Researcher Jianbin Su

Jianbin Su

Defense or growth: a complicated balance

April 7, 2021 By Lauren Hines in Research Tags: gene expression, plant immune system, plant science, TOPLESS gene family

By Lauren Hines | Bond LSC

The plant immune system isn’t active all the time. Plants must decide to either defend against disease or grow, but not simultaneously.

The reason behind this process is not fully understood, and the Walter Gassmann lab at Bond Life Sciences Center is searching for answers.

The lab recently found a link between members of the TOPLESS gene family, the immune receptor SNC1 and a negative regulator SRFR1. The relationship revealed when members of the gene family are absent in a plant, the immune system intensifies, and growth is stunted. The findings were published in February in the journal PLoS Genetics.

“As scientists, we try to simplify a model but sometimes the more we know, the more complicated we realize it to be,” said Jianbin Su, a research scientist in the Gassmann lab.

The study focused on TPR2 and TPR3, two genes within the TOPLESS family.

After studying these two genes, Gassmann said they did not act as he expected when partnered with SNC1. It turns out the genes act as “brakes” so then the immune system doesn’t go on forever.

“If you were to keep stimulating a plant with pathogens, you would see reduced growth over the long term,” said Gassmann, director of Bond LSC. “Plants have to balance whether they grow or if they defend, but we can artificially remove genes in the repertoire of a plant so that the immune system is on all the time from the get-go, and that manifests itself as stunted growth.”

This balance is the main obstacle facing researchers who want to increase crop yield and resistance to disease. Technically, researchers could increase the level of resistance in plants today but increasing the defense system often costs too much growth and yield.

Instead, the Gassmann lab proposes to modify the natural regulation of the plant’s immune system and bypass artificially increased resistance like pesticides.

“In the end, we would like to be able to generate crop plants that are more resistant to a wide swath of pathogens once we understand their regulatory system better,” Gassmann said.

Now, all the Gassmann lab needs to do is figure out how the system works. Easier said than done.

However, there are theories as to why the plant must choose between growth and defense. Previous theories believe there isn’t enough energy for plants to defend and grow at the same time. Gassmann said the theory doesn’t make a lot of sense to him. Even though the plants at Bond LSC are “pampered” and live in a “luxurious environment,” they stop growing whenever their immune systems are stimulated.

“I think evolutionarily, it is an advantage for plants to have a genetic circuit that makes them decide whether to grow or to defend themselves,” Gassmann said. “So, it’s not an energy limitation. It is genetic pathways that we can study to understand how that recognition works. And if there’s a genetic circuit, then we can tweak it and improve on it.”

Even with these theories, there’s more to this system than just genetics. While TPR2 and TPR3 interact with the immune receptor SNC1 and a negative regulator SRFR1 — a molecule that puts a stop or pause on a cellular process — that doesn’t mean their proteins interact in the cell.

“In terms of protein-protein interaction, many people think, ‘Oh it’s just as we interact physically,’ but actually, the cell is alive,” Su said. “In microscopes, they are moving. Sometimes the protein interaction needs a trigger to induce the protein-protein interaction.”

This interaction at the protein level still needs to be further analyzed, but it can explain why both SRFR1 and TPR2 must be absent for the plant to stop growing and be smaller.

“We think they actually work at different points in the circuit, and that’s why you get an additive effect on plant growth,” Gassmann said. “We’d be really interested to find out what those points are exactly, so there’s always more work to be done.”

While the Gassmann lab has found a new interaction revealing a bit more of the plant immunity process, there is still more to understand.

“Knocking out SRFR1 causes smaller plants, but the more accurate mechanism is still, I think, largely unknown,” Su said. “These genetic interactions with TPR2 are just one part of SRFR1 as a negative regulator in plant immunity.”

Plant vs. Pathogen

October 7, 2020 By Lauren Hines in Research Tags: plant immune system

Research scientist Jianbin Su studies the immune system in lettuce on the third floor of the Bond Life Science Center.

By Lauren Hines | Bond LSC

Scientist Jianbin Su’s research lately took him outside to look at patches of grass and cracks in sidewalks around Mizzou’s campus, searching for a subject in the wild. He found his subject in the form of wild lettuce.

That search can potentially help Su — a research scientist in the Walter Gassmann lab at Bond Life Sciences Center — better understand the immune system of lettuce and therefore protect it against diseases like Downy Mildew and Xanthomonas, which would increase lettuce crop yield.

Su’s paper under review about how the pathogen effector protein, AvrRps4, interacts with lettuce’s immune system will hopefully soon be accepted in the journal Molecular Plant-Microbe Interactions.

“Scientists in Florida are still focusing on lettuce resistance to Xanthomonas,” Su said. “If we can find a mechanism where lettuce recognizes our protein, this finding can be applied to make lettuce immune to Xanthomonas.”

Xanthomonas causes bacterial leaf spots and is a serious seed-borne disease that results in significant losses for the lettuce industry

To infect a plant successfully, the bacterium must inject 30 to 40 protein effectors, like AvrRps4, in the cell and interact with multiple plant cell functions at once to overcome the host. Effectors for a pathogen can bind to proteins that affect the biological activities of the plant, letting the disease invade the plant, suppress its immune system and allow Xanthomonas to survive.

However, when the plant cell’s receptors recognize the pathogen, it can trigger its immune response. To stop the pathogen from growing, the plant cell initiates a hypersensitive response by killing itself. If the plant can’t stop the pathogen, it will multiply and affect much larger areas of the leaf. This will ultimately destroy the plant tissue and cause the characteristic round, brown dead spots on the lettuce leaves.

“Plants can afford the hypersensitive response because their developmental program isn’t set in stone like in most animals,” said Walter Gassmann, interim director for Bond Life Sciences Center. “They can adjust their growth in real-time…so losing a leaf is not a big deal to a plant, not like us, losing a limb or something like that.”

Wild Lettuce Found on Campus — While studying lettuce immunity, research scientist Jianbin Su took photos of wild lettuce growing on campus. | photo contributed by Jianbin Su.

Once AvRrps4 enters the plant cell, it splits up into two parts: AvRrps4-C and AvRrps4-N. Some plants like flowers, tomatoes and melons only recognize the C part, but lettuce only recognizes the N part of the effector.

“The C part of AvrRps4 has been studied by many labs, and they’ve already found some mechanisms,” Su said. “The C part attacks a group of important proteins that are required for plant immunity. That’s the function of the C part, but the function of the N part is not clear. That’s what I’m focusing on in lettuce.”

Recognition is important because, without it, plant cells can’t respond to fight off the pathogen.

Su is studying lettuce not only because it hasn’t been studied as much, but so far, it’s the only plant that requires recognition of both parts to initiate immunity.

This means lettuce evolved to recognize and attack AvRrps4-C. In turn, the effector evolved by adding a second part to prevent recognition by plants.

This evolutionary choice, if you will, is odd. Instead of getting around the immune response by getting rid of the protein that is recognized, the protein added a second part to itself. This means AvRrps4-N, the original part, must possess a vital function for the pathogen worth keeping.

“That’s why we think this effector arose in nature,” Gassmann said. “It’s because the first part triggered a very strong immune response, something else got tacked on to it to weaken that immune response to give the pathogen a leg up.”

This evolutionary battle can be seen in Mizzou’s very own backyard. Su found five different types of wild lettuce. After testing if the types were able to recognize the N part of the effector, he found two of the five did.

Since some did and others did not, Su thinks the receptor for recognizing the effector has been lost in some wild lettuce types due to evolution and the absence of the pathogen in certain areas.

“We haven’t found the lettuce receptor but based on this information we can narrow it down,” Su said. “Right now, we have 36 candidates. We are already sure that among the 36, there’s 99.999% that there is one receptor that recognizes our protein.”

Su still has much work left to do but, for now, he resubmitted his paper Oct. 5.

“Once we identify the receptors that recognize our protein, our research will go into the next direction, and maybe have some application purpose for our research,” Su said.