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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.”

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.

A love story closes LSSP 2017

Jim Obergefell’s love endured through his partner’s death and all the way to the Supreme Court.
Jim ObergefellJim Obergefell speaks about winning the landmark Supreme Court case that granted equal marraige 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.

McKibben urges climate action in campus lecture

Bill McKibben explained the impact of increasing carbon emissions on the global climate and explored solutions to slowing the trend

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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

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.

 

Small steps to treat neuromuscular disorder

Researchers find evidence of a genetic modifier that can improve symptoms of Spinal Muscular Atrophy

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Chris Lorson examines axons through a microscope. Lorson’s lab recently published results that showed evidence that the protein plastin 3 affects the severity of SMA. | Photo by Eleanor Hasenbeck, Bond LSC

Eleanor Hasenbeck | Bond Life Sciences Center

Two new potential treatments might improve the lives of patients living with Spinal Muscular Atrophy.

Researchers in the Lorson lab at Bond Life Sciences Center recently produced a new drug that increases the lifespans of mice with SMA, and they found evidence that an increased level of the protein plastin 3 lengthened life span and improved the animal’s nerve function.

Two genes impact Spinal Muscular Atrophy, SMN1 and SMN2. In a healthy body, SMN1 creates a protein called SMN that helps maintain motor neurons controlling muscle movement. If someone is born without SMN1, their body relies on SMN2 to produce this protein, but a small change in the SMN2 gene causes it to make much less of the protein than needed. This leads to SMA, a disorder where an individual loses motor and nervous function, often starting in childhood, over a number of years.

Although rare, sometimes siblings develop SMA, providing an unusual insight into SMA development. Discordant siblings — or siblings that both have SMA but have different severities of the disorder— suggest that other factors could contribute to SMA.

Researchers are investigating why this happens. One theory is that a “genetic modifier,” another gene or protein elsewhere in the DNA, impacts the severity of SMA. The protein plastin 3 could be this modifier.

Plastin 3 doesn’t improve the severe SMA mice, but extended the lives of mice with more mild cases of the disorder. The Lorson lab created its own SMA drug, an antisense oligonucleotide that allows SMN2 to produce a functional protein. The drug is capable of extending survival of SMA mice from approximately 13 days up to 150 days from a single treatment. The typical lifespan of a lab mouse is 1.3 to 3 years.

Kevin Kaifer, a graduate student in the Lorson lab, gave the SMA mice a low dose injection of the drug, increasing their lifespan to about 30 days. Then, they modified a gene in the mice to increase the level of plastin 3. Mice that received the drug and the plastin 3 therapy lived about 40% longer than mice that received only the drug.

Lorson said the results provide proof of concept that plastin 3 does not make more SMN, but actually decreased disease severity. The SMA mice showed improved neuromuscular junctions, the sites where nerve cells fire electrical impulses to the muscles in the body.

“That’s really where plastin 3 is designed to function, at the neuromuscular junction,” Lorson said. “So that brings the idea of plastin 3 full circle; it does not increase SMN, but it does improve the function of the nerve which is where plastin 3 is supposed to function normally.”

This discovery shows promise for a future treatment to some with the disease.

“SMA is a very broad clinical spectrum disease, so there are patients who have an incredibly severe form, and patients that don’t develop disease until adulthood,” said Chris Lorson, a Bond LSC scientist. “Perhaps one therapy is not going to address that very broad clinical spectrum, and you’re going to need to address different parts of the disease with different therapeutics.”

Despite it’s relative rarity as a disease, new treatments for SMA are hitting the market. In December, the Food and Drug Administration approved Spinraza, an antisense oligonucleotide similar to the drug the Lorson lab. But the infrequency of SMA means treatment comes at a cost: $750,000 for the first year of Spinraza and $375,000 for subsequent years. Spinraza is an FDA-designated orphan drug, meaning it’s a treatment for a disease that affects less than 200,000 people in the U.S. To incentivize research into rare diseases, The Orphan Drug Act allows pharmaceutical companies longer exclusive patent rights. Drugs that treat rare diseases that impact children, including Spinraza, can be allowed priority review, basically putting these drugs on a faster track from lab to market. Though the act has led to more research in certain diseases, it has sparked controversy as patients with no other treatment options are burdened with the resulting drugs’ high cost.

Still, it’s the first FDA approved treatment available to the 9,000 Americans living with SMA.

“I think collectively this is a very exciting time in the SMA field, whether we’re talking about SMN targeting compounds or drugs that are capable of augmenting function,” Lorson said.  “To have a rare disease that has so many shots on goals, so to speak is really exciting.”

“The SMA community is really a model for how foundations, families, patients and government agencies can come together,” Lorson said. He said families and government agencies are often in the same room as academics, biotechnology and pharmaceutical companies during meetings.

“The amount of support from the patients, the families and the non-profit world has really helped drive SMN research… I think that’s really helped push SMA from an unknown 20 years ago, to an approved drug.”

Christian Lorson is a professor of veterinary pathobiology at the Bond LSC. His research focuses on spinal muscular atrophy.
The results of this study were published in an article in JCI Insight, “Plastin-3 extends survival and reduces severity in mouse models of spinal muscular atrophy.” This work is partially funded by grants from the Muscular Dystrophy Association, FightSMA, the Gwendolyn Strong Foundation, and the Missouri Spinal Cord Injury/Disease Research Program. CureSMA provided the initial support for the development of the drug/antisense oligonucleotide used in these studies.

