Photo: Kochia, southwest Montana. © 2020 Delena Norris-Tull
Herbicide Resistance in Invasive Plants
Summaries of the research and commentary by Dr. Delena Norris-Tull, Professor Emerita of Science Education, University of Montana Western, October 2020.
In a 1999 report on the impact of herbicide resistant weeds in Kansas, Peterson reports, “Monocropping and repeated use of the same or similar herbicides in some areas of the state has resulted in the development of herbicide-resistant weeds. The development of herbicide-resistant weed populations has an immediate and a long- term effect on the efficiency and cost of controlling weeds.” Kochia was one of the first noxious weeds known to develop herbicide-resistance, first documented in Kansas in 1976 “from populations found along rail-road right-of-ways, where high rates of triazine herbicides were used for nonselective residual weed control.” (Peterson, 1999).
Green, 2007, conducted a review of the research on the history and mechanisms of herbicide-resistant weeds and the development of herbicide-resistant crops. Glyphosate, a postemergence herbicide, has been an effective control for most of the world’s worst weeds for decades, and has been used to control more than 300 herbaceous weed species and woody brush and trees. As of 2007, “11 glyphosate-resistant weed species have been identified” (Green, 2007). Glyphosate resistant weeds developed slowly over nearly two decades of use. First identified in 1996, “glyphosate-resistant rigid ryegrass… took 15 years to evolve in response to two annual applications of glyphosate. …. Goosegrass took 10 years to evolve glyphosate resistance with up to eight applications of glyphosate each year…. The first weed discovered to be resistant to ALS-inhibiting herbicides was prickly lettuce… which evolved after 5 years of chlorsulfuron applications… [As of 2007,] 95 weed species have been reported that are ALS- resistant…. Not all ALS-resistant weed biotypes become cross-resistant to other classes of ALS-inhibiting herbicide” (Green 2007).
Dong, et al., 2016, found that by 2015, “A total of thirty-one weed species have evolved resistance to glyphosate worldwide,” with 14 of those weeds in farmland in the US. “By 2012, glyphosate-resistance weeds had infested 25 million hectares of U.S. cropland…. The evolution and spread of glyphosate-resistance weeds may jeopardize the economic and environmental benefits of herbicide-tolerant crops as farmers shift to more frequent tillage and apply more toxic and/or more expensive herbicides.” Dong, et al., 2016, developed a tool to evaluate the extent to which farmers adopt various best management practices for preventing the development of herbicide-resistant weeds. Refer to the results of that study below.
Green, 2007, states that in 1975, “scientists at America Cyanamid and Dupont independently discovered herbicides that inhibited acetolactate synthase (ALS)…. Today more than 50 ALS-inhibiting herbicides from five different chemical classes (sulfonylureas…, imidazolinones…, triazolopyrimidines…, pyrimidinylthiobenzoates… and sulfonylamino-carbonly-triazolineones) are commercial. These herbicides control a wide spectrum of grass and broadleaf weeds at relatively low application rates… ALS does not occur in mammals and thus ALS-inhibiting herbicides have low mammalian toxicity.”
The emergence of herbicide resistant noxious weeds has greatly increased agricultural costs. A number of invasive plant species now have developed resistance to a variety of herbicides. John Samson, from the Wyoming Department of Transportation, told me, “Kochia has become resistant to the triazines [a broad spectrum, Group 5 herbicide]. We used to use triazines but we no longer use them due to the damage they did to some crops on alkaline soils. We had a similar problem with dicamba and wind drift, and a lot of the Group 2 herbicides (ALS inhibitors). A lot of herbicides have the same mode of action, which is why an invasive species will eventually become resistant not just to one herbicide, but a variety of herbicides in that Action Group.”
“Triazine-resistant pigweeds (Amaranthus spp.) were not confirmed until almost 20 yr later than kochia … Resistance to acetolactate synthase (ALS)-inhibiting herbicides was confirmed first in kochia from a wheat…field near Liberal, KS, in 1987… The development and incidence of ALS-resistant kochia increased more quickly than triazine-resistant kochia, probably because ALS resistance apparently has no fitness penalty and can be spread through pollen transfer, whereas triazine resistance results in a fitness penalty and is inherited only maternally… ALS-resistant common waterhemp (Amaranthus rudis) and Palmer amaranth (Amaranthus palmeri) were confirmed first in Kansas in 1993... The ALS-resistant Palmer amaranth biotype was collected from a field with a history of intensive use of ALS-inhibiting herbicides and was cross-resistant to all sulfonylurea, imidazolinone, and triazolopyrimidine herbicides….ALS-resistant common cocklebur (Xanthium strumarium), shattercane (Sorghum bicolor), and common sun- flower (Helianthus annuus) were confirmed in Kansas in 1997… Common sunflower exhibited various patterns of cross-resistance among the sulfonyl-urea, imidazolinone, and triazolopyrimidine herbicides, reflecting historical herbicide use patterns in and adjacent to the collection sites.” (Peterson, 1999).
