Marianne Emery is a Ph.D. candidate in Ruthie Angelovici’s Lab in Bond LSC. | photo by Allison Scott, Bond LSC
By Allison Scott | Bond Life Sciences Center
“#IAmScience because it leads to innovation that makes for a better world, which is an awesome thing to be a part of.”
It’s good to have a role model, and Marianne Emery has always looked up to female pioneer scientists.
One of her favorites is Barbara McClintock, a Nobel prize winning botantist who studied how the chromosomes of corn change during reproduction.
It is from women like McClintock that Emery is encouraged to always be impactful with her research and overcome obstacles with grace.
“I think it’s inspiring to see these women in positions that have typically been male-dominated,” Emery said. “You lose your confidence sometimes when things just don’t work. You’re continuously met with obstacles, but you have to keep going.”
And that she has.
Emery works in Ruthie Angelovici’s lab at Bond LSC to understand what controls protein levels in seed. She primarily spends her time on the computer working with large data sets and trying new software, but is always excited about the findings she’s able to uncover.
“I enjoy developing new skill sets every day,” Emery said. “The most important thing I’ve learned so far is how to communicate my science and how to communicate when I’m having an issue. Conveying a problem and problem-solving in general can be hard.”
Still, Emery continues to focus on improving on a daily basis. She hopes to work for a company like Monsanto after earning her Ph.D.
“I really like the business side of science,” Emery said. “Ultimately, a bigger company would be the best fit. I also really like policy and the patenting process.”
Wherever Emery ends up, though, she hopes to become like the women who pioneered science.
“Female scientists have been so inspiring to me,” Emery said. “I hope that one day I can be a leader and a role model for other young women who aspire to be involved with science.”
What companies aren’t telling you about their merchandise
Cheryl Rosenfeld, a Bond Life Sciences Center investigator and professor of biomedical sciences at the University of Missouri. | photo by Jinghong Chen, Bond LSC
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.
Lab explores how parvo wins in tug of war with cells
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.
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.
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.
Vivek Shrestha, a Ph. D candidate, works in Dr. Ruthie Angelovici’s lab at Bond LSC. | photo by Allison Scott, Bond LSC
By Allison Scott | Bond Life Sciences Center
“#IAmScience because it provides me with a platform to make that which seems impossible possible.”
Agriculture is a mainstay in Nepal, where Vivek Shrestha was born and raised. He grew up in a small farming family, but he was surprised that although a significant portion of the country was involved with agriculture, food insecurity was prevalent.
“Nepal is a small, developing nation that is naturally beautiful,” Shrestha said. “Agriculture is huge, but still a lot of people are food insecure.”
Shrestha saw this need and decided to study plant sciences as an undergraduate at Tribhuvan University in Nepal. From there, he earned his master’s degree from South Dakota State University before coming to Mizzou to pursue his Ph.D.
“The overall goal of my study is to understand the genetic architecture of seed amino acid composition,” Shrestha said. “Seed amino acid composition is a complex metabolic trait and, despite having tremendous importance in biofortification efforts in seed crops, the underlying genetics are not clearly understood.”
Currently, Shrestha works in Dr. Ruthie Angelovici’s lab at Bond LSC studying the trait to better grasp its genetic breakdown.
“The {research} quality of amino acids has a tradeoff with the quantity, which makes it more challenging,” Shrestha said. “However, our research is of paramount importance because it has millions of beneficiaries.”
Shrestha’s research helps not only with food stability in places like Nepal, but also in cutting costs for the livestock feed industry in developed nations like the United States.
“Maize is a huge part of the feed industry for the United States,” Shrestha said.
This dual interest makes Shrestha’s work that much more rewarding. Although the amino acids are complex — having multiple cellular processes and interactions — the complexity gives Shrestha motivations and excitement in what he does.
“Every day is a fresh, new day for me to explore and enjoy science,” Shrestha said.
Bond LSC’s Jay Thelen was recently part of a team that looked at how short laser pulses might be used to modify peptides and proteins to make foods edible for those with specific allergies.
Thelen, a biochemistry professor, joined scientists from his department, engineering and Denmark to explore this possibility. What they found was a way to modify molecules quicker and more cheaply than current chemical methods. This could potentially lower costs for specific applications in medicine, pharmacology, biotechnology and more.
We don’t want to give everything away, so read the whole story from MU’s College of Engineering.
