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Drew Lyon: Hello. Welcome to the WSU Wheat Beat podcast. I’m your host, Drew Lyon, and I want to thank you for joining me as we explore the world of small grains production and research at Washington State University. In each episode, I speak with researchers WSU and the USDA-ARS to provide you with insights into the latest research on wheat and barley production. If you enjoy the WSU Wheat Beat podcast do us a favor and subscribe on iTunes or your favorite podcasting app and leave us a review while you’re there so others can find the show too.
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Drew Lyon: My guest today is Dr. Ian Burke. Ian is a professor of weed science at Washington State University. His research program is focused on basic aspects of weed biology and ecology with the goal of integrating such information into practical and economical methods of managing weeds in the environment. Ian teaches the undergraduate courses in weed science and cropping systems. Hello, Ian.
Dr. Ian Burke: Hi, Drew.
Drew Lyon: I put out a call for questions from listeners thinking we might put together an issue or an episode with where we try to answer all those. But one question I got that I thought deserved maybe a little more attention was the discussion of weed resistance. This person said he’s particularly interested in addressing how when we use certain Group 2 longer residual grassy weed herbicides, why the Group 2 herbicide activity falls off so dramatically in subsequent years using most any other Group 2 herbicides. So I thought maybe just a general discussion of herbicide resistance as it relates to Group 2s. And then that question of, you know, what happens when we use some of these longer residual herbicides today. You know, have a different influence than some short-lived Group 2. So maybe start off with where we’re at in our in the world of herbicide resistance as it relates to our group, to our ALS inhibiting herbicides.
Dr. Ian Burke: Okay. Yeah, that’s a really complicated question. There’s a lot to unpack in that topic.
Drew Lyon: [ laughter ] One question and a lot of things to talk about.
Dr. Ian Burke: You know, there’s a lot of biochemistry involved in that answer. So, you know, hopefully, everyone’s ready for a ride. So, you know, interestingly, the Group 2 herbicides, you know, the first reported instances of resistance to those herbicides actually occurred here in the PNW, and it was Kochia and prickly lettuce and a few other broadleaf weeds that were identified as being resistant back in the late 1980s. And all lot of work was good work done by University of Idaho, Carol Mallory Smith, and Don Tell. And that really sort of set the tone for what we became, whereas evolved into a pretty complex stories. There’s an incredible array of Group 2 herbicides, something like 70 plus herbicides that interact with what we call acetolactate synthase enzyme. And, you know, that’s a story in of itself. It’s certainly the most numerous mode of action we have. So each herbicide is unique, it’s different, it’s got a different shape, but they all interact with that same enzyme. And so it’s allowed us to explore the mechanisms of resistance to the Group 2 herbicides and a little bit different way than almost any other herbicide class. So you go through the top-level story, when I talk about herbicide resistance in the Group 2s is there’s two real flavors, although there’s probably more based on recent experience with other resistance types. There’s what we call target site resistance, where that the enzymes have been modified in some way through a genetic mutation in the gene. And now the herbicide doesn’t bind to it as well. And then there’s metabolism-based resistance, where through a separate enzyme pathway, the weeds have evolved the capacity to break down the herbicide very rapidly, often within hours. And so that understanding of herbicide resistance to the Group 2 herbicides hasn’t changed over the last 30 years. What has changed is our understanding of where those herbicides are binding to the enzyme. Over the years, there’s been documentation of as many as different, eight different changes in the enzyme. And they occur within the binding region of the, you know, where the herbicide binds, we know where the actually substrate binds into the enzyme that can occur just outside that binding area and still change the shape of the binding region. And so, you know, when you have that many eight. So it’s not as simple as just eight. Right. So because of the way these enzymes are coded at the genetic level, there could be several other amino acid residues at each one of those mutation sites. And so instead of it’s like eight to the fourth different permutations, you can wind up with for changes in that binding pocket. And with 70 active ingredients to throw at it, there’s really it’s really very challenging to predict exactly what’s going to happen within the herbicide and a particular weed species. So hopefully that gives your listeners a little bit of some sense of the complexity of what we’re dealing with here with just this mode of action. That’s really pretty fascinating.
