SoyKB: Leading the convergence of wet and dry science in the era of Big Data

Yaya Cui, an investigator in plant sciences at the Bond Life Sciences Center examines data on fast neuron soybean mutants that are represented on the SoyKB database.

Yaya Cui, an investigator in plant sciences at the Bond Life Sciences Center examines data on fast neuron soybean mutants that are represented on the SoyKB database.

The most puzzling scientific mysteries may be solved at the same machine you’re likely reading this sentence.

In the era of “Big Data” many significant scientific discoveries — the development of new drugs to fight diseases, strategies of agricultural breeding to solve world-hunger problems and figuring out why the world exists — are being made without ever stepping foot in a lab.

Developed by researchers at the Bond Life Sciences Center, SoyKB.org allows international researchers, scientists and farmers to chart the unknown territory of soybean genomics together — sometimes continents away from one another — through that data.

 

Digital solutions to real-world questions

As part of the Obama Administration’s $200 million “Big Data” Initiative, SoyKB (Soy Knowledge Base) was born.

The digital infrastructure changes the way researchers conduct their experiments dramatically, according to plant scientists like Gary Stacey, Bond LSC researcher, endowed professor of soybean biotechnology and professor of plant sciences and biochemistry.

“It’s very powerful,” Stacey said. “Humans can only look at so many lines in an excel spreadsheet — then it just kind of blurs. So we need these kinds of tools to be able to deal with this high-throughput data.”

The website, managed by Trupti Joshi, an assistant research professor in computer science at MU’s College of Engineering, enables researchers to develop important scientific questions and theories.

“There are people that during their entire career, don’t do any bench work or wet science, they just look at the data,” Stacey said.

The Gene Pathway Viewer available on SoyKB, shows different signaling pathways and points to the function of specific genes so that researchers can develop improvements for badly performing soybean lines.

“It’s much easier to grasp this whole data and narrow it down to basically what you want to focus on,” Joshi said.

A 3D-protein modeling tool lends itself especially to drug design. A pharmaceutical company could test the hypothesis and in some situations, the proposed drug turns out to yield the expected results — formulated solely by data analysis.

The Big Data initiative drives a blending of “wet science” — conducting experiments in the lab and gathering original data — and “dry science” — using computational methods.

Testament of the times?

“Oh, absolutely,” Joshi said.

 

Collaboration between the “wet” and “dry” sciences

Before SoyKB, data from numerous experiments would be gathered and disregarded, with only the desired results analyzed. The website makes it easy to dump all of the data gathered to then be repurposed by other researchers.

“With these kinds of databases now, all the data is put there so something that’s not valuable to me may be valuable to somebody else,” Stacey said,

Joshi said infrastructure like SoyKB is becoming more necessary in all realms of scientific discovery.

“(SoyKB) has turned out to be a very good public resource for the soybean community to cross reference that and check the details of their findings,” she said.

Computer science prevents researchers having to reinvent the wheel with their own digital platforms. SoyKB has a translational infrastructure with computational methods and tools that can be used for many disciplines like health sciences, animal sciences, physics and genetic research.

“I think there’s more and more need for these types of collaborations,” Joshi said. “It can be really difficult for biologists to handle the large scope of data by themselves and you really don’t want to spend time just dealing with files — You want to focus more on the biology, so these types of collaborations work really well.

It’s a win-win situation for everyone,” she said.

The success of SoyKB was perhaps catalyzed by Joshi. She adopted the website and the compilation of data in its infant stages as her PhD dissertation.

Joshi is unique because she has both a biology degree and a computer science background. Stacey said Joshi, who has “had a foot in each camp,” serves as an irreplaceable translator.

Most recently, the progress of SoyKB as part of the Big Data Initiative was presented at the International Conference on Bioinformatics and Biomedicine Dec. 2013 in Shanghai. The ongoing project is funded by NSF grants.