Ronnie LaCombe, a Ph. D candidate in biological sciences at MU, stands near her lab station in D Cornelison’s lab in Bond LSC. | photo by Allison Scott, Bond LSC
By Allison Scott | Bond LSC
“#IAmScience because I feel most alive when I’m talking to people, both in and out of my field, about my work.”
While other kids were playing with Legos and dolls, Ronnie LaCombe was exploring the world through a microscope.
Alongside her cousins, LaCombe used science at an early age as both a way of learning and for entertainment.
“I’ve always wanted to be a scientist,” LaCombe said. “In third grade I told everyone I was going to be planetologist — a scientist who studies planets. Although that didn’t pan out, I guess I always knew science was the path for me.”
Years later she’s working in D Cornelison’s lab studying protein interactions in cells of rhabdomyoscarcoma, a form of childhood cancer. Specifically, the fifth-year biological sciences Ph.D. candidate is trying to uncover why a protein that’s typically on the outside of a cell is located inside the nucleus in this form of cancer.
“I was looking at the cells and saw that this protein was in the nucleus and not on the outside,” LaCombe said. “At first, I thought it was fake. I followed up on it, and it ended up being something potentially significant.”
After noticing the unusual location of the protein in the cell, LaCombe and others in her lab looked into other species to see if it existed in them, too. When they saw the structure was the same in both dogs and mice they knew it meant something.
“We were jumping up and down once as we saw it was in three different species,” LaCombe said. “That validated what we had thought earlier about it being something significant and not a mistake.”
Now, the lab’s test is to figure out why the protein is there and if it’s functioning the in the same way it would if it were outside of the cell.
“Cells touch each other and talk to each other through the proteins on the outside of the cell,” LaCombe said. “We’re trying to figure out what the protein is doing since it’s in the nucleus rather than at the surface.”
At this point, they’re still looking into how this is possible and what it means for this type of cancer.
“The hope is to figure out a method that can be used in other forms of cancer,” LaCombe said.
Until that solution is discovered, LaCombe is happy to put the puzzle together piece-by-piece.
“Research is like one very long, often very difficult, puzzle that you don’t always have all the pieces to,” LaCombe said. “I enjoy the challenge, though, and the difficulty of it makes solving the puzzle even more satisfying.”
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, Arabidopsisthaliana. 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.
Jim Obergefell’s love endured through his partner’s death and all the way to the Supreme Court.
Jim Obergefell speaks about winning the landmark Supreme Court case that granted equal marriage rights to same-sex couples. Obergefell received a standing ovation after his lecture. Photo by Eleanor Hasenbeck | Bond Life Sciences
By Eleanor C. Hasenbeck | Bond Life Sciences
Jim Obergefell had a destination wedding, but not by choice. On a chartered medical jet on a tarmac in Baltimore, Obergefell married John Arthur, his partner of 20 years, in a union that would result in a landmark Supreme Court decision.
Obergefell was the named plaintiff in the landmark decision that granted same-sex couples the right to marry, Obergefell v. Hodges. He closed the Life Sciences and Society Symposium, The Science of Love, Friday, October 13, with a lecture and book signing.
Obergefell and his partner John met and began their life together in Cincinnati, Ohio, around the time the city passed an ordinance prohibiting any city laws that would protect LGBTQ people. In 2004, Ohio passed a state Defense of Marriage Act that explicitly prohibited marriage between same-sex couples in Ohio. In 2013, the Supreme Court handed down the Windsor decision, which struck down a key portion of the federal Defense of Marriage Act and gave same-sex marriages federal recognition.
When Obergefell learned this news, he leaned over, hugged and kissed his partner, and said “let’s get married.”
This was more complicated than your run-of-the-mill, spontaneous wedding. Due to marriage prohibitions in Ohio, the couple had to get a dying man to a state that would marry same-sex couples. Jim’s partner, John Arthur, suffered from Amyotrophic Lateral Sclerosis, Lou Gehrig’s disease. ALS is a degenerative disease of the nervous system. Nerves that control voluntary movements like breathing, walking and chewing deteriorate and die. A dead nerve cell cannot send pulses to the muscles, so a person with ALS will gradually lose all ability to move, talk and breathe. Arthur was entering the later stages of the disease, and he was confined to a wheelchair with little ability to move.
They settled on Maryland, because it didn’t require both spouses be present to obtain a marriage license. Obergefell got the license, and the couple’ family and friends helped them charter a medical jet to fly to their wedding. Because of Arthur’s illness, they said their vows in the tiny plane’s cabin on the tarmac, with the ceremony officiated by Arthur’s aunt.