Drew Lyon: And so, you know, we often speak in broad terms, you know, the ALS inhibitors, but you’re telling us there’s a lot of difference in among those, so. While the message is simple. You know, try to avoid using ALSI inhibitors all the time. It’s really more complex if you want to dove into it.
Dr. Ian Burke: And there’s opportunity there in science to understand how a particular mutation that confers resistance to herbicide X might affect a number of other herbicides that you would use on that same weed species. And it’s not as simple or clear, cut it. There’s a lot of pretty critical science that would need to be done to understand and be able to predict the outcomes of the development of resistance to that that one herbicide and how it might confer a cross-resistance, other herbicides. Normally, we just work that out by trying something else. Right? So you go try another Group 2 herbicide. So, downy brome comes to mind is Italian ryegrass. We’ll go try PowerFlex. That doesn’t work. We’ll go try Osprey that doesn’t work, maybe we’ll try Olympus. And I’ve just there are three different chemical classes just in those three herbicides, all with a new, very unique chemical structure that all bind to the same place. Generally speaking, on this enzyme. And so it’s it becomes quite complicated to understand how we could predict it in retrospect, we can look back and say, okay, so this group of we know this subset of downy browne, all of them are resistant to PowerFlex. Some are resistant to Beyond, some are resistant to Osprey but we can kind of begin to see patterns emerge and associate that with the point mutation that we can find when we go looking in the weed. It doesn’t necessarily help growers out unless they’re trying to identify one, an additional herbicide that will work. But they often can just go spray to figure that out, too.
Drew Lyon: I know people send in a seed of plants they suspect of being resistant and you have a program to screen them and you’ve shared those results with me. And it seems like all the different, you know, some of them are resistant to all the Group 2s some of them are just resistant to the one that the person sent it in for. Some were resistant to a mix of them. So it’s really it’s a different story almost in every situation.
Dr. Ian Burke: And like I said, it’s hard to predict. Hard to predict.
Drew Lyon: So that you were talking about the early development of ALS resistance here in Washington, and that that example is with a product called chlorsulfuron, which is one of these long-lasting Group 2s. So getting to the grower’s question about how does the use of something with long residual effect other Group 2s is there? Is it the same mixed message that you just gave us, or is it or is there something about these long residual Group 2s that’s different than others?
Dr. Ian Burke: Yeah, the long residual Group 2s present a much greater selection pressure than Group 2 herbicides that maybe don’t last as long. It’s also important to remember that it could be long residual. And not necessarily be a significant selection pressure if the activity of the group to herbicide isn’t that great on a particular weed species. But with chlorsulfuron, that herbicide is very active and very, very low doses on a number of different weed species, particularly some of the ones we saw develop resistance pretty quickly to. And so you couple of hypersensitivity in the long residual, and it’s a very strong selection, pressure exercised over a long period of time, often measured in years because there are some residual of the herbicide present that the germinating weed seedlings are going to encounter. And so instead of just applying a selection pressure to the emerged weed, you might be treating your functionally applying a selection pressure to all the germinating seedlings that are going to come up for the next two years. And that number is dramatically higher in terms of the number of weeds you’re selecting against. And so we’ve come to terms with with thinking about these long residual herbicides is a bit of a recipe for very quick and rapid evolution to herbicides. And if you do work with a long residual and I can think of one that’s just come on the market now that I’d probably want to pay close attention to, Idaziflam totally. It’s not a Group 2. It’s a Group 29. So so those biosynthesis inhibitors, but it’s a very long-lived residual soil active herbicide that controls annual grasses. And the lessons we’ve learned with a Group 2 herbicides is that when you have a herbicide like that, it’s really important to make sure that you have a program in place so that there’s selection, there’s multiple modes of action active during that long duration of residual activity of that one herbicide. That’s how you integrate the herbicide modes of action.
Drew Lyon: Okay, and that probably wasn’t the case way back when. As I recall, I was actually around as a graduate student back to those days, although in the Midwest, not here. And basically, they just sprayed Glean and that’s all they needed to do. And so there was no other mode of action. And that’s really a lesson of herbicide resistance, is we’ve learned it may be a little too late, or if we knew it, we didn’t communicate well, that you just need to bring more than one mechanism of action to bear on these weeds or you’re eventually going to have resistance issues.