MU Scientists Successfully Transplant, Grow Stem Cells in Pigs

New line of pigs do not reject transplants, will allow for future research on stem cell therapies

Story by Nathan Hurst/MU News Bureau

COLUMBIA, Mo. – One of the biggest challenges for medical researchers studying the effectiveness of stem cell therapies is that transplants or grafts of cells are often rejected by the hosts. This rejection can render experiments useless, making research into potentially life-saving treatments a long and difficult process. Now, researchers at the University of Missouri have shown that a new line of genetically modified pigs will host transplanted cells without the risk of rejection.

Roberts, Mike

Mike Roberts, courtesy of MU News Bureau

“The rejection of transplants and grafts by host bodies is a huge hurdle for medical researchers,” said R. Michael Roberts, Curators Professor of Animal Science and Biochemistry and a researcher in the Bond Life Sciences Center. “By establishing that these pigs will support transplants without the fear of rejection, we can  move stem cell therapy research forward at a quicker pace.”

In a published study, the team of researchers implanted human pluripotent stem cells in a special line of pigs developed by Randall Prather, an MU Curators Professor of reproductive physiology. Prather specifically created the pigs with immune systems that allow the pigs to accept all transplants or grafts without rejection. Once the scientists implanted the cells, the pigs did not reject the stem cells and the cells thrived. Prather says achieving this success with pigs is notable because pigs are much closer to humans than many other test animals.

Randall Prather, courtesy of MU News Bureau

Randall Prather, courtesy of MU News Bureau

“Many medical researchers prefer conducting studies with pigs because they are more anatomically similar to humans than other animals, such as mice and rats,” Prather said. “Physically, pigs are much closer to the size and scale of humans than other animals, and they respond to health threats similarly. This means that research in pigs is more likely to have results similar to those in humans for many different tests and treatments.”

“Now that we know that human stem cells can thrive in these pigs, a door has been opened for new and exciting research by scientists around the world,” Roberts said. “Hopefully this means that we are one step closer to therapies and treatments for a number of debilitating human diseases.”

Roberts and Prather published their study, “Engraftment of human iPS cells and allogeneic porcine cells into pigs with inactivated RAG2 and accompanying severe combined immunodeficiency” in the Proceedings of the National Academy of Sciences.

This study was made possible through grants from Konkuk University in South Korea and the National Institutes of Health.

Roberts has appointments in the MU College of Food, Agriculture and Natural Resources (CAFNR) and the MU School of Medicine and is a member of the National Academy of Sciences. Prather has an appointment in CAFNR and is the director of the NIH-funded National Swine Resource and Research Center.

New screening tool gives scientists more control over genetic research

A tangled spool of yarn represents DNA, while the fingers holding the section represent the insulators just added by MU researchers to improve a scientific, screening tool. | Paige Blankenbuehler

A tangled spool of yarn represents DNA, while the fingers holding the section represent the insulators just added by MU researchers to improve a scientific, screening tool. | Paige Blankenbuehler

Here’s a scenario: You are trying to find a lost section of string in the world’s most massively tangled spool of yarn. Then try cutting that section of yarn that’s deeply embedded in the mess without inadvertently cutting another or losing track of the piece you’re after.

For researchers, this problem is not unlike something they encounter in the study of genetic information in the tangled spool that is DNA.

A new tool will help scientists straighten things out.

The tool, developed by University of Missouri Bond Life Sciences Center investigators helps researchers effectively screen cell behavior by limiting epigenetic silencing, which occurs when a cell packages and stows away important genetic information, much like an accountant puts a client’s information away in a filing cabinet.

The cell can go digging to find that information when it absolutely needs it, but otherwise that information is tucked away and inactive.

Professors of biochemistry Mark Hannink, Tom Mawhinney and research assistant professor Valeri V. Mossine used insulators to develop the piggyBac transposon plus insulators, a better reporter of signaling between cells that makes improved screening possible.

This simple addition to an existing screening tool used in laboratories will help streamline research and contribute to screening products like vitamins and supplements and medicines for authenticity, Hannink said.

This is why the insulator addition to the piggyBac reporter assay by MU researchers is a game changer in the scientific world.

