S8 E14 - Novel Genetic Methods for Pigweed Control

with you today. What I work on. I'm really interested in the genetics of wheat, understanding how they do what they do, and why they're so successful, and no matter the very best ideas we have to get rid of them and manage them that they're always seeming to come up with a way to respond and to understand that from the genetics angle, whether that's herbicide resistance, whether that's shifts In emergence, you know, how can we understand from their genetic diversity background, how weeds

are responding to our management practices?

first one for the model plant, Arabidopsis. It's a little mustard that it's kind of a wild plant and northern latitudes around the world. That genome was completed in the year 2000 and it's really interesting to think that, you know, altogether, that effort, you know, probably cost somewhere roughly in the range of ten million you know, in terms of

the sequencing and the time. And it was a many, many year project, and that genome still continues to be updated, but it's a really incredibly valuable reference for plant biology, understanding at a very basic level how plants work. And then you zoom forward to, you know, probably in the range of about 10 years after that, a lot of people are starting to think, could we do genomes for weeds and genomes for major crops were

getting done. You know, Rice was done, corn was done and appointed there millet and people working on tomato and soybean, wheat was a more challenging one, a bigger genome coming later. But certainly, you know, you could see a lot of value and reason to invest in doing these crop genomes, and they were at that point becoming, you know, maybe multi million dollar projects, but less than 10 million. So still,

you know, to do a weed species, very, very expensive. And so there are a lot of conversations, particularly at the Weed Science meetings around maybe, could we pick a model weed and find the resources to make that happen, and it really never, kind of got moved out of that. Then we moved into the era of next generation sequencing, as it's called, and this brought an incredible drop in the cost of getting DNA sequence. So it's kind of like, you know, just like the computer processors in

our computers get faster. They sort of double in capacity about every 18 months. There's this thing called Moore's law that sort of describes that, that they're going faster and faster all the time. And you know that, right? If you have a two year old computer, suddenly it's like, why is this so slow, you know? And you get a new one, and that's essentially what happened. There's this incredible change in the technology that now we could get huge amounts of data and the

cost dropped by orders of magnitude. So then people could start to work with the RNA, with the expressed genes. And so we can call that the transcriptome. Each RNA is called the transcript, and those are, again, the instructions for the genes that make the proteins that do everything in the plant. And that really became feasible for weeds in the range of 10 to

12 years ago. And you start seeing people using that to study herbicide resistance in particular, start to find new mutations for resistance for things like group one you know, your grass herbicides and. And some work was also done on group four herbicides, the auxins. But still, it didn't give us a picture of the whole genome, you know, all the other information

in addition to the genes. So again, this is going along in about 2016 there's an international Weed Science meeting in Prague, and there's a workshop there on weed genomics. And so a lot of people where they're talking and thinking, Okay, this cost has come down. We have these important weed species. We see reasons why we'd want to do this. That was when people started thinking, how could we actually make this

happen? And the idea came together that a lot of the crop protection companies, you know, that discover and market herbicides. They were doing some of this work, and a few of them had maybe a genome or two, or maybe some of these transcriptomes. But of course, they had that information

themselves. They're using it for their own projects. And the thought was, is there a way that if these companies could come together and pool some resources that these genomes could get done and then be shared with the whole Weed Science community. And that's that started the ball rolling on these conversations and more workshops, more meetings, and it was eventually by actually in 2020. Was another kind of milestone into the first really complete, well done genome of what we call a real

weed was done. That was horseweed, can I say, conyza canadensis, that was done by a group from mag, Canada. And then in that same year was when the plan really solidified for the International weed Genomics Consortium. So that brought together the companies, including BASF, Bayer crop science, Syngenta and Corteva agrascience, which, you know,

kind of at that time, had just formed. And that was a really interesting opportunity, because it brought together the, there's a was a big genomics group in Iowa with the former DuPont side. And then, of course, the a lot of the herbicide folks on the former Dow side in Indianapolis. So what the consortium does is, with the funding from the companies, and then corteva, with their genomics core in Iowa, they're actually doing the sequencing that brought us this place.