That wasn’t the end of their love story. The following week, a human rights lawyer showed them a blank death certificate and told them when Arthur died, the state of Ohio wouldn’t recognize their marriage. Arthur would be listed as single, and in the eyes of their state government, Obergefell wouldn’t be his widow.
“I loved John,” Obergefell said. “I loved my husband, and I was willing to fight for that, and I was not willing to let my state, Ohio, tell me that I was not his widower. That wasn’t something that I was going to give up.”
Eight days after their wedding, Obergefell filed suit against the state of Ohio and the city of Cincinnati. Three months after the cases first hearing, Arthur died. Obergefell ordered 20 copies of his death certificate, knowing the state of Ohio wouldn’t get it right. The Sixth Circuit Court ruled against the couple, opening the case up for Supreme Court review.
It took two years from their wedding, but the Supreme Court ruled in their favor and granted equal marriage rights to same-sex couples on July 26, 2015. Obergefell left the courtroom to a crowd of cheers, cries, high-fives and slaps on the back. He received a phone call from President Barack Obama. He only remembered what he said after watching himself speak to the President on CNN News.
Today, he calls himself an “accidental activist.” He tells his story at speaking events across the country. He said he feels proud each time an audience member tells him he’s given them the bravery to come out to their friends and family. 20th Century Fox bought the movie rights to his book, Love Wins, and he’s starting a business selling LGBTQ-themed wines, with a portion of the proceeds benefitting organizations advancing LGBTQ equality.
As he spoke, it marked four years since his husband’s passing. Now ordained himself, he married two of his friends, a same-sex couple, earlier this week. For him, the Supreme Court’s decision marks his partner’s greatest legacy.
“You know, I’d give it all back for John to be here,” Obergefell said. “I couldn’t prevent John from dying of ALS, but I’m really happy I could help create a legacy of love for millions of people in his memory.”
Obergefell spoke as part of the The 13th annual Life Sciences and Society Symposium, The Science of Love, Oct. 6-13, 2017. It featured six experts that research various aspects of love, relationships and connection. Obergefell’s book, Love Wins, is available now.
Bill McKibben explained the impact of increasing carbon emissions on the global climate and explored solutions to slowing the trend
Bill McKibben responds to an audience member’s question at his lecture on Oct. 4 in Jesse Hall. The screen behind him shows demonstrators blocking an oil rig from leaving harbor. McKibben called them “kayak-tivists.” Photo by Eleanor Hasenbeck | Bond Life Sciences
Eleanor Hasenbeck | Bond Life Sciences Center
Climate writer and activist Bill McKibben spoke to a packed house at the Missouri Theater Wednesday, October 4. With more than 300 people in attendance, McKibben discussed the changing climate, its impacts and his activism. The lecture was part of the Lloyd B. Thomas Lecture & Performance Series.
“It’s happened a hell of a lot faster and pinched a hell of a lot harder than we thought it would,” said McKibben of climate change.
McKibben said the signs of a warming planet first became apparent in the 1970s. Today, the oceans have become 30% more acidic as the world’s salt water takes in carbon dioxide from the atmosphere. Hurricanes are breaking records in the amount of rainfall and monetary damage they bring, McKibben said.
The solution lies in consuming less and using alternative energy, he continued. Last year, half of Denmark’s energy was generated by wind. Solar panels are so affordable now that homes in east Africa once lit by kerosene lanterns are powered by solar panels on the roofs of small homes.
“If we actually wanted to, we could move with real speed to make this transition,” McKibben said.
Why aren’t we then? McKibben blames the fossil fuel industry. Internal communications from Exxon Mobil show the corporation took steps to protect its drilling rigs from rising sea levels and increasing severe weather at the same time it was working to block regulations that would decrease carbon emissions.
“It took me far too long to figure out that we were not in argument at all,” McKibben said, referring to the so-called debate as to whether a warming climate is caused by human impact. “We were in a fight, and a fight is always about money and power. The fossil fuel industry was the richest and the most powerful industry on the planet, and the fact that it had lost the argument made very little difference to it. It was winning the fight day after day after day.”