 

How it works

DNA stretches out to nearly 10 feet when it’s uncoiled. That’s 10 feet of your body’s deepest secrets coiled into a microscopic package and tucked away into each and every one of your cells. The human body, by the way, holds an estimated 10 trillion cells. An inconceivable number, right?

Let’s go back to our yarn analogy. You’re trying to find one specific piece to cut but it’s deeply tangled in the mass of yarn. You need to find the piece that you really care about and clamp your fingers onto the yarn to reduce the slack — straighten it out — so you can cut it easily.

Think of your fingers as the insulators.

The insulators of the new piggyBac transposon tool perform the same task of stretching out the DNA so certain expressions through signaling pathways are held open, enabling the investigation of specific genetic material.

Hannink hypothesizes this new reporter could provide answers to questions like: Does an anti-migraine medicine have the component that will relieve that ailment? Does a multi-vitamin deliver all of the nutrients on its label?

“A lot of botanicals are said to have anti-inflammatory benefits,” Hannink said. “By using an assay like this, we can easily determine if they actually do and if so, what molecules in these complex mixtures are in fact the cause of the punitive inflammatory activity.”

 

 

Reproducing results

Replication is a critical part of verifying scientific discovery and epigenetic silencing is a big headache for investigators trying to reproduce results.

Scientists studying genetic material can open certain expressions with other reporter tools but often, the cell will turn expressions off and block signaling pathways, causing an expected result to fail because of epigenetic silencing.

The new assay preserves conditions of an experiment so the same results can be reached. Cell behavior under the same conditions and expressions that were switched on during the experiment will be expressed.

The new version of the reporter assay is being used at the MU Center for Botanical Interaction Studies to understand how botanical compounds affect the immune system and in other research on the central nervous system and on the development of prostate cancer.

This research appeared in the Dec. 20, 2013 edition of PLoS ONE. It was funded by the University of Missouri Agriculture Experiment Station Laboratories and grants from the National Center for Complementary and Alternative Medicines, Office of Dietary Supplements and the National Cancer Institute.

Trail to a Cure, Inc. helps fund training of future scientists, physcians

Over the weekend, Bond LSC HIV researchers Stefan Sarafianos, Marc Johnson and Donald Burke-Aguero joined Trail to a Cure, Inc., a Columbia nonprofit organization that helped fund important HIV research.

Since 2008, the organization has raised $74,000 for HIV/AIDS research, with some of that funding going directly to the Bond LSC providing additional hours of lab research. The 2014 online fundraising is still open and donations can be made to Trail to a Cure, Inc. until the end of the month.

The funding from Trail to a Cure helps Bond LSC researchers train future scientists and physicians in labs and in some cases, training them on the development of next generation therapies, Johnson said.

 

Bond LSC HIV researchers Stefan Sarafianos (left), Marc Johnson (center), and Donald Burke-Aguero (right) at the 7th annual Trail to a Cure along Katy Trail in Rocheport on May 3. | Credit: Trail to a Cure, Inc..

Bond LSC HIV researchers Stefan Sarafianos (left), Marc Johnson (center), and Donald Burke-Aguero (right) at the 7th annual Trail to a Cure along Katy Trail in Rocheport on May 3. | Credit: Trail to a Cure, Inc..

Trail to a Cure, Inc., a Columbia-based nonprofit, has raised $74,000 for HIV/AIDS since 2008. Part of the raised funds go to HIV research in the LSC, providing additional hours of lab research. | Credit: Trail to a Cure, Inc.

Trail to a Cure, Inc., a Columbia-based nonprofit, has raised $74,000 for HIV/AIDS since 2008. Part of the raised funds go to HIV research in the LSC, providing additional hours of lab research. | Credit: Trail to a Cure, Inc.

A drug that packs a punch: new compound works better against resistant HIV

Virologist Stefan Sarafianos stands in the atrium of the Bond LSC.

Bond LSC researcher Stefan Sarafianos stands in the LSC atrium. The virologist is an associate professor of molecular microbiology and immunology and Chancellor’s Chair of Excellence in Molecular Virology with appointments in MU’s School of Medicine and the Department of Biochemistry.