Yeah, 2020 and 2021, we launched, there's matching funding from the foundation for food and agriculture research, and it finally solved this problem. Because I think for years before this, people had said, hey, you know, we want to do a genome. So, you know, if you're at a university, you write up a grant proposal and you send it in, and then you get

the comments back. Well, you've never done a genome. We don't think you know how to do it, and it's going to take you three years to get it done, and you're not gonna be able to do all the cool work that you want to do with it. And we're not interested in just funding a genome. And so that really made this possible, so that now I think currently, there are over 61 genomes in the database. You can go to weedgenomics.org and

check out a lot more information. It's where we put together the species that are there, their chromosome number, their genome size. And then you can link to the data in what's called weedpedia. That's another site, but you just go that you can it's free to request an account, and you can get a login. They can go in and actually find your favorite weed and search for your favorite genes and get all the

information there. And more and more of those are coming online as we're getting these genomes, now that they've gone through the assembly the annotation process, where we understand, you know what, all genes are there and and everything. And then, then they're posted. So that's been, it's been a great time. A lot of people involved, and as well, a lot of good conferences and training along the way. I think it's another

part. Is for folks in Weed Science you know are coming from, maybe from an agronomy background, chemistry background, and these genomics tools requires another set of training and knowledge about what to do. So we've had some great meetings, both standalone and in combination with the WSSA in the US, the European weed Research Society, and meeting in

Australia, where we have opportunities for training. So also, if somebody wants to get some basics, maybe on molecular biology or on how to run an RNA Seq experiment, for example, how to run a blast. We have some training videos on the weedgenomics.org website. You can check those out as well.

can look at the target site gene. And if you look at a typical grad student, probably 15 to 18 years ago, their whole PhD would have been cloning and sequencing the ALS gene and finding that mutation that had been quite an accomplishment and difficult to do in a new weed species, but now we can go into this database, and you have the sequence at hand for all 30 to 40,000 genes in the species, including ALS, and you can easily develop the tools, molecular tools, that you need

to go in and sequence it and analyze it. So it gives us a big head start, just in the sense of, if we're going after a target site gene and looking for a target site mutation, really will help things go faster. So that's a that's a nice advantage. And then we have the cases of mechanisms where we don't really know what's going on, and this is still the case for quite a few things. For example, when it comes to glyphosate, there's some mechanisms that we know about.

We're talking pigweeds. You know, they typically have extra copies of the target site gene that's called epsps, and that can occur different ways, but there are quite a few cases where there's some kind of non target site mechanism that we still just don't really know, actually how that works. Maybe they they're not translocating glyphosate as much, but we're still not the point where we could say, here is the gene with its mutation and it causes that change in that resistance. So

what can we do now? Because we have these genomes, we have the whole map of the DNA. It enables us to do genetic mapping. And this is what people in plant breeding would do when they want to identify a new disease resistance gene, or, you know,

those kind of things. We can take a resistant and a susceptible individual, cross them, and then you self pollinate that you get an f2 and what that does is it kind of shuffles the genetic deck so that now you know all these things that might have been associated with resistance, just through population history, shared ancestry, that kind of stuff. We can shuffle it all up with the susceptible, and then

we can use genetic markers across the whole genome. For example, Palmer amaranth has 17 chromosomes, and the whole genome is about 450 million base pairs. So you think about that, that's a lot of information, but with these advanced sequencing

technologies. Now, by the way, I meant to mention that if the you know, the first plant reference genome cost more than, you know, the most expensive house in the country, essentially, you know, now you can sequence the genome of Palmer Amaranth for about the cost of a Big Mac. So that's a gives you a sense of the cost. Now, you've got to do something with that data once you get it. But, you know, you can generate millions and millions of base

pairs of sequence data for, you know, 10s of dollars. So that's kind of amazing. So now we can get those genetic markers across, those 17 chromosomes of Palmer amaranth, for example, and find out where does the sequence that comes from the resistant parent associate with the resistance trait. So it's kind of like you almost run an ANOVA on each of these markers and find out which one is is associated with being resistant. Now you can zoom in on a region of the genome to give a few