Dr. Ian Burke: And when I reflect on what we’ve done with downy browne with a series of pretty amazing herbicides that have come along to control it, post-emergence in our wheat. The mistake I feel like we’ve really made over the years is leaving a small residual out of the program. You know, Metribuzin was one that was around in the 70s and 80s, and it was sort of a mainstay. And when these Group 2 post-emergence herbicides came out for controlling downy brome, we really kind of stopped using Metribuzin. And that was an error. We should have kept that as an integrated part of our strategy, even though it can be touchy and sometimes difficult to use. And timing can be problematic and there can be replant issues. The loss of a Group 2 herbicide post-emergence herbicides is far greater than any kind of inconvenience we might have encountered with the use of views. And so, you know, those are important lessons that we have to apply as we move forward.
Drew Lyon: I remember in the 90s telling growers in this case, western Nebraska that they would never be able to selectively take downy brome out of their winter wheat, and then and then Maverick came around and I was proven wrong. But now, 20 years later, that message might have to revive that message. [ laughter ] You’re not going to be able to selectively take downy brome from winter wheat because of resistance, unfortunately, because we didn’t manage it the way we probably should have. Because those were that was amazing technology. I mean, I really was amazed when they came out with something that took a grass weed out of winter wheat that way.
Dr. Ian Burke: There was in many ways were the glory days of herbicide discovery in an introduction, I don’t know that we’ll ever see the numbers of herbicides appear in that way again.
Drew Lyon: So that’s the Group 2s, which I think is the most used group in small grain production. Do we have similar things going on with other modes of action, or is that the one that’s really capturing a lot of your attention and focus?
Dr. Ian Burke: I guess I would say that that the question is also quite relevant for the Group 1 herbicides, where we’ve had we have multiple active ingredients that interact with what is called the ACCas enzyme. And even those herbicides don’t have any soil residual activity. You can still see some pretty interesting cross-resistance patterns. So if you’ve used a lot of what we call the fops, so things like Assure II or Fusillade or some of these other fops-based herbicides, and you can sometimes see that that confers cross-resistance to all the fop herbicides at a stroke and sometimes cross-resistance to the active ingredient and axial pinoxaden. By far, the worst kind of target sight resistance, though, in the ACCas herbicide, families target sight resistance to clethodim. And it’s been documented in several different occasions where you can have a target sight resistance to clethodim, and that at a stroke confers cross-resistance to all the other ACCas herbicides. And so that’s a looming possibility for ryegrass. And as we see, these ACCas inhibitors deployed in our canola rotations are, you know, legume rotations and then also now in the aggressor system. So that’s a real possibility that we could be nearing the end of the utility of an entire mode of action because of that, our ability to convert cross-resistance with clethodim.
Drew Lyon: Okay, that sounds like a very strong word of caution. [ laughter ] Be careful how frequently and how you use clethodim in your system. All right. Well, I think we’ve discussed what really is a very complicated issue when you drill down into it, but in some ways, also a simple message that don’t rely on a single mode of action too much. Make sure you bring in some different modes of action in either the crop or within the cropping system. Thank you, Ian.
Dr. Ian Burke: Thank you, Drew.
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Drew Lyon: Thanks for joining us and listening to the WSU Wheat Beat podcast. If you like what you hear don’t forget to subscribe and leave a review on iTunes or your favorite podcasting app. If you have questions or topics, you’d like to hear on future episodes please email me at drew.lyon — that’s email@example.com –(firstname.lastname@example.org). You can find us online at smallgrains.wsu.edu and on Facebook and Twitter @WSUSmallGrains. The WSU Wheat Beat podcast is a production of CAHNRS Communications and the College of Agricultural, Human and Natural Resource Sciences at Washington State University. I’m Drew Lyon, we’ll see you next time.
The views, thoughts, and opinions expressed by guests of this podcast are their own and does not imply Washington State University’s endorsement.