Resistance is the price of success when it comes to treating HIV.

Virologists at the Bond Life Sciences Center are helping to test the next generation of anti-AIDS medication to quell that resistance.

Stefan Sarafianos’ lab recently proved that EFdA, a compound that stops HIV from spreading, is 70 times more potent against some HIV that resists Tenofovir – one of the most used HIV drugs.

“HIV in patients treated with Tenofovir eventually develop a K65R RT mutation that causes a failure of this first line of defense,” said Sarafianos, virologist at Bond LSC. “Not only does EFdA work on resistant HIV, but it works 10 times better than on wild-type HIV that hasn’t become Tenofovir resistant.”

Sarafianos and a team of researchers found that EFdA (4′-ethynyl-2-fluoro-2′-deoxyadenosine) is activated by cells more readily and isn’t broken down by the liver and kidneys as quickly as similar existing drugs.

“These two reasons make it more potent than other drugs, and so our task is to look at the structural features that make it such a fantastic drug,” he said.

 

From soy sauce to virus killer

The path from EFdA’s discovery to current research is a bit unorthodox.

A Japanese soy sauce company named Yamasa patented this molecule, which falls into a family of compounds called nucleoside analogues that are very similar to existing drugs for HIV and other viruses. EFdA was designed and synthesized by Hiroshi Ohrui (Chem Rec. 2006; 6 (3), 133-143Org. Lett. 2011; 13, 5264) and shown by Hiroaki Mitsuya, Eiichi Kodama, and Yamasa to have potential usefulness against HIV. Samples sent for further testing confirmed EFdA’s potential usefulness against HIV. This started more than a decade of research to pinpoint what makes the compound special.

EFdA joins a class of compounds called nucleoside reverse transcriptase inhibitors (NRTIs) that includes eight existing HIV drugs. Like all NRTIs, EFdA hijacks the process HIV uses to spread by tricking an enzyme called reverse transcriptase (RT). RT helps build new DNA from the RNA in HIV, assembling nucleoside building blocks into a chain. Since EFdA looks like those building blocks, RT is tricked into using the imposter. When this happens the virus’ code cannot be added to the DNA of white blood cells it attacks.

“NRTIs are called chain terminators because they stop the copying of the DNA chain, and once incorporated it’s like a dead end,” Sarafianos said.

 

A little help from some friends

Sarafianos isn’t alone in studying EFdA.

The virologist’s lab works closely with University of Pittsburgh biochemist Michael Parniak and the National Institutes of Health’s Hiroaki Mitsuya to explore the molecule’s potential. Mitsuya had a hand in discovering the first three drugs to treat HIV and Parniak has spent years evaluating HIV treatments using cultured white blood cells.

Sarafianos’ focus requires him to take a very close look at EFdA to define how it works on a molecular level. He uses virology, crystallography and nuclear magnetic resonance to piece together the exact structure, bonding angles and configuration of the compound.

By looking at subtle differences in EFdA’s sugar-like ring, his lab identified the best structure that looks the most like actual nucleosides, doesn’t break down easily and is activated readily by CD4+ T lymphocyte white blood cells.

“The structure of this compound is very important because it’s a lock and key kind of mechanism that can be recognized by the target,” Sarafianos said. “We’re looking at small changes and the ideal scenario is a compound bound very efficiently by the target and activating enzyme but not efficiently by the degrading enzymes.”

 

Treatment for the future

The research of Sarafianos, Parniak and Mitsuya continue to uncover the magic of EFdA. In 2012, they showed that the drug worked incredibly well to treat the HIV equivalent in monkeys.

“These animals were so lethargic, so ill, that they were scheduled to be euthanized when EFdA was administered,” said Parniak. “Within a month they were bouncing around in their cages, looking very happy and their virus load dropped to undetectable levels. That shows you the activity of the molecule; it’s so active that resistance doesn’t come in as much of a factor with it.”

HIV prevention is the newest focus in their collaboration.

By recruiting formulation expert Lisa Rohan at the University of Pittsburgh, they are now putting EFdA in a vaginal film with a consistency similar to Listerine breath strips.