examples of this. We're working on a case of 2,4-D resistance in another conyza horseweed species from Brazil. And it's a bit unusual in that the plants actually have this very rapid response to 2,4-D they die. You know, the cells start when you see reactive oxygen species and membrane leakage and everything within about 15 minutes after treating the plant, our mapping

shows that it's probably a single gene. And what we've done then is we've made one of these mapping populations and re sequenced it, and from the whole genome of that species, that's about a billion based Pairs. We've narrowed it down to a region that's about 20 million base pairs. So that's still a lot. You know, there's still maybe 100 genes or so in that region, but, you know, talk about sort of making a much smaller haystack to find your needle in, right? You know, the

gene with this mutation has to be in there somewhere. So that's making some progress. Similar things have happened with Dicamba resistance, for example, in Kochia, you know, particularly in the West, Dicamba resistance has been an issue for quite some time. Dicamba is used a lot in the no till fallow part of the cropping cycle, as well as whenever you've got corn in the system. So there's been a lot of selection pressure for Dicamba resistance and Kochia, and we

recently had a project where we did this as well. We crossed and resistant by susceptible, mapped it, and we're able to find a region on the chromosome. And then going a bit further, we found that there's this target gene. It's one of the CO receptors for auxin, and it had a mutation. Is an unusual mutation, and that something called a transposon had inserted into the gene. So these transposons, you know, might be familiar with it from corn. Barbara McClintock studied this.

You know, in corn you can get these, the kernels will have different colors, right, and different patterns, and that's due to transposons moving around and disrupting the pigment synthesis genes. And so their transposons are really common in plants, and some of them are not moving. Some of them do move, but it just happens as one moved into that gene, and by doing so, it changed the sequence right at the Dicamba binding site, and it enabled it that then now that version of the protein doesn't

bind to Dicamba anymore. So that was kind of a really interesting one, again, that we can map. And then, more recently, in palmer amaranth, working people working on glufosinate resistance. You know, people in Arkansas have been looking at this for a little while, and previously with Palmer amaranth that was known that there's this thing called an extra chromosomal, circular DNA. Now, what is that? It's I told you, a Polymer has

17 chromosomes. That's its normal genome. But somehow, and this is something we still need to learn a lot more about, but this extra circle of DNA has formed, so kind of think about it like a very small chromosome, but it's a circle, and it's about 400,000 base pairs long, and it has roughly 60 coding genes in it that A lot of them are expressed, and it just happens that somehow that circle of DNA picked up epsps, the target gene for glyphosate, and that then gives it an over

expression, and it makes them, those plants resistant to glyphosate. That's how that's generally working in Palmer amaranth. Now, the people looking at glufosinate went back to that ECC DNA and sequence it again, and it turns out that the target gene of glufosinate is now in their glutamine synthetase. And so the same way that the plant has this mechanism to over express a gene now is also over expressing

glutamine synthetase and surviving glufosinate. So that's another case where having this genomic information, as well as the sequencing tools allowed really fast progress to be made to figure out, hey, you know, here's what's going on and and how it's organized. Now, when we think about some of the big issues out there, 2,4-D and dicamba resistance in pigweeds, we don't have a clear picture on that. It's kind of coming

together. I think a lot of people are working on studying it, but now these tools are available, and we can compare, for example, a waterhemp genome reference against a resistant one. People will be able to use that, maybe to find 2,4-D Dicamba resistance mechanisms. There is an interesting example of 2,4-D resistance in waterhemp that comes from before the use scenario in soybean and cotton. It's from a place in Nebraska where they're producing bluegrass seed, perennial grass

seed. So they're using 2,4-D for years to control broad leaves in that and they selected for a really high level of resistance to 2,4-D in waterhemp. Turns out, those plants, rather than having one of these target site mutations, they're able to break down 2,4-D really rapidly, and they do so through a pathway that is kind of similar to what the grasses do, because grasses can break down 2,4-D pretty rapidly. So these waterhemp

