationship in a more constructive way. Finkel said this is one that doesn’t take much time and doesn’t need both couples. One way to do this, Finkel explained, is by writing about your fights from a third party perspective. A study that asked participants to do this showed that marriage quality stopped declining and the individual reported feeling less angry.
  • Recalibrating: This technique involves lowering your expectations. Floyd elaborated by speaking explaining that people are relying more on their spouse to satisfy theirto how marriage has taken on more of individuals’ social social,, emotional and psychological needs. Research shows that people who have more diversified social networks are happier than those who don’t.

“It’s an interesting time to be married,” Finkel concluded. “The average marriage is a little bit worse than before but those of us who are able to flourish while asking these ambitious things are able to have a level of marital fulfillment that was out of reach previously.”

The 13th annual Life Sciences and Society Symposium, The Science of Love, started Friday, Oct. 6 and Saturday, Oct. 7. It features six experts that research various aspects of love, relationships and connection. The event will conclude on Friday, Oct. 13 with its last speaker, Jim Obergefell, who was the plaintiff in the 2015 Supreme Court case on marriage equality.

Examining the African American marriage

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Charlandra Bryant reveals some of her findings on what influences African Americans’ marriage quality. Bryant spoke on the effects of health on African American couples on Saturday, Oct. 7. | Photo by Roger Meissen, Bond LSC

By: Samantha Kummerer, Bond LSC

“Race matters, even in marriage,” Charlandra Bryant said to open her talk on the marital functions of African American couples.

Bryant asked the crowd that gathered for the Annual Life Sciences & Society Program Symposium on Saturday, October 7, to name successful African American couples.

After naming the Obama’s, many people’s minds come up empty, and Bryant attributes this to the tendency of the media and literature to highlight single African American households.

Few studies explore how African Americans’ marriage quality relates to interactions between the couple.

Bryant wanted to explore factors like entering marriages with kids and poverty that are unique characteristics to African American relationships. Her project dives into the connection between African American marriages and health.

Over the years, she has collected data from hundreds of newlywed African American couples. The couples’ variance in other key demographics like age, education level and income, produced a result that realistically encompassed African American marriages.

Health

Weight was one aspect of Bryant’s research that impacted the health of a relationship.

She found that heavier husbands were more likely to be depressed, but their weight did not affect their wives’ happiness. However, if a wife was heavier, the husband often showed more signs of depression.

While this effect was interesting, Bryant said the most revealing part of this research was that if couples felt very close to their partner the link between depression and weight decreased. This behavioral closeness, in sum, improved their lives.

Stepfathers

The effect of stepfathers on relationships was another theme Bryant explored. Her research explored how stepfathers affected things like commitment, trust, marital happiness and love. Not surprisingly, she found stepfathers who had positive relationships with their stepchildren reported better marriage quality.

Racial Discrimination

Bryant’s work found that wives who experienced racial discrimination also reported less physical affection and hostile husbands. She said this association stumped her for a while.

Now, she theorizes that husbands may be frustrated by their lack of ability to help their wife to deal with the discrimination, so they displace their anger towards their wives, such as perhaps raising their voice asking “Why didn’t you stand up for yourself?” The wife who could be sensitive to the experience could interpret this as a hostile behavior.

The Role of Genes

Little is known about the effect that genes play in social relationships, Bryant explained, but that didn’t stop her from asking questions.

For one study, male participants were asked to spit into a cup. Those samples were then paired with participants’ responses on hostility and warmth within their marriages along with depression and marriage satisfaction.

It found men at high-risk for depression were more responsive to positive and negative effects. In essence, husbands with a higher risk for depression can actually report higher levels of marital satisfaction when they receive high levels of warmth than the husbands who are at low-risk for depression.

While individuals can’t change their genetic makeup, Bryant said knowing if your spouse is susceptible to depression could help in your relationship.

Goals

The goal of Bryant’s ongoing research is to help improve intervention techniques. She said not all interventions work for everyone; sometimes they need to be culture-specific so she hopes her findings can help improve the techniques used for African American couples.

The 13th annual Life Sciences and Society Symposium, The Science of Love, started Friday, Oct. 6 and Saturday, Oct. 7. It features six experts that research various aspects of love, relationships and connection. The event will conclude on Friday, Oct. 13 with its last speaker, Jim Obergefell, who was the plaintiff in the 2015 Supreme Court case on marriage equality.