“The only way we are going to make a difference with HIV is prevention,” Parniak said. “If we can prevent transmission, this approach could make a huge difference in minimizing the continued spread of the disease when combined with existing therapies for people already infected.”

While AIDS in the U.S. occurs mostly in men, the opposite is true in sub-Saharan Africa where more than 70 percent of HIV cases occur. Since a film has a better shelf life than creams or gels, it could benefit those at risk in extreme climates and third-world countries.

“We have nearly 30 drugs approved for treating HIV infected individuals, but only one approved for prevention,” Sarafianos said. “Women in Africa would benefit from a formulation like this as a means to protect themselves.”

Despite this success, Sarafianos and Parniak aren’t slowing down in figuring out how EFdA works so well.

“We want to understand how long EFdA stays in the bloodstream and cells,” Parniak said. “If we understand structurally why this drug is so potent it allows us to maybe develop additional molecules equally potent, and a combination of those molecules could be a blockbuster.”

Grants from the National Institutes of Health fund this research.

In 2013 and 2014, the journals Retrovirology, Antimicrobial Agents and Chemotherapy and The International Journal of Pharmaceutics published this group’s work on EFdA. Sarafianos is an associate professor of molecular microbiology and immunology and Chancellor’s Chair of Excellence in molecular virology with MU’s School of Medicine and a joint associate professor of biochemistry in the MU College of Agriculture, Food and Natural Resources. 

Frogs help researchers find genetic mechanism for mildew susceptibility in grapevine

Powdery mildew on a cabernet sauvignon grapevine leaf. | USDA Grape genetics publications and research

Powdery mildew on a cabernet sauvignon grapevine leaf. | USDA Grape genetics publications and research

A princess kisses a frog and it turns into a prince, but when a scientist uses a frog to find out more information about a grapevine disease, it turns into the perfect tool narrowing in on the cause of crop loss of Vitis vinifera, the world’s favorite connoisseur wine-producing varietal.

MU researchers recently published a study that uncovered a specific gene in the Vitis vinifera varietal Cabernet Sauvingon, that contributes to its susceptibility to a widespread plant disease, powdery mildew. They studied the biological role of the gene by “incubating” it in unfertilized frog eggs.

The study, funded by USDA National Institute of Food and Agriculture grants, was lead by Walter Gassmann, an investigator at the Bond Life Sciences Center and University of Missouri professor in the division of plant sciences.

The findings show one way that Vitis vinifera is genetically unable to combat the pathogen that causes powdery mildew.

Gassmann said isolating the genes that determine susceptibility could lead to developing immunities for different varietals and other crop plants and contribute to general scientific knowledge of grapevine, which has not been studied on the molecular level to the extent of many other plants.

The grapevine genome is largely unknown.

“Not much is known about the way grapevine supports the growth of the powdery mildew disease, but what we’ve provided is a reasonable hypothesis for what’s going on here and why Cabernet Sauvingon could be susceptible to this pathogen,” Gassmann said.

The research opens the door for discussion on genetically modifying grapevine varietals.

Theoretically, Gassmann said, the grapevine could be modified to prevent susceptibility and would keep the character of the wine intact — a benefit of genetic modification over crossbreeding, which increases immunity over a lengthy process but can diminish character and affect taste of the wine.

Grapevine under attack

Gassmann’s recent research found a link between nitrate transporters and susceptibility through a genetic process going on in grapevine infected with the powdery mildew disease.

Infected grapevine expressed an upregulation of a gene that encodes a nitrate transporter, a protein that regulates the makes it possible for the protein to enter the plant cell.

Once the pathogen is attracted to this varietal of grapevine, it tricks grapevine into providing nutrients, allowing the mildew to grow and devastate the plant.

As leaves mature, they go through a transition where they’re no longer taking a lot of nutrients for themselves. Instead, they become “sources” and send nutrients to new “sink” leaves and tissues. The exchange enables plants to grow.

