Contributed by Dr. Drew Lyon, Washington State University
Humans like easy answers. Unfortunately, few things in life are as easy as we like to believe they are. Not that long ago, herbicide resistance was considered rather straight forward. A single gene mutation results in a binding site/protein change and a given herbicide can no longer bind to the target site allowing the resistant plant to grow and reproduce in the presence of the herbicide. This “target-site” resistance was the first herbicide-resistance mechanism identified, and it is still a very widespread type of resistance. An effective strategy for managing target-site resistance is to use herbicides with different effective modes of action, either by overlapping residual herbicides, using both a residual herbicide and a postemergence herbicide, tank mixing postemergence herbicides, or rotating herbicides. Using two effective modes of action in the same crop has been shown to be more effective than herbicide rotation for delaying target-site resistance. I have been discussing this approach for managing herbicide resistance for many years. But woe to the man who begins to feel comfortable with what he thinks he knows.
In recent years, a new form of herbicide resistance has been identified in plants: non-target-site resistance. With non-target-site resistance, a process within the plant prevents the herbicide from reaching the intended site of action. There are several ways that this occurs in various plants, but the most concerning way is known as enhanced metabolism or metabolic resistance. Herbicide metabolism is generally a three-phase process that first involves a slight modification of the herbicide molecule followed by combining the modified molecule with another compound such as sugar or glutathione, that allows transport enzymes to move the modified herbicide into the cell vacuole (a small enclosed space in a cell that is often referred to as the cell’s garbage can) or outside the cell in the intracellular space. The movement of the herbicide to these areas isolates the herbicide from the target site, rendering the herbicide ineffective. Metabolic resistance is concerning because it can result in plants developing resistance to specific or multiple herbicide groups without any previous exposure to those herbicides. This makes managing metabolic resistance difficult by the traditional practice of mixing or rotating the use of effective herbicide modes of action, as discussed above. Unfortunately, non-target-site resistance is increasingly common, and scientists are still trying to identify potential alternative herbicide strategies to manage these kinds of resistance.
Fortunately, cultural, mechanical, and preventative management strategies are still effective for managing both target-site and non-target-site herbicide resistance. PNW754, Best Management Practices for Managing Herbicide Resistance, discusses these various strategies and how they could be implemented in the dryland cropping systems of Eastern Washington, Oregon, and northern Idaho. Additional information on managing herbicide resistance can be found on the Herbicide Resistance Resources page of the WSU Wheat and Small Grains website.
My colleague, Dr. Ian Burke, has been screening weeds for herbicide resistance for several years (see the Resistance Testing Program webpage for how to submit a sample for testing). He reports that greater than 80% of the resistance he now sees in Italian ryegrass and downy brome is the result of non-target-site resistance. This was a surprise to me, but it probably shouldn’t have been. The lesson here is to never become too comfortable in what you think you know. The world is a complicated place despite our desire for simplicity.