plants now are able to detoxify 2,4-D, very quickly. Again, we used mapping and the reference genome of at the time, originally with a crop amaranthus, the grain amaranth. But now, you know, we can do that mapping in the waterhemp genome itself, and we're able to find a region that it looks like there's some some of these herbicide metabolism genes there. So still working on trying to figure out exactly

which one it is. But you know, again, the bottom line is, there's a similar type of technology as what people are using in human medicine. And you know, all these areas where there are a lot of breakthroughs, we can now access that same technology in agriculture and even in Weed Science, and that lets us study more complicated things and move faster and get better answers to help us understand what's going on out there,

some of that. I'm just curious if that is, if that question has been asked using this type of approach,

yeah, what happened? How did it emerge from the desert and become one of our main, you know, row crop weeds across such a huge area and continuing to expand. Because not only, you know, is it spreading across the northern us, as we know, you know, fairly recently, in places like Minnesota and New York and Michigan, it's becoming a problem in Spain and Italy and Turkey and Israel. It's in China, it's in Japan. It's in

South Africa. Recently spending some time in Australia, and they're gearing up their monitoring system because, you know, that's the only continent that is not on yet. And so they're very aware that it's a big problem. They don't want it. But, yeah, exactly the Why was the explanation for this? What is, are there certain things that have been selected? Is there something that mutated and, you know, new kind of capacity evolved? That's definitely the question people

are asking. I think it's and with these tools now, it's where there's there's one area of genomics called the pan genome. So it's kind of like you have a reference genome, you know, from a single individual, but now you can also get the whole genome of another individual, and start to ask, where does it have does it have extra copies of certain genes? Has it lost certain genes? Are there some of these transposons that have moved

around? Is the expression of certain genes changing? That's a big question, and I think that it's one that people are looking at, and I feel hopeful that in a few years, we'll start to have at least some initial answers for that.

silencing in weeds. Could you tell us a little bit about that work and maybe any potential for control?

turn it on. So the RNA is this kind of temporary instruction molecule that goes and then that's used to actually make the protein that goes and does the thing, whatever it is the reaction or the structure in the cell. So the, you know, plant cells are constantly turning these genes on and off, and there's certain RNAs that are around. Now, when we think about our main we management tool that's small molecule herbicides, nearly every one of them is going, you know, you're

got to enter the plant, right? It's either got to pass the cuticle of the leafAnd get into the cells, or it's going to come in through the root with the water stream and get into the cells. It'll go in and it's going to bind to some kind of protein and either inhibit its reaction or stop it from doing a structural thing, you know, in the case of tubulin, something like that. But they're all a small molecule that is binding to a protein, and we're so we're working at that protein level.

If we can knock out that protein, some of these proteins are really essential, so losing its function is lethal, or sometimes knocking it out creates something that's lethal, like if we interfere the, you know, the group five herbicides that interfere with photosynthesis, if you block that, then now we get electrons and free radicals and that kind of thing. However, now if we talk about gene silencing, we switch from trying to target the protein to targeting that RNA.

So like I said, that RNA is there, but it's transient and it's a fairly fragile molecule. So there are a number of ways in which this can be done. There's a major pathway that's called RNAi, which stands for RNA interference. And this kind of technology is actually already in the field for insect management. So there are, there are things where you can actually, you can do a transgene into the crop genome and make

one of these RNAi molecules. What it is is you basically do the backwards version of the RNA sequence, and it will complementary base pair bind to its target, RNA. So he's just, you know, kind of taking the reverse of it the plant cells making that so then when it recognizes that certain RNA, in this case, say, an insect, you know, a beetle or a moth larvae, that's going to be feeding on the plant, it's going to ingest that, that RNAi trigger, and it's going to silence that gene

in the insect and control it. So those are out there. And also, there's a company called Green Light bioscience that this year has one of these spray on RNAi products for, I think it's Colorado potato beetle. And so again, you spray it on, you spray on this double it's called the double strand RNA. Normally, RNA is a single strand, but this double strand is there on the plant, for example, and the insect will eat it, and triggers this gene, silent team pathway, RNAi. So that works for critters

that are chomping on plants, right? But what about weeds we've got to actually spray it on. So what's the challenge there? You know, a typical small molecule herbicide has, you can measure the size of a molecule in a unit called Daltons, or kilo Daltons. So just the to give you a sense that a typical herbicide is in the range of 30 to 40 kilo Daltons, and so that's that's a size that is able to go into a plant cell and cross cell walls and go through the cuticle and all that stuff.