The powdery mildew pathogen, which requires a living host, tricks the grapevine into using its nutrient transfer against itself. Leaves turn into a “sink” for the pathogens, and nutrients that would have gone to new leaves, go instead, to the pathogen, Gassmann said.

“We think that what this fungus has to do is make this leaf a sink for nitrate so that nitrate goes to the pathogen instead of going to the rest of the plant,” Gassmann said.

Walter Gassmann, of the Bond Life Sciences Center at the University of Missouri was the lead investogator on the research. Much of his work has been on grapevine susceptibility to pathogens.

Walter Gassmann, of the Bond Life Sciences Center at the University of Missouri was the lead investogator on the research. Much of his work has been on grapevine susceptibility to pathogens. | Roger Meissen, Bond Life Sciences Center

According to a report by the USDA, powdery mildew can cause “major yield losses if infection occurs early in the crop cycle and conditions remain favorable for development.”

Powdery mildew appears as white to pale gray “fuzzy” blotches on the upper surfaces of leaves and thrives in “cool, humid and semiarid areas,” according to the report.

Gassmann said powdery mildew affects grapevine leaves, stems and berries and contributes to significant crop loss of the Vitas vinifera, which is cultivated for most commercial wine varietals.

“The leaves that are attacked lose their chlorophyll and they can’t produce much sugar,” Gassmann said. “Plus the grape berries get infected directly, so quality and yield are reduced in multiple ways.”

Pinpointing a cause

Solutions to problems start with finding the reason why something is happening, so Gassmann and his team looked at a list of genes activated by the pathogen to find transporters that allowed compounds like peptides, amino acids, and nitrate to pass.

Genes for nitrate transporters, Gassmann said, pointed to a cause for vulnerability to the mildew pathogen.

Over-fertilization of nitrate increases the severity of mildew in many crop plants, according to previous studies sited in Gassmann’s article in the journal of Plant Cell Physiology.

The testing system for isolating and analyzing the genes began with female frogs.

Gassmann used frog oocytes (unfertilized eggs), to verify the similar functions of nitrate transporters in Arabidopsis thaliana, a plant used as a baseline for comparison.

A nitrate transporter, he hypothesized, would increase the grapevine’s susceptibility to mildew.

“The genes that were upregulated in grapevine showed similarity to genes in Arabidopsis that are known to transport nitrate,” Gassmann said. “We felt the first thing we had to do was verify that what we have in grapevine actually does that.”

The eggs are very large relative to other testing systems and act as “an incubating system” for developing a protein. Gassmann and his team of researchers injected the oocyte with RNA, a messenger molecule that contains the information from a gene to produce a protein. The egg thinks it’s being fertilized and protein reproduces and is studied.

“The oocyte is like a machine to crank out protein,” Gassmann said. “We use that technique to establish what we have is actually a nitrate transporter.”

The system confirmed that the gene isolated from grapevine encodes a nitrate transporter.

“We contributed to the general knowledge of the nitrate transporter family,” Gassmann said. “It turned out to be the first member of one branch of nitrate transporters that, even in Arabidopsis haven’t been characterized before.”

The mounting knowledge of Vitis vinifera genes could make genetically modifying the strain to prevent the susceptibility easier.

“Resistance is determined sometimes by a single gene,” Gassmann said. “Until people are willing to have the conversation of genetic modification, the only way to save your grapevines is to be spraying a lot.”

Sharon Pike, Gassmann, other investigators from the MU Christopher S. Bond Life Sciences Center and post-doctoral student, Min Jung Kim from Daniel Schachtman’s lab at the Donald Danforth Plant Science Center in Saint Louis, Mo. contributed to the report.

The article was accepted November 2013 into the Plant Cell Physiology journal.

Chemical beacons: LSC scientist discovers how plants beckon bacteria to attack

Scott Peck studies Arabidopsis and how bacteria perceive it before initiating an infection. Roger Meissen/ Bond LSC

Scott Peck, Bond LSC scientist and associate professor of biochemistry, studies Arabidopsis and how bacteria perceive it before initiating an infection. Roger Meissen/ Bond LSC

Sometimes plants inadvertently roll out the red carpet for bacteria.