Peterson, 1999, reported that, “The recommended management strategies for herbicide-resistant weed problems include an integrated system of crop rotation, rotation of herbicide modes of action, tank-mixes of herbicide modes of action, and cultivation… However, tank-mix partners must be mutually effective on the target weeds or this strategy will not be effective for resistance management…Switching to different herbicides is effective only if adequate alternatives are available to provide similar weed control at a comparable price…Unfortunately, farmers who have not encountered an herbicide resistance problem tend to continue with a successful herbicide program until it fails…. The greatest long-term costs of herbicide-resistant weeds are the loss of herbicide performance and weed population shifts…The initial phases of herbicide resistance development often result in a tremendous increase in the seed bank of the resistant species because of weed control failures...The increased weed pressure often requires an intensified weed control program for several years…Sequential weed management programs consisting of planting time residual herbicides followed by postemergence herbicides and cultivation have been recommended…Sequential herbicide programs have the added cost of another application but can provide more consistent weed control with reduced risk of failures compared to single-pass programs.”
Herbicide resistance to 2,4-D and Dicamba
Schulz and Segobye, 2016, studied the cause of noxious weed resistance to 2,4-D. They found that, “Despite its decades-long worldwide use, resistance against 2,4-D has been found in only 28 different weed species.” They examined the research on how 2,4-D resistance develops in noxious weeds. Research by Goggin, et al., 2016, concluded that, “The herbicidal mechanism of action of 2,4-D [in wild radish] is considered to be activation of the auxin receptor system (TIR1 and related receptor proteins), which results in permanent up-regulation of auxin responses in plants.” Schulz & Segobye, 2016, concluded that, “The molecular understanding of herbicide resistance mechanisms is still in its infancy. However, recent progress promises a better understanding and provides more options for developing informed strategies to deal with the problem in weeds, such as use of RNAi technology to overcome resistance.”
Goggin et al., 2018, conducted experiments to examine the mechanism of 2,4-D and dicamba resistance in the noxious weed, wild radish, in Australia. They treated various populations of wild radish with varying strengths of 2,4-D and dicamba. Wild radish populations already known to be resistant to 2,4-D were labeled R populations. Populations of wild radish known to be susceptible to 2,4-D were labeled S populations. The populations were grown in isolation from each other, to avoid cross-pollination. Various genetic crosses of some of the R populations were also produced and included in the treatments.
Goggin et al., 2018, commented that, “Very recently, the first target site mutation conferring auxinic herbicide resistance in a weed species was identified in the conserved domain II region of the auxin co-receptor IAA16 in dicamba-resistant Kochia scoparia (LeClere, et al., 2018). There was also evidence that the mutation caused cross-resistance to 2,4-D but not to the natural auxin indole-3-acetic acid (IAA) or the synthetic 1-naphthyleneacetic acid (NAA).”
In their experimental treatments, Goggin et al., 2018, discovered that, “Although 2,4-D and dicamba had similar effects on the biomass of the R survivors, S survivors were less affected by dicamba than by 2,4-D at doses of 125–500 g ha–1…The effects of 2,4-D and dicamba on the biomass of the surviving plants were not subjected to a GR50 analysis, because the biomass of some R populations was not greatly affected at any herbicide dose…Instead, the mean biomass of survivors across all herbicide doses was compared. Almost all of the R populations had a significantly (P < 0.05) higher biomass than the S populations, but again there were no consistent patterns between R populations. There were significant positive correlations between plant survival (LD50) and survivor biomass under both 2,4-D and dicamba treatment.”
Goggin et al., 2018, stated that, “2,4-D resistance in wild radish appears to result from subtly different auxin signaling alterations in different populations, supplemented by an enhanced defence response and, in some cases, reduced 2,4-D translocation. This study highlights the dangers of applying knowledge generated from a few populations of a weed species to the species as a whole.”