When we're talking about some of these RNA eye triggers or spray on gene silencing, they might be in the range of 5000 to 10,000 kilodaltons. So they're much, much larger, and they're also very water soluble, and they're potentially easily degraded. Plants have lots of defenses against these small RNAs, because that's typically what a plant virus is going to look like, is going to they're also, they're the form of a of an RNA. So plants have lots of enzymes and things that break down,

break down our RNA. So what can we do about that? You know, we can figure out how to have a better formulation. So think, you know, it really draws on the same kind of formulation technology that we use with herbicides. You know, can we adjust the ratio of the lipophilic component and the hydrophilic component? Are there things we can do to spread out the droplet or or make it have a sharper angle, to drive a concentration gradient? The same kind of questions are the things

we're looking at. So we can put, let's call it a nucleic acid, so that just is a term for, you know, a little piece of one of these RNAi triggers. We can put a tag on that with fluorescent tags. We could see it under a microscope. And we'll do experiments where we might try, you know, maybe a surfactant that's more has more hydrophilic component, or more lipophilic, you know, whatever it might be. And then we can look at it, that leaf under the microscope, and figure out how much is actually

going into the cuticle, how much is going into the cells. We can have markers for the DNA, the nucleus of the cell, and see how much is getting there, but that is really, you know, the kind of research that I've been working on, and other groups have been working on, you know, probably for about five years now, in terms of how can we get solve this problem of getting what is a very large and delicate molecule into the plant. But

progress is being made there now. Talk on the other side of it, what happens when we actually get it in because we're going after the RNA? Now, potentially, there's a whole new playbook or toolkit of things that we can go after, because herbicides are somewhat limited by you've got to get find an effective inhibitor of a protein. It's got to be a

protein that, if you knock it out, it's lethal. But now we could go after any RNA we want, as long as we can get this the it's the chemical properties of the of the trigger are essentially the same no matter what Gene we're going after. And also, now that we have all these genomes with all this information, we can go after things that are currently herbicide targets, but you go after things that are not, you know, there's a whole lot of information in Plant Biology

about, if you knock out this gene, the plant can't live. So, hey, let's try that. Then I think this is where this gets really fun. So, you know, how could this be better? Like, you know? So herbicides work really well. We have issues with resistance. You know, it can be a lot of challenging as far as the stewardship of these molecules and their registration and all the things that come with that. So what's better about gene silencing? For one thing, off target effects, by

design, we can really minimize the risk of that. So because we design, for example, one of these triggers needs to be they're usually 22 bases long. So you design that so it exactly matches. For example, the target pigweed, it doesn't target the crop. So this as long as it has to be a perfect match. So if there are two or three bases that don't match, it doesn't

affect the crop. It's safe for the person applying it that you know will not there's no match to any RNA in the in the people who are using it and and interacting with it, consuming the product. Later. When you think of the soil microbiome, you know, there's no you make sure, we can check it against all these databases and make sure there's no match there, you think of off target, maybe endangered species, birds, fish, amphibians, etc. They can make sure that it's not having any

effect on anything else. That can be very, very precise and very selective. So, you know, we think of, we spend a lot of time thinking about crop safety and balancing that with weed management. And this should be, you know, a very precise tool. Now, with that precision comes a bit of a trade off, and that, you know, there's not going to be, because you can't have one trigger that controls all your broad leaves and all your grasses, right? Because they're going to have different

sequences. However, I think a nice way to think about this is, you know, when you go you want to paint room in your house, right? And you look at all the options, and you that's the favorite color I want. The store doesn't have all of those colors mixed up, right? They have the base colors, and they know how