Researchers at the University of Missouri Bond Life Sciences Center recently discovered how a plant’s own chemicals act as a beacon to bacteria, triggering an infection. Proceedings of the National Academy of Sciences published their study April 21.

“When bacteria recognize these plant chemicals it builds a needle-like syringe that injects 20-30 proteins into its host, shutting down the plant’s immune system,” said Scott Peck, Bond LSC plant scientist and lead investigator on the study. “Without a proper defense response, bacteria can grow and continue to infect the plant. It looks like these chemical signals play a very large role in mediating these initial steps of infection.”

The question of how bacteria actually know they are in the presence of a plant has puzzled scientists for years. Being able to identify the difference between a plant cell and, say, a rock or a piece of dirt, means the bacteria saves energy by only turning on its infection machinery when near a plant cell.

“Our results show the bacteria needs to see both a sugar – which plants produce quite a bit of from photosynthesis – and five particular acids at the same time,” Peck said. “It’s sort of a fail-safe mechanism to be sure it’s around a host before it turns on this infection apparatus.”

Peck’s work started with one mutant plant called Arabidopsis mkp1.

Discovered several years ago by Peck’s lab, this little mustard plant acts differently than others by rebuffing the advances of bacteria. Lab tests confirmed that this mutant didn’t get infected by Pseudomonas syringae pv. tomato DC3000, a bacterial pathogen that causes brown spots on tomatoes and hurts the model plant Arabidopsis. Along with MU biochemistry research scientist Jeffrey Anderson and post doc Ying Wan, they showed that this mutant didn’t trigger the bacteria’s Type III Secretion System, the needle-like syringe and associated proteins that lead to infection.

Pacific Northwest National Laboratory (PNNL) worked with Peck’s team to compare levels of metabolites between the mutant Arabidopsis and normal plants. This comparison helped Peck identify a few of these chemicals – created from regular plant processes – that existed in much lower levels in their special little mutant.

Using the PNNL work as a guide, the team found five acids collectively had the biggest effect in turning on a bacteria’s infection: aspartic, citric, pyroglutamic, 4-hydrobenzoic and shikimic acid.

“The key experiment involved us simply adding these acids back into the mutant,” Peck said. “Suddenly we saw the mutant plant wasn’t resistant anymore and the bacteria were once again capable of injecting proteins to turn off the plant’s immune system.”

First contact and recognition means all the difference, whether bacteria or plant. Just a slight jump out of the starting blocks by one or the other could change who will win a battle of health or infection.

While low concentrations of these five acids trigger the bacteria’s attack, high levels blind it to the plant’s presence, leading Peck to believe it could be used to hinder bacterial growth. If this actually thwarts the bacteria’s head start, it could mean stopping disease in crops and could lead to a different approach in the field.

“A lot of the winning and losing occurs within the first 2-6 hours and it seems to be that if the microbe is too slow to turn off the immune system, the plant can actually fight off the infection,” Peck said. “In the future we could possibly make a new generation of anti-microbial compounds that don’t try to kill the bacteria, but rather just make them no longer virulent by blocking these chemical signals so the natural plant immune system can basically take over.”

Peck’s team believes at least some other bacteria will respond to these chemical signals, and he plans to test other bacterial pathogens to make certain. They also want to test bacteria to see if they are more virulent in humans once primed for attack by these plant chemical signals.

“In the long run the question is how far this extends. A lot of people get salmonella or listeria infections through a food source,” Peck said. “The question is do other bacteria that come in through plant food sources have similar perception systems and end up being more infectious in humans because they are already primed for infection.”

A $500,000 grant from the National Science Foundation supported this research.

Bond LSC Investigator Chris Pires in Shanghai, Wuhan

Recently, one of our investigators, J. Chris Pires traveled to Fudan University in Shanghai and the Wuhan Vegetable Research Institute for the 19th annual Crucifer Genetic Workshop and Brassica 2014 Conference in Wuhan, China.

Pires was invited to the esteemed event as the keynote speaker of the Brassica Conference. He led workshops as part of the three-day conference March 30 through April 2 and also visited Fudan University in Shanghai during the trip.