 

Old friends, new ideas

A partnership between MU and Gyeongsang National University in South Korea has created lasting connections

By Eleanor Hasenbeck | Bond Life Sciences Center

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Discussion went global this week as researchers converged from Gyeongsang National University in South Korea, MU and Washington University at Bond Life Sciences Center for the sixth MU-GNU International Joint Symposium in Plant Biotechnology.

Plant biologists from each university shared their research, ranging from molecular biology and signaling to breeding soybeans for improved yields. The symposium is held every two years, alternating locations between the U.S. and South Korea. This conference marks the eleventh year of collaboration between GNU and MU.

“Every trip that comes over, new collaborations develop,” said Gary Stacey, a Bond LSC scientist of soybean biotechnology and chair of the symposium’s local organizing committee. “Just at dinner the other night, you could hear people talking and saying ‘We should do that together.’ You get people together and they collide, and good things come from that. The whole idea of these symposiums is try to increase those collisions.”

As those involved share new research and ideas, these collaborations create opportunities. A former student in Stacey’s lab recently received a doctoral degree from both universities as part of a joint-doctoral degree program. Undergraduate Korean students can also complete a “2+2” degree, where students can begin their studies with two years at GNU and finish with two years at MU.

The schools also exchange faculty members. GNU researchers Jong Chan Hong and Woo Sik Chung completed sabbaticals at MU. Stacey has spent time in Korea, and his lab receives funding from Korean grants.

“Getting our students to interact with Korean students and Korean faculty expands their horizons, gets them in contact with other cultures and is really part of creating an intellectual environment where students can grow,” Stacey said.

For Stacey, the symposium has also brought valued friendships. “After you’ve been over there, and you know these guys for eleven years, it’s like your cousin coming home,” he said. “You’re not a visitor anymore. You’re like part of the family.”

For more information about the science exchanged, visit http://staceylab.missouri.edu/symposium.

The next Martians: the common bean?

Researchers in the Mendoza-Cozatl lab grow beans in a soil that simulates Martian soil
By Eleanor C. Hasenbeck | Bond Life Sciences

As NASA works to send people to Mars, researchers at the Mendoza-Cozatl lab at Bond Life Sciences Center are exploring the possibility of sending beans to the red planet. The journey from Earth to Mars alone would take somewhere between 100 to 300 days. To feed astronauts on these longer missions, scientists are studying space horticulture.

Norma Castro, a research associate in the lab, studies how common beans grow in a soil that simulates Mars’ red soil. The common bean is a good candidate for interstellar cultivation. Beans are a very nutritious crop, and their affinity for nitrogen-fixing bacteria can improve soil health while requiring less fertilizer. Castro is trying to understand how different varieties of beans could grow in the soil.

“This kind of research not only will tell us the right plants to take to Mars, but also which kind of technology needs to be developed,” Castro said.

Harvard researcher to speak at Life Sciences Week

Jessica Whited studies the genetics behind how salamanders grow severed limbs

By Eleanor Hasenbeck | Bond LSC

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An axolotl rests at the bottom of its tank at Menagerie du Jardin des Plantes in Paris. | photo by Jack Baker, Flickr

It takes about two months for an axolotl to regenerate a lost limb. Humans, as you probably know, don’t regenerate limbs.

But, a basic understanding of how the Mexican salamander regrows limbs advance regenerative medicine in humans according to Jessica Whited, a researcher at Brigham Women’s Hospital and assistant professor at Harvard Medical School.

Whited will speak at 3:30 p.m., Thursday April 13, in Monsanto Auditorium as part of Missouri Life Sciences Week at Bond Life Science Center. Her lecture, “Identifying roadblocks to regeneration in axolotl salamanders” will present the lab’s discoveries and evidence that a specific gene in axolotls can block the animal’s ability to regenerate.

Whited’s lab found axolotls can exhaust their ability to regenerate. When a limb is severed repeatedly, the salamander stops producing blastemas, the mass of cells capable of regeneration that allow the limb to grow back. This could be due to a dysregulated gene blocking the animal’s ability to produce them.

The Whited Lab sequenced the mRNA in axolotls that could regenerate limbs and that could no longer regenerate. They found 912 genes that differed between the two groups. Whited will discuss one of these genes, which her lab considers a potential inhibitor to regeneration.

“It’s much more common for people to think “Oh, what are the things that promote limb regeneration?’ than it is to think about the things that we might have to block to make it happen,” Whited said. “This project has the potential to uncover the roadblocks, which could turn out to be equally critical.”

An MU alumna, Whited received the National Institutes of Health New Innovator Award in 2015 for her work with this unique regenerative salamander. She earned a PhD in biology at the Massachusetts Institute of Technology, and two undergraduate degrees in biological sciences and philosophy at MU.

Whited attended MU as a Bright Flight and Curator’s Scholar. And though it happened nearly 20 years ago, she said receiving those two scholarships were among the most important things that happened in her career. As a high school student, she knew she would go to college, but financially, she didn’t know how it would happen. She also credits her education and undergraduate research experience at MU for preparing her to think at the research bench.

“You have to get an undergraduate education, and it totally prepared me even for graduate school at MIT, which is one of the top programs in the world, in many subjects, but in biology especially,” Whited said. “The idea that you could find a career where you’re using your brain as your primary asset, I figured that out while I was at the University of Missouri, because there were people, our professors, doing that.”

Whited’s lecture is free and open to the public as part of Missouri Life Sciences Week. It occurs at 3:30 on Thursday, April 13 in Bond LSC’s Monsanto Auditorium. See more about events during the week at bondlsc.missouri.edu/life-sciences-week.