to mix up that exact one. Well, that's what we could start to do, is you could go in and say, hey, well, in my field, you know, I've got palmer amaranth, I've got waterhemp, and I've got barnyard grass I want to mix for that, you know, I don't care about velvetleaf or I don't care about prickly sida or whatever,

and you get the ones just your custom mix for what you need. Go even a little bit further, you know, you think of the precision spray technologies we've got now, and can we get to a place where those are even able to identify the species you might actually have, you could have, you know, 10 different of these gene silencing triggers loaded in the system and the and the spray is recognizing, okay, that's Palmer amaranth. It draws that and sprays it, you know. Okay, that's a grass it brings

that one in and sprays it again. You know, maybe that's all getting a bit complicated, but with this precision, come will come the opportunity to do potentially new things that we haven't thought about doing before as well. There's resistance, just as we think about it with herbicides. We've got to think about it in this sense as well, because now you know of mutation, and this is what weeds are good at as mutations. We'll make it so that that one doesn't match anymore.

So how can we monitor that and respond? Well, if the population does have a mutation, we can design another oligo that matches that form, add it to the mix. We can have multiple targets, maybe that are applied at once. So maybe you're targeting three or four genes with the spray. You could potentially Think about it like a flu vaccine. You know, every year the manufacturer comes out with a different mix of gene

targets. So even as the applicator, you're not even in a situation where you could be using the same thing two years in a row, because there's enough options. You can always be mixing it up, combining that with now our genomics understanding and the low cost these tools to monitor for these mutations that are out there. I think, you know, if we can solve this problem around the delivery and we've got to figure out, you

know, how does this fit? How does this work? I think that there's just a. Incredible range of of options, of how this could be applied to make it, you know, a really nice additional partner and another tool in the toolbox.

cheap molecule. So yeah, if I've got waterhemp and kochia, I can do my water hemp and kosher RNA blend, and then glyphsate will take care of the rest. And just one, one of the simple ways of possibly integrating it, before we go down to all the potentially more complicated and complex routes that we could end up at one day.

mutation, potentially somewhere in some individual. So if you start using this kind of technology on that broad sense, what it's going to reveal very quickly are the mutant individuals that have a mismatch in that right. So it is almost whereas we often can think about like a if, let's say we had a new herbicide. Theoretically, a resistant mutation is roughly anywhere in the range of about one in 10,000,001 in 20 million.

That's a pretty good guess. And you know, how much area does it take to have 20 million Palmer Imran individuals, not that much, unfortunately, but it's a it doesn't, you know, obviously, when we start, if we did have a new herbicide, it's not like the first year you start seeing survivors and resistance. But these, what I'm trying to say is the potential frequency of resistance is higher. So I think you need to, right away have a very sort of proactive and reactive resistance management.

And that's but how we do that then is the kind of combination approach. So if we have, you know, a target for Gene one and a target for Gene two, now the probability of an individual having mutation to both of those drops a lot. If you're bringing a third one, you get that number very, very low. Then, if you're changing those each year and not putting the selection pressure on one, that's where you drop it really low. Now, does that become practical from a manufacturing and a use

perspective? I think those are questions and challenges that have to be addressed. But I think that with a there could be a good design to help reduce that risk of resistance, although it's still definitely be a concern, you'd want all the monitoring and and integrated, you know, non chemical practices get rid of survivors. All those same things would be especially important.

anymore? You know? All you know, if we've learned anything from herbicide resistance, it's just about anything can be possible. Yeah.