Pires is an associate professor in biological sciences and focuses much of his research on the evolution of plants. His talk at Fudan University discussed his research on whole genome duplications and the origins of novelty in plants.

Chris Pires, investigator and associate professor in biological sciences at the Bond Life Sciences Center at Fudan University in Shanghai.

Chris Pires, investigator and associate professor in biological sciences at the Bond Life Sciences Center at Fudan University in Shanghai.

Pires-china-conference3

Pires with Hong Ma, the dean of life sciences at Fudan University (right) and an assistant professor (left). Pires traveled to Shanghai to lead a workshop at the university over his research in whole genome duplications in plants.

Pires-China-workshop2

Pires at the 19th Crucifer Genetic Workshop and Brassica 2014 at the Wuhan Vegetable Research Institute in Wuhan, China. Pires was the keynote speaker at the conference.

Bond LSC staff prepares boat for April 12 fundraiser

Made completely of cardboard and Popeye themed, Bond LSC facilities crew say this boat could be the winner of the 3rd Annual Flot Your Boat for the Food Bank Race on April 12 — BLANKENBUEHLER

Made completely of cardboard and Popeye themed, Bond LSC facilities crew say this boat could be the winner of the 3rd Annual Flot Your Boat for the Food Bank Race on April 12 — BLANKENBUEHLER

Every year the College of Agriculture, Food and Natural Resources puts on a Float Your Boat for the Food Bank Race. All proceeds go to the Columbia Food Bank and last year, with 45 participants, more than $17,000 was donated.  All participants craft their own boat and obey one golden rule: cardboard only.

The Bond LSC crew are returning to the race, this year on April 12, with a Popeye themed boat they say will win it all. Cash donations are being accepted until the race day by Maureen Kemp in 106 at the Bond Life Sciences Center. The People’s Choice Award is given to the boat with the team that raised the most money for the Food Bank.

Barbie Reid, Bond LSC office support assistant, will dress as Olive Oil for this year's race. — BLANKENBUEHLER

Barbie Reid, Bond LSC office support assistant, will dress as Olive Oil for this year’s race. — BLANKENBUEHLER

The Bond LSC ATCP is a streamlined, perfectly buoyant  cardboard boat. ATCP are the letters of DNA sequencing. — BLANKENBUEHLER

The Bond LSC ATCP is a streamlined, perfectly buoyant cardboard boat. ATCP are the letters of DNA sequencing. — BLANKENBUEHLER

The Bond LSC facilities department crafted mock spinach cans to play up the Popeye theme for this year's Float Your Boat for the Food Bank Race— BLANKENBUEHLER

The Bond LSC facilities department crafted mock spinach cans to play up the Popeye theme for this year’s Float Your Boat for the Food Bank Race— BLANKENBUEHLER

Choi honored for distinguished dissertation

Jeongmin Choi (left), Gary Stacey (center) and postdoc Kiwamu Tanaka recently discovered the first plant receptor for extracellular ATP.

Jeongmin Choi (left), Gary Stacey (center) and postdoc Kiwamu Tanaka recently discovered the first plant receptor for extracellular ATP. Choi received the 2014 Distinguished Dissertation Award for her part in this work.

A former Bond LSC graduate student is being recognized for a dissertation that stands out from the crowd.

Jeongmin Choi received the 2014 Distinguished Dissertation Award this month from MU’s Graduate Faculty Senate for her work identifying the first plant receptor for extracellular ATP. The journal Science published Choi’s “Identification of a plant receptor for extracellular ATP”  Jan. 17, 2014.

Choi completed her dissertation working as a member of Gary Stacey’s lab team. Stacey, a Bond LSC researcher, nominated her work for this award. This is the second year work completed in Bond LSC garnered this award after Lefteris Michailidis won in 2013 for work on the HIV drug EFdA.

Choi has since received her Ph.D. and now resides in Cambridge, England.

Read more about her work in Bond LSC team identifies first plant receptor for extracellular ATP published in January.