Goggin et al., 2018, also found that, “There was evidence of differential auxin selectivity in the different populations. All of the 2,4-D-resistant populations were also resistant to a dicamba foliar spray, but there was no correlation between the levels of resistance to 2,4-D and to dicamba as measured by survival or biomass increase following foliar spraying. Similarly, whilst all of the populations were 2,4-D resistant in the root elongation assays, some were not dicamba resistant and other (different) populations were not resistant to NAA. It is well known that different auxins interact with components of the auxin signalling and transport machinery in distinct ways,… so the observed differences in auxin selectivity between the 2,4-D-resistant wild radish populations, and in their relative resistance levels, strengthen the hypothesis that 2,4-D resistance is conferred by different alterations in auxin signalling in different populations... In view of the recent discovery of a mutation conferring evolved dicamba and 2,4-D resistance in the IAA16 protein of Kochia scoparia…, it is tempting to speculate that these signalling alterations may be due to mutations in various Aux/IAA proteins in the different populations.”
Goggin et al., 2018, concluded that “it is unlikely that a universal chemical or genetic solution (e.g. compounds restoring translocation or bypassing the putative block in auxin signaling; use of the CRISPR/Cas9 gene drive) could be found to control 2,4-D-resistant wild radish. As most of these populations are also resistant to one or two other herbicide modes of action…, the best control options would involve strategic mixtures of still effective modes of action plus non-chemical measures, namely prevention of seed bank replenishment at harvest… and increased competition from the crop.”
in my interviews with Weed Scientists, I gained valuable insights into the history of the emergence of noxious weeds that are resistant to herbicides. Refer to the various interviews. In particular, I recommend reading my interview with Dr. George Beck at Colorado State University.
References:
Links to additional information on Herbicide Resistance:
Next Sections on Herbicides and other Pesticides:
Herbicide Resistance in Invasive Plants
Summaries of the research and commentary by Dr. Delena Norris-Tull, Professor Emerita of Science Education, University of Montana Western, October 2020.
In a 1999 report on the impact of herbicide resistant weeds in Kansas, Peterson reports, “Monocropping and repeated use of the same or similar herbicides in some areas of the state has resulted in the development of herbicide-resistant weeds. The development of herbicide-resistant weed populations has an immediate and a long- term effect on the efficiency and cost of controlling weeds.” Kochia was one of the first noxious weeds known to develop herbicide-resistance, first documented in Kansas in 1976 “from populations found along rail-road right-of-ways, where high rates of triazine herbicides were used for nonselective residual weed control.” (Peterson, 1999).
Green, 2007, conducted a review of the research on the history and mechanisms of herbicide-resistant weeds and the development of herbicide-resistant crops. Glyphosate, a postemergence herbicide, has been an effective control for most of the world’s worst weeds for decades, and has been used to control more than 300 herbaceous weed species and woody brush and trees. As of 2007, “11 glyphosate-resistant weed species have been identified” (Green, 2007). Glyphosate resistant weeds developed slowly over nearly two decades of use. First identified in 1996, “glyphosate-resistant rigid ryegrass… took 15 years to evolve in response to two annual applications of glyphosate. …. Goosegrass took 10 years to evolve glyphosate resistance with up to eight applications of glyphosate each year…. The first weed discovered to be resistant to ALS-inhibiting herbicides was prickly lettuce… which evolved after 5 years of chlorsulfuron applications… [As of 2007,] 95 weed species have been reported that are ALS- resistant…. Not all ALS-resistant weed biotypes become cross-resistant to other classes of ALS-inhibiting herbicide” (Green 2007).
Dong, et al., 2016, found that by 2015, “A total of thirty-one weed species have evolved resistance to glyphosate worldwide,” with 14 of those weeds in farmland in the US. “By 2012, glyphosate-resistance weeds had infested 25 million hectares of U.S. cropland…. The evolution and spread of glyphosate-resistance weeds may jeopardize the economic and environmental benefits of herbicide-tolerant crops as farmers shift to more frequent tillage and apply more toxic and/or more expensive herbicides.” Dong, et al., 2016, developed a tool to evaluate the extent to which farmers adopt various best management practices for preventing the development of herbicide-resistant weeds. Refer to the results of that study below.
Green, 2007, states that in 1975, “scientists at America Cyanamid and Dupont independently discovered herbicides that inhibited acetolactate synthase (ALS)…. Today more than 50 ALS-inhibiting herbicides from five different chemical classes (sulfonylureas…, imidazolinones…, triazolopyrimidines…, pyrimidinylthiobenzoates… and sulfonylamino-carbonly-triazolineones) are commercial. These herbicides control a wide spectrum of grass and broadleaf weeds at relatively low application rates… ALS does not occur in mammals and thus ALS-inhibiting herbicides have low mammalian toxicity.”