that's really driving it along. So you could, you know, if you're to do a search for RNAi companies, there are a lot of them out there. So people are really working on this. Weeds are probably the most challenging. You know, I'd say insects the best application. Fungal pathogens have good applications for this. The challenge is to get these gene silos and triggers into weeds. So how quickly can we solve

that? And then how quickly can this product come to market? You know, there are questions on just how does this look like from a regulatory perspective? For example, you know, if we have a given 22 base pair sequence of a given RNAi trigger, and you change three base pairs of it, is that a whole new molecule that needs a new registration package? Or is that a variant that, you know can go under the same safety and

assessment package? You know, I certainly don't have the answers to those kind of things, and so, you know, that will be a step in bringing it to market. Certainly is the the safety assessment and regulation. How does that fit in manufacturing questions? You know, I think it's a solvable problem, but it's one of these things that you can make tons of these, of these nucleic acid

triggers. But right now the cost of doing that is very high. You need to, you need to switch to a different scale, to different chemistry, to make them at that large scale. And you wouldn't do that unless you have a need or market for it, right? It's like, so you can bring the cost of it way down. You need to have a reason to do so. So how somebody's gonna have to navigate that kind of, you know, production and demand divide,

but it's, I think it's technically feasible. So let me just you know, I hope that in the range of seven to 10 years, we would could have something like this in the market. I really do, and I know I'm certainly getting up every day and working on this to try to do my part to help make that happen. And but it'll be a lot of people, and we'll need breakthroughs in various spaces to get it there.

different mutant form of our target gene. We can change what we're synthesizing to target it, if it's you know, through that pathway. So I think that there's a way to we can incorporate this faster information about resistance, as well as resistance to our our regular herbicides to make better decisions, and maybe even come to more like a personalized weed

management kind of approach. You know that, you know here's what you've got going on in this field, your soil types, your precipitation patterns, your cropping goals, the weeds you've got, what is going to work on them, what's not and put that all into your mix, as well as with these precision technologies, see and spray kind of things that you can know. Okay, here's my best option of the best weed management at the

least cost and the longest productivity. So it's really, I think that the genomic side allows us to have better diagnostics. You know, we could potentially get to something where you can walk out in the field and crush up a leaf and put it in a little test strip and have an answer, you know, is it resistant or not? So, you know, if you're working with the consultant or the you know, whoever the advisor, you can make your decision right then and not say, well, we'll send it

off to a lab, and maybe we'll know in a month. You know that I think that we could get to a place of timely information and then expand the toolbox so that, again, we just have more information and we can make better choices.

they are to pigweed that is 100 miles away, 500 miles away? What do you think is the answer for that? Let's say Palmer amaranth. What would you predict?

just about every gene in the genome. And there's a huge amount of genetic diversity, because they, you know, they have to outcross, and also that there's something in that question you asked earlier about, why is this such a successful weed? That's one idea that a lot of people are talking about is, you know, can weeds actually generate more mutations in their genome, whether through transposons, whether through

things like this circular DNA. We are talking about that, even just a few weeds there, they've got a ton of genetic diversity. So that's why I think my answer would be, No, there's not a silver bullet. Because no matter what that silver bullet is, there is some kind of genetic variant out there that is going to allow those weeds to escape it, and it doesn't have to be resistant to that particular you know, if it's a chemical control

option, think of weed shifts, right? One of the, I think an amazing story with Kochia is that there's this kind of long term weed management study in western Nebraska at Scottsbluff, and they noticed that Kochia was surviving in a lot of these plots that got a group 27 pre emergence, early in the season for years. So they thought, okay, maybe we've got HPPD resistance here. Got samples of those seeds go the greenhouse. No resistance whatsoever. They're completely sensitive.

However, what was that population doing? It had shifted its its germination was delayed about 30 days after that herbicide breaks down, right? So it's just able to escape. So you know, and that you know, the population that's not its ideal time to germinate. But is there a variation for that late germination, even in a 10 by 30 foot plot? You bet it's there. So I think that, you know, no matter what we do, if we find something that works really well, and we keep doing it over

and over, as weeds will will shift. There's there's variation out there that is going to come back and get us

would you do with all these wheat genomes, really? And so we have this paper that talks about, kind of all the different ideas that people have thought of and how we can use wheat genomes. We've mostly talked about herbicides today, but can we look at biology and dormancy and ecology and all these things? With weeds. And so that paper is in a journal called Genome biology, and Jake Montgomery is the first author.

And I can send you that link for that paper. It's an open access one, so anybody can take a look at it if you really want to dive into the topic.

to catch you next week on the war against weeds. Podcast.