Research Highlights

Research Highlights
Understanding Biochemistry to Fight Herbicide Resistance in Palmer Amaranth

Photo: United Soybean Board

By Laura Temple

Palmer amaranth has grown into one of the biggest weed problems in soybean fields throughout the country — literally. It germinates throughout the growing season, rapidly growing to heights of 6 to 8 feet and producing enormous volumes of seed. It continues spreading to new areas and developing resistance to multiple herbicides, stealing soybean yields in the process.

“Palmer amaranth can grow anywhere, like in concrete cracks and under drought conditions,” observes Naveen Kumar Dixit, extension specialist and associate professor for the University of Maryland Eastern Shore Extension. “The plants are fascinating.”

Noticing how the weed thrives in a wide range of conditions and environments sparked Dixit’s curiosity. 

“What happens in their cells at a biochemical level that allows them to grow?” he asks. 

He believes the answers can help manage herbicide resistance in the weeds and reveal traits that could improve cash crops. Research funded by the Delaware Soybean Board in 2022 allowed Dixit to begin exploring answers, with a focus on managing herbicide resistance.

Through photosynthesis, plants fix carbon dioxide into a carbon compound while releasing oxygen. Dixit explains that most plants, including soybeans, are C3 plants, meaning that the first carbon compound created in the process has three carbon atoms. However, Palmer amaranth is a C4 plant, creating a compound with four carbon atoms and using a slightly different biochemical process for photosynthesis.

“When temperatures are high, C3 plants actually lose carbon dioxide during photosynthesis,” he says. “C4 plants like Palmer amaranth continue to fix carbon dioxide in those conditions. They also have high water and nitrogen use efficiencies. That partly allows them to grow well under stress.”

Uncontrolled, Palmer amaranth can cause up to 79% yield loss in soybeans and 91% yield loss in corn, Dixit reports. It has been classified as a noxious weed in several states, including Delaware and Maryland, requiring by law that it be controlled. However, the weed’s ability to develop herbicide resistance quickly makes that challenging.

He says the development of herbicide resistance in weeds is a natural process. While it can’t be stopped, it can be slowed down. 

Understanding how weeds like Palmer amaranth develop resistance to those herbicides helps farmers figure out how to slow the development of resistance in their fields. 

Developing Resistance: When Targets Inside Weeds Change

Farmers rely on biochemical reactions when they apply herbicides to control weeds. Most herbicide active ingredients target a specific enzyme. 

For example, glyphosate, the active ingredient in Roundup and similar herbicides, targets 5-enolpyruvylshikimate-3-phosphate synthase, or EPSP synthase. This enzyme is involved in creating the amino acids tryptophan, tyrosine and phenylalanine, which plants need to make protein. As an EPSP inhibitor, glyphosate binds to EPSP enzymes so that they can’t function. When a critical enzyme like this doesn’t work, the plants die.

“It’s like a lock and key,” Dixit explains. “Glyphosate is like a key that fits the EPSP lock. Other herbicides do the same with other enzymes. However, plants can evolve so that the enzyme lock dimensions change. Then the enzyme no longer accepts the herbicide key. In this case, glyphosate no longer binds to the EPSP enzyme.”

He says this evolution in weeds is called target-site resistance, because the biochemical site targeted by a herbicide changes to resist herbicide control. This is the type of resistance seen in Palmer amaranth and other weeds with resistance to many herbicides, like glyphosate, ALS inhibitors and PPO inhibitors.

Developing Resistance: When Weeds Detox

Weeds can also develop non-target-site resistance to herbicides, using a different biochemical process. 

Every cell of a plant contains glutathione S-transferase, or GST, an enzyme that allows plants to detoxify as a defense mechanism. When activated, molecules of GST bind with foreign material in the plant and takes it to a storage area in the cell called a vacuole. When that happens to a herbicide, it becomes inactive.

“Spraying herbicides can activate the production of GST,” Dixit says. “The GST binds to the herbicide active ingredient and stores it away so that the herbicide key never reaches the intended lock, or target site.”

Herbicide Impact on Palmer Amaranth Biochemistry

To learn how Palmer amaranth, an aggressive weed, handles herbicide applications at the biochemical level, Dixit and his team started in the lab. They collected weed seed from the research farm, grew them in the greenhouse and identified the six or seven most common herbicide treatments used to control them in the field. 

Leaf pieces from those weeds floated first in solutions of herbicide treatments and then in distilled water under selected light intensities. Biochemical analysis of those pieces revealed how enzyme levels changed due to each treatment.

“We looked for changes in GST production in the leaves,” Dixit shares. “A minimal change in GST levels indicates that the herbicides are more likely to reach their targets. Using herbicide treatments that trigger less GST also prevents development of non-target-site resistance.”

His team found that glyphosate triggered the highest increase in GST levels in Palmer amaranth. That indicates that the herbicide is captured in the plant detox system and never gets a chance to bind to the targeted EPSP synthase. However, when glyphosate combined with other modes of action in a treatment, the leaf cells produced less GST.

“In the lab, we consistently see that just one herbicide mode of action triggers release of more GST, while using two or more modes of action produces less GST,” he reports.

Dixit is also examining how herbicide applications influence production of hydrogen peroxide, a molecule toxic to plants, but released when they experience stress. His team is looking for an association between GST production and hydrogen peroxide. 

“When more hydrogen peroxide is present, we want to see if that kills Palmer amaranth cells before they produce enough GST to detoxify,” he says. 

He plans to compare lab results with results in the field during 2024. Coordinating with farmers, his team hopes to pull leaves from Palmer amaranth in soybean fields shortly after they are sprayed. 

“The biochemical activity triggered by herbicides starts shortly after application, so looking at leaves just a couple hours after spraying will help us compare in-field conditions to our lab observations,” Dixit explains. “Then, we can make recommendations for Palmer amaranth control based on the herbicide combinations that trigger less GST production and more hydrogen peroxide to help farmers delay resistance.”

He notes that the principles his team is exploring apply to other weeds. This research can inform work to slow the development of resistance in other problem weeds. Dixit also believes that what they learn about biochemical reactions in weeds can point to characteristics that could benefit crops in the future. 

Published: Feb 12, 2024

The materials on SRIN were funded with checkoff dollars from United Soybean Board and the North Central Soybean Research Program. To find checkoff funded research related to this research highlight or to see other checkoff research projects, please visit the National Soybean Checkoff Research Database.