The emergence of herbicide resistant noxious weeds has greatly increased agricultural costs. A number of invasive plant species now have developed resistance to a variety of herbicides. John Samson, from the Wyoming Department of Transportation, told me, “Kochia has become resistant to the triazines [a broad spectrum, Group 5 herbicide]. We used to use triazines but we no longer use them due to the damage they did to some crops on alkaline soils. We had a similar problem with dicamba and wind drift, and a lot of the Group 2 herbicides (ALS inhibitors). A lot of herbicides have the same mode of action, which is why an invasive species will eventually become resistant not just to one herbicide, but a variety of herbicides in that Action Group.”
“Triazine-resistant pigweeds (Amaranthus spp.) were not confirmed until almost 20 yr later than kochia … Resistance to acetolactate synthase (ALS)-inhibiting herbicides was confirmed first in kochia from a wheat…field near Liberal, KS, in 1987… The development and incidence of ALS-resistant kochia increased more quickly than triazine-resistant kochia, probably because ALS resistance apparently has no fitness penalty and can be spread through pollen transfer, whereas triazine resistance results in a fitness penalty and is inherited only maternally… ALS-resistant common waterhemp (Amaranthus rudis) and Palmer amaranth (Amaranthus palmeri) were confirmed first in Kansas in 1993... The ALS-resistant Palmer amaranth biotype was collected from a field with a history of intensive use of ALS-inhibiting herbicides and was cross-resistant to all sulfonylurea, imidazolinone, and triazolopyrimidine herbicides….ALS-resistant common cocklebur (Xanthium strumarium), shattercane (Sorghum bicolor), and common sun- flower (Helianthus annuus) were confirmed in Kansas in 1997… Common sunflower exhibited various patterns of cross-resistance among the sulfonyl-urea, imidazolinone, and triazolopyrimidine herbicides, reflecting historical herbicide use patterns in and adjacent to the collection sites.” (Peterson, 1999).
Peterson, 1999, reported that, “The recommended management strategies for herbicide-resistant weed problems include an integrated system of crop rotation, rotation of herbicide modes of action, tank-mixes of herbicide modes of action, and cultivation… However, tank-mix partners must be mutually effective on the target weeds or this strategy will not be effective for resistance management…Switching to different herbicides is effective only if adequate alternatives are available to provide similar weed control at a comparable price…Unfortunately, farmers who have not encountered an herbicide resistance problem tend to continue with a successful herbicide program until it fails…. The greatest long-term costs of herbicide-resistant weeds are the loss of herbicide performance and weed population shifts…The initial phases of herbicide resistance development often result in a tremendous increase in the seed bank of the resistant species because of weed control failures...The increased weed pressure often requires an intensified weed control program for several years…Sequential weed management programs consisting of planting time residual herbicides followed by postemergence herbicides and cultivation have been recommended…Sequential herbicide programs have the added cost of another application but can provide more consistent weed control with reduced risk of failures compared to single-pass programs.”
Herbicide resistance to 2,4-D and Dicamba
Schulz and Segobye, 2016, studied the cause of noxious weed resistance to 2,4-D. They found that, “Despite its decades-long worldwide use, resistance against 2,4-D has been found in only 28 different weed species.” They examined the research on how 2,4-D resistance develops in noxious weeds. Research by Goggin, et al., 2016, concluded that, “The herbicidal mechanism of action of 2,4-D [in wild radish] is considered to be activation of the auxin receptor system (TIR1 and related receptor proteins), which results in permanent up-regulation of auxin responses in plants.” Schulz & Segobye, 2016, concluded that, “The molecular understanding of herbicide resistance mechanisms is still in its infancy. However, recent progress promises a better understanding and provides more options for developing informed strategies to deal with the problem in weeds, such as use of RNAi technology to overcome resistance.”
Goggin et al., 2018, conducted experiments to examine the mechanism of 2,4-D and dicamba resistance in the noxious weed, wild radish, in Australia. They treated various populations of wild radish with varying strengths of 2,4-D and dicamba. Wild radish populations already known to be resistant to 2,4-D were labeled R populations. Populations of wild radish known to be susceptible to 2,4-D were labeled S populations. The populations were grown in isolation from each other, to avoid cross-pollination. Various genetic crosses of some of the R populations were also produced and included in the treatments.