But for all the doom and gloom surrounding climate change, McKibben still has hope that we can slow the process. He founded 350, an organization working to use grass roots movements to oppose fossil fuels. According to 350.org, 350 is named after an acceptable concentration of carbon in the atmosphere, 350 parts per million. Demonstrations through the organization have taken place across the world, from American cities to places most susceptible to rising sea levels, like the Maldives and Haiti.
At Bond LSC, some are taking their own steps to slow down the rate of the world’s warming. Cheryl Rosenfeld studies Bisphenol A, a chemical component of many plastics. She recently installed solar panels on her home, and she earns credits for the energy they generate. She uses reusable bags at the grocery store to reduce the waste generated from plastic and the fossil fuels consumed to produce them.
“Each of us could be making the decisions in our own lives that can make a change,” Rosenfeld said. “If we all come together like that, we can make an impact.”
There are several ways to reduce your own carbon footprint:
Use renewable energy to power your home. You can find utilities companies that generate at least half their power through renewable energy
Weatherize your home to make your heating and cooling systems more efficient.
Invest in energy-efficient appliances. Use a power strip or unplug your devices when they are fully charged or not in use.
Reduce food and water waste. About 10 percent of American energy goes to food production, and about 40 percent of our food is wasted. You can save money and energy by eating what you buy.
Install solar panels on your home. Right now, you can earn a 30 percent federal solar tax credit. The city of Columbia also offers rebates to encourage utilities customers to use solar energy and invest in more energy efficient utility systems. The city also maintains a list of solar providers that meet its requirements for rebates.
The most important thing, said McKibben, is inspiring policy changes like carbon taxes or renewable energy programs.
“We’re so far deep into this problem that we can’t solve it one person at a time. What we need is a change in policy, said McKibben. “The best individual action is not to be an individual. It’s to come together in movements big enough – that doesn’t take an enormous movement. It takes between four or five percent of people coming together in a movement to force change in policy that might give us some chance.”
Bill McKibben is author of sixteen books about environmental issues and founder of 350. He frequently contributes articles and editorials to organizations such as the New York Times, the Guardian and Mother Jones. You can learn more about his writing and activism at his website.
Bond Life Sciences Center sponsored the 2016 LSSP Symposium, Confronting Climate Change, which brought experts in the field to MU to speak about its pressing issues.
Katy Guthrie, a Ph.D. candidate, works in Dr. Paula McSteen’s lab in Bond LSC. | photo by Allison Scott, Bond LSC
By Allison Scott | Bond LSC
“#IAmScience because I want to take the knowledge I gain and teach it to other young scientists so they share in this excitement, too.”
Katy Guthrie grew up as one of five girls. All five sisters took very different paths —one ended up in hospital management, another in marketing and advertising, one became an engineer and the other works in logistics for a start up.
But Guthrie took a different route.
Her love of science started long before she enrolled in classes at Northwest Missouri State University, but there she discovered her true love of plants. Guthrie took a required botany class, and less than a week into the course she was hooked.
“All biology students had to take zoology and botany,” said Guthrie. “I had an awesome botany professor second semester of my freshman year — her enthusiasm for the subject was captivating — and she and I developed a great relationship. It was in that class I discovered that plants are what I want to study for the rest of my life.”
As part of Dr. Paula McSteen’s lab, Guthrie studies the reproductive organs of maize and how its genes allow it to produce flower-bearing structures in pairs, while other plants only produce these structures singly.
“If you count the number of rows on a corn cob, it’s always even,” Guthrie said. “That’s because maize produces two flowers at a time instead of one. My research is essentially trying to figure out which genes are responsible for that doubling trait.”
It’s not an easy process, though, so Guthrie nurtures a unique approach to finding the solutions.
“I take ears of corn that make one flower-bearing structure and work backwards to try and find what’s missing,” Guthrie said. “If I can find that, I can assume that’s what’s making the difference.”
Although her work can be painstaking, Guthrie noted that science is all about learning from mistakes.
Ultimately, Guthrie wants to duplicate the gene that causes the doubling trait in other crops, such as rice, wheat and barley. This could have a big impact on cereal crop reproduction.
“We’re hoping to apply what we learn about maize other crops,” Guthrie said.
After finishing her studies at Mizzou, Guthrie plans to return to the classroom as a professor, preferably teaching undergraduates.
“The whole reason I decided to go to graduate school was to be able to teach,” Guthrie said. “I want people who aren’t necessarily interested in science initially to get invested in it. I also want to incorporate research into the classes I’ll teach because not every college is a research campus like Mizzou.”