Goggin et al., 2018, commented that, “Very recently, the first target site mutation conferring auxinic herbicide resistance in a weed species was identified in the conserved domain II region of the auxin co-receptor IAA16 in dicamba-resistant Kochia scoparia (LeClere, et al., 2018). There was also evidence that the mutation caused cross-resistance to 2,4-D but not to the natural auxin indole-3-acetic acid (IAA) or the synthetic 1-naphthyleneacetic acid (NAA).”
In their experimental treatments, Goggin et al., 2018, discovered that, “Although 2,4-D and dicamba had similar effects on the biomass of the R survivors, S survivors were less affected by dicamba than by 2,4-D at doses of 125–500 g ha–1…The effects of 2,4-D and dicamba on the biomass of the surviving plants were not subjected to a GR50 analysis, because the biomass of some R populations was not greatly affected at any herbicide dose…Instead, the mean biomass of survivors across all herbicide doses was compared. Almost all of the R populations had a significantly (P < 0.05) higher biomass than the S populations, but again there were no consistent patterns between R populations. There were significant positive correlations between plant survival (LD50) and survivor biomass under both 2,4-D and dicamba treatment.”
Goggin et al., 2018, stated that, “2,4-D resistance in wild radish appears to result from subtly different auxin signaling alterations in different populations, supplemented by an enhanced defence response and, in some cases, reduced 2,4-D translocation. This study highlights the dangers of applying knowledge generated from a few populations of a weed species to the species as a whole.”
Goggin et al., 2018, also found that, “There was evidence of differential auxin selectivity in the different populations. All of the 2,4-D-resistant populations were also resistant to a dicamba foliar spray, but there was no correlation between the levels of resistance to 2,4-D and to dicamba as measured by survival or biomass increase following foliar spraying. Similarly, whilst all of the populations were 2,4-D resistant in the root elongation assays, some were not dicamba resistant and other (different) populations were not resistant to NAA. It is well known that different auxins interact with components of the auxin signalling and transport machinery in distinct ways,… so the observed differences in auxin selectivity between the 2,4-D-resistant wild radish populations, and in their relative resistance levels, strengthen the hypothesis that 2,4-D resistance is conferred by different alterations in auxin signalling in different populations... In view of the recent discovery of a mutation conferring evolved dicamba and 2,4-D resistance in the IAA16 protein of Kochia scoparia…, it is tempting to speculate that these signalling alterations may be due to mutations in various Aux/IAA proteins in the different populations.”
Goggin et al., 2018, concluded that “it is unlikely that a universal chemical or genetic solution (e.g. compounds restoring translocation or bypassing the putative block in auxin signaling; use of the CRISPR/Cas9 gene drive) could be found to control 2,4-D-resistant wild radish. As most of these populations are also resistant to one or two other herbicide modes of action…, the best control options would involve strategic mixtures of still effective modes of action plus non-chemical measures, namely prevention of seed bank replenishment at harvest… and increased competition from the crop.”
in my interviews with Weed Scientists, I gained valuable insights into the history of the emergence of noxious weeds that are resistant to herbicides. Refer to the various interviews. In particular, I recommend reading my interview with Dr. George Beck at Colorado State University.
References:
- Dong, F., Mitchell, P.D., Hurley, T.M., & Frisvold, G.B. (2016). Quantifying adoption intensity for weed-resistance management practices and its determinants among U.S. soybean, corn, and cotton farmers. Journal of Agricultural and Resource Economics, 41(1):42-61.
- Goggin, D.E., Kaur, P., Owen, M.J., Stephen B., & Powles, S.B. (2018). Annals of Botany, 122: 627–640. doi: 10.1093/aob/mcy097
- Green, J.M. (Apr-June, 2007). Review of glyphosate and ALS-inhibiting herbicide crop resistance and resistant weed management. Weed Technology, 21(2): 547-558.
- Peterson, D.E. (July-Sept., 1999). The impact of herbicide-resistant weeds on Kansas agriculture. Weed Technology, 13(3):632- 635.
- Schulz, B., & Segobye, K. (2016). 2,4-D transport and herbicide resistance in weeds. Journal of Experimental Botany, 67 (11):3177-3179. doi: 10.1093/jxb/erw199
Links to additional information on Herbicide Resistance:
- Herbicide Resistant Crops
- Controlling herbicide-resistant weeds in herbicide-resistant crops
- Best Management Practices
Next Sections on Herbicides and other Pesticides:
Previous Sections on Herbicides: