Herbicide Tolerant Crops
Genetic engineering (GE) refers to techniques used to manipulate the genetic composition of an organism by adding specific genes. The enhancement of desired traits has traditionally been undertaken through conventional plant breeding. GE crops are often broken down into two categories, herbicide tolerant and Plant-incorporated protectants (PIPs).Crops are also engineered or “stacked” to express multiple traits like crops that are resistant to multiple herbicides or are resistant to herbicides and incorporates insecticides.
Herbicide tolerant crops are designed to tolerate specific broad-spectrum herbicides, which kill the surrounding weeds, but leave the cultivated crop intact. Currently, the only varieties Cultivated in the U.S. are engineered to be tolerant to glyphosate. However, the U.S. Department of Agriculture (USDA) is currently in the process of deregulating other new varieties of crops that are resistant to 2,4-D and other herbicides.
Glyphosate Tolerant Crops
Monsanto first introduced glyphosate-resistant soybean in 1996 and later introduced glyphosate-resistant corn in 1998. These crops, commonly called “Roundup Ready”, have become ubiquitous in American agriculture with 93% of soybeans, 82% of cotton, and 85% of corn planted engineered to be glyphosate resistant. This increase in glyphosate-resistant crops has led to an increase in herbicide use, herbicide-resistant weeds (also known as “superweeds”), and numerous other environmental and human health impacts.
Pesticide resistance, the ability of an organism to withstand a poison, is a predictable consequence of repeated pesticide use. How quickly pesticide resistance develops depends on: the frequency of use, the mechanisms of resistance, the genetics of the resistance mechanism, the size of the gene pool and how quickly the organisms reproduce.
- A study published by Washington State University’s research professor Charles Benbrook, PhD, found that the use of herbicides in the production of three GE crops—cotton, soybeans and corn—had increased. This finding contradicts industry claims that the technology would reduce pesticide applications. According to the study, the emergence and spread of glyphosate-resistant weeds is by far the most important factor driving up herbicide use on land planted with GE crops. Glyphosate-tolerant weeds were practically unknown before the introduction of Roundup-tolerant crops in 1996. But heavy reliance on the herbicide Roundup, whose active ingredient is glyphosate, has placed weed populations under progressively intense and unprecedented selection pressure, triggering a perfect storm for the emergence of glyphosate-resistant weeds. “Resistant weeds have become a major problem for many farmers reliant on GE crops, and are now driving up the volume of herbicide needed each year by about 25 percent,” Dr. Benbrook said.
- Glyphosate resistance issues have led farmers to request emergency exemptions to use untested herbicides on now glyphosate-resistant weeds. For example, in November 2012, the U.S. Environmental Protection Agency (EPA) granted an emergency exemption for the use of fluridone, an aquatic herbicide that has never undergone scrutiny for its effects on endangered species, on GE cotton crops in order to control resistant weeds.
Increased Herbicide Use
- A recent USDA report found that herbicide use on GE corn increased from around 1.5 pounds per planted acre in 2001 to more than 2.0 pounds per planted acre in 2010. Herbicide use on non-GMO corn has remained relatively level during that same time frame.
Loss of Habitat
- The increased use of glyphosate-resistant crops has led to declines in pollinator habitat. Historically, for butterflies in the U.S., their key source of food, milkweed, was found in several key states where the butterfly feeds and breeds: Iowa, Minnesota, Wisconsin, Illinois, Indiana, parts of Ohio and the eastern Dakotas. Now fields have been planted with more than 120 million acres of corn and soybeans genetically engineered to be tolerant to glyphosate, as well as other herbicides, allowing farmers to use glyphosate to kill milkweed in the field. According to researchers, the utilization of these GE crops has all but eliminated milkweeds from these fields, thus eliminating the butterfly’s source of food.
Glyphosate in the Environment
- A second 2011 study, Fate and transport of glyphosate and aminomethylphosphonic acid in surface waters of agricultural basins, conducted by USGS monitored water concentrations of glyphosate. The study found glyphosate persists in streams throughout the growing season of GE crops in Iowa and Mississippi, but is generally not observed during other times of the year. The degradation product of glyphosate, aminomethylphosphonic acid (AMPA), which has a longer environmental lifetime, is also frequently detected in streams and rain.
Allowing GE crops to be grown close to organic and non-GE conventional produceincreases the riskof genetic cross-contamination, as pollen from GE crops has the potential to drift onto non-GE crops and produce offspring. Because GE crops are prohibited under organic standards organic farmers may suffer significant financial losses if certified organic crops become polluted with genetically-engineered pollen.
- A recent Survey produced by Food & Water Watch, Organic Farmers Pay the Price for GMO Contamination, found that a third of U.S. organic farmers have experienced problems in their fields due to the nearby use of GE crops, and over half of those growers have had loads of grain rejected because of unwitting GE contamination.
- In May of 2013, USDA announced that unapproved GE wheat was found growing in an Oregon wheat field. After this discovery Japan cancelled its order to buy U.S. western white wheat. Monsanto has not conducted field trials in Oregon since 2001 when it reportedly withdrew from the state.
- In September of 2013, the U.S. Department of Agriculture (USDA) refused to take action or investigate after it was confirmed that GE alfalfa contaminated non-GE alfalfa in Washington State. USDA claimed the contamination is a “commercial issue” and should be addressed by the marketplace and not the government.
Human Health Risks
- The increased use of glyphosate on glyphosate resistant crops could lead to increases in human health problems. Glyphosate-formulated herbicides have been linked to numerous health problems including cancer, particularly non-Hodgkin’s lymphoma in three separate peer-reviewed studies (1,2,3), ADHD, rhinitis, and hormone disruption. Short term health effects include lung congestion and increased breathing rates. Chronic exposures at levels above Maximum Contaminant Levels (MCL) are likely to produce kidney damage and reproductive effects. Click here to see Beyond Pesticides’ comments to the EPA concerning the reregistration of glyphosate.
2,4-D Tolerant Crops
Recently, USDA released for public input itsDraft Environmental Impact Statement(DEIS), which calls for the deregulation of GE corn and soybeans engineered to be tolerant to the herbicide 2,4-D. Much like glyphosate, these new varieties of GE corn and soybeans are set to usher in dramatic increases in 2,4-D. Dow AgroSciences produces these new GE crops under the brand name “Enlist” which will be stacked with glyphosate resistance.
Increased use of 2,4-D could have dramatic impacts on human and environmental health. Scientists around the world have reported increased cancer risks in association with its use, especially for non-Hodgkins Lymphoma (NHL). It is also neurotoxic, genotoxic, and an endocrine disruptor.
2,4-D has a high potential to leach from soils and can be a potential ground water contaminate. Environmental monitoring detected the herbicide in streams, groundwater and even drinking water. Studies document 2,4-D’s negative impacts on a wide range of animals. In birds, 2,4-D exposure reduced hatching success and caused birth defects. Toxic to fish, 2,4-D can bio-accumulate inside the fish. 2,4-D also is toxic to honey bees and earthworms.
For more information please read Beyond Pesticides' comments to USDA on its recent DEIS.
Extension > Agriculture > Crops > Weed management > Resistance management > Herbicide resistant weeds
Herbicide resistant weeds
Jeff L. Gunsolus, Extension agronomist - weed science
Resistance of weeds to herbicides is not a unique phenomenon. In fact, resistance to pesticides is a world wide problem that is not confined to any single pest category. The first report of insects resistant to insecticides was in 1908, of plant pathogens resistant to fungicides in 1940, and of weeds resistant to herbicides (triazines) in 1968. By 1991,120 weed biotypes that were resistant to triazine herbicides and 15 other herbicide families were documented throughout the world. Results of a 1992 North Central Weed Science Society survey of the north central United States and Canada reflect a world wide trend of increasing appearance of herbicide resistance. Twelve states or provinces reported biotypes of 19 weed species resistant to triazine herbicides (Table 7). Five states or provinces reported biotypes of three weed species resistant to lipid biosynthesis inhibitors (Table 4), 10 states or provinces reported biotypes of four weed species resistant to amino acid biosynthesis inhibitors (Table 2), four states or provinces reported biotypes of two weed species resistant to dinitroaniline herbicides (Table 5), and Manitoba reported resistance of a wild mustard biotype to growth regulator herbicides (Table 1). Indeed, pests have proven to be ecologically and biochemically adaptable to agrichemicals.
Why worry about herbicide resistance?
In corn, soybean, and small grains there are many herbicide options. Why then should a crop producer be concerned whether a weed biotype is resistant to a particular herbicide? There are several reasons. Many herbicide options could quickly be lost for several crops if a weed biotype is resistant to more than one herbicide (i.e. cross resistance). Obviously, a loss of herbicide options could have important economic and environmental consequences to agriculture. Also, in an era of high re-registration costs for older herbicides and high development costs for new herbicides, the possibility for replacement of the herbicides lost due to resistance diminishes. Finally, in most cases, it will not be easy nor inexpensive to assess resistant weed biotypes. Due to cross resistance, many resistance problems may have to be solved by trial and error, which could be quite expensive to the crop producer.
The herbicide resistance issue does have solutions and perhaps the best place to start is to consider herbicides as a resource that needs to be preserved. Strategies for resistance prevention follow from there.
Figure 1 Enzymes--Enzymes function as steps in biological processes. Enzymes are also extremely specialized in their function. As a result, many different enzymes are involved with the many different biological processes that occur within a plant. Some herbicides can stop specific enzymes from functioning, resulting in a disruption of specific plant processes; this often leads to the death of the plant. This herbicide-enzyme relationship is very specific and any chemical modification of the herbicide or enzyme can eliminate herbicidal activity.
Figure 2 Photosynthetic Inhibitors--The photosynthetic process occurs within a plant cell's chloroplasts. Certain herbicides can inhibit photosynthesis by binding to specific sites within the chloroplast. The relationship of a herbicide to the chloroplast binding site is very specific and any modification of the herbicide or binding site can eliminate herbicidal activity.
Site of action refers to the biochemical site within the plant with which the herbicide directly interacts. Some herbicide site of action interactions are well understood, others are unknown. Many of the well-known sites of action are enzymes or proteins essential to plant growth and development (Figure 1 and Figure 2). Also, some herbicides are believed to act at multiple sites.
Metabolism refers to the biochemical processes within the plant that generally modify herbicides to less toxic compounds. Differential rates of metabolism between crops and weeds is a primary method of crop selectivity to herbicides. One metabolic process may affect several different families of herbicides.
Herbicide families are a convenient way of organizing herbicides that share a common chemical structure and have similar herbicidal activity. Two or more herbicide families may affect the same site of action and therefore express similar herbicidal activity and injury symptoms.
A biotype is a group of plants within a species that has biological traits that are not common to the population as a whole. For example, the Pursuit resistant corn hybrid Pioneer 3377 IR is a biotype of Pioneer 3377 and atrazine-resistant common lambsquarters is a biotype of common lambsquarters. Therefore, in most instances, specific biotypes are not easily recognizable by casual observation.
Selection intensity in regard to herbicide resistance is the degree to which weed control measures (e.g. herbicides) in a cropping system give a competitive advantage to a weed or crop biotype resistant to a particular herbicide.
Herbicide susceptibility means a particular weed or crop biotype is killed by the recommended use rate of the herbicide.
Herbicide resistance refers to the inherited ability of a weed or crop biotype to survive a herbicide application to which the original population was susceptible. Currently, the three known resistance mechanisms that plants employ are: an alteration of the herbicide site of action, metabolism of the herbicide, and removal of the herbicide from the target site (sequestration).
Herbicide cross resistance refers to a weed or crop biotype that has evolved a mechanism or mechanisms of resistance to one herbicide that also allows it to be resistant to other herbicides. Cross resistance can occur with herbicides within the same or in different herbicide families and with the same or different sites of action. For example, after the extensive use of herbicide A in a field, selection of a weed biotype resistant to herbicide A is found to also be resistant to herbicide B, although herbicide B was never used in that field.
Herbicide multiple resistance refers to a weed or crop biotype that has evolved mechanisms of resistance to more than one herbicide and the resistance was brought about by separate selection processes. For example, after a weed or crop biotype developed resistance to herbicide A, then herbicide B was used and resistance evolved to herbicide B. The plant is now resistant to herbicides A and B through two separate selection processes.
How does selection of resistant weed biotypes occur?
Figure 3 Selection for herbicide resistance begins when a herbicide resistant biotype survives a particular herbicide application. The resistant biotype survives, matures, and sets seed. If the same herbicide continues to be applied and the resistant weeds reproduce, eventually the majority of the weeds will be resistant to the herbicide.
Selection for change in weed populations begins when a small number of plants (a biotype) within a weed species have a genetic makeup that enables them to survive a particular herbicide application. Where this difference in genetic makeup originated is not clear. However, herbicides are not known to directly cause the genetic change (i.e. mutation) that allows resistance. The resistant biotype, therefore, is present in low numbers in natural populations and when a herbicide is applied, most of the susceptible weeds die but the few resistant weeds survive, mature, and produce seed. If the same herbicide continues to be applied and the resistant weeds reproduce, the percentage of the weed population that is resistant will increase (Figure 3).
It is difficult to predict exactly which weed species will have biotypes resistant to a given herbicide. However, we have learned from previous pesticide resistance problems that the occurrence of herbicide resistant weeds is linked directly to the herbicide program used, the weed species present, and the crop management practices employed.
Selection intensity - the key to prevention
Selection intensity acts, in a sense, like a filter that can screen out susceptible weed biotypes while leaving resistant biotypes. Herbicides by definition are effective weed killers; therefore, they have the potential to exert heavy selection intensity on weeds. The more susceptible a weed species is to a given herbicide (i.e. the greater the weed control) the greater the selection intensity. As a result, the rate of selection for resistance can be quite rapid if the same herbicide or herbicides with the same site of action are repeatedly used in a particular field.
Figure 4 Simulated progression of resistant kochia exposed to repeated annual applications of Glean. This simulation assumes an initial seed population of 100,000/m2 with a 1 in 10,000,000 occurrence of resistant biotypes in the initial population and 90% weed control.
With such highly effective herbicides, one would think that the increase in the number of herbicide resistant biotypes would be readily observable. This is not the case. Resistant biotypes generally are only detectable when they make up about 30% of the population. During the first several years of a weed control program that relies on only one herbicide, the proportion of resistant biotypes is very low (less than 1% of the population). As long as the application of this herbicide continues and the resistant biotypes reproduce, the proportion of the population that is resistant will increase. It is very common to go from excellent control of a particular weed species to very poor control within one growing season. A gradual decline in performance is seldom seen. Figure 4 illustrates the predicted rapid increase in the proportion of a kochia population that is resistant following repeated annual applications of the sulfonylurea herbicide Glean. In field situations, resistance to sulfonylurea herbicides has been reported to occur after 3 to 5 years of repeated use. With triazine herbicides, resistance has generally appeared after seven or more years of repeated use. Therefore, depending upon the proportion of the population that was initially resistant to a herbicide, repeated use of a product for more than two years could develop a herbicide resistance problem.
Herbicide factors that increase selection intensity
The herbicide characteristics that affect herbicide resistance are as follows:
- Herbicides that act on a single site of action.
- Herbicides that are applied multiple times during the growing season.
- Herbicides used for several consecutive growing seasons or repeated application of herbicides with the same site of action to the same or different crops.
- Herbicides used without other weed control options (e.g. cultivation) and are considered "stand alone" weed control programs.
Single site of action herbicides
Figure 5 Development of resistance to single site of action herbicides is more likely than to multiple site of action herbicides because a change (mutation) in only one gene may be enough to affect a herbicide's binding potential to a single action site. It is less likely that the appropriate mutations will occur at multiple action sites.
Several herbicide families interfere with only a single site of action. Tables 2 - 5 and 7 - 9 list the herbicides associated with specific sites of action. Herbicides that interfere with single sites of action are generally more likely to select for resistant weeds because a change in only one gene may be enough to affect a herbicide's binding potential to the site of action. Therefore, it is more probable that a resistant weed population will develop if a difference of only one gene is required (Figure 5).
Multiple site of action herbicides
Based on the line of reasoning presented for single site of action herbicides, if a herbicide has multiple action sites it is less likely existing biotypes will have the genetic differences at all of the sites of action that will result in resistance (Figure 5). Therefore, it is less likely that weeds will evolve resistance to herbicides with multiple action sites. Tables 1 and 6 list herbicides with multiple sites of action.
Herbicide cross resistance and site of action
Figure 6. Changes (mutations) in a site of action may or may not result in resistance to other herbicides in the same family or that interact at the same site of action. The outcome is dependent upon the herbicide site of action relationship. For example, herbicides A and B may share part of a binding site on a particular enzyme, whereas herbicide C may bind at an entirely different site on the enzyme. Therefore, a genetic change that affects the enzyme may have different effects on any particular herbicide-enzyme relationship and any corresponding effects on crop injury or weed control.
A change in a site of action that results in resistance to a particular herbicide may or may not result in resistance to other herbicides that are active at the same site of action. The reason for this is there can be many different binding sites at a particular site of action (e.g. an enzyme) and those binding sites can be very herbicide specific. Therefore, several different herbicides may bind to the same enzyme but at different sites on the enzyme (Figure 6). As a result, it is not possible to predict herbicide cross resistance; however, the greatest potential for herbicide cross resistance exists among herbicides of the same family and having the same site of action.
To illustrate cross resistance, both the imidazolinone (e.g. Pursuit and Scepter) and sulfonylurea (e.g. Classic) herbicide families are ALS enzyme inhibitors (Table 2). However, imidazolinone resistant (IR) corn hybrids are resistant to imidazolinone herbicides and are cross resistant to the sulfonylurea herbicides. The imidazolinone tolerant (IT) corn hybrids are resistant to Pursuit and soil-applied Scepter but are not cross resistant to sulfonylurea herbicides.
Herbicide resistance via altered metabolism
Regardless of whether a herbicide is active at single or multiple site(s) of action, it is often metabolized by crops or weeds before reaching the primary site(s) of action. Therefore, the rate at which a herbicide is metabolized plays a key role in determining crop injury and weed control. The genetic regulation of a metabolic process will influence the likelihood of developing herbicide resistance due to altered metabolism. For example, a change in only one gene has altered the rate of metabolism of atrazine in some biotypes of atrazine-resistant velvetleaf (Abutilon theophrasti). Most metabolic processes are thought to be controlled by multiple genes, thereby reducing the probability but not eliminating the possibility of weed biotypes that are resistant to herbicides due to enhanced metabolic capabilities or altered metabolic processes. Metabolic resistance could be especially challenging if it were to occur, because a metabolic process often affects several families of herbicides that do not share a common site of action. Regardless of the resistance mechanism, the key to prevention of herbicide resistance is to reduce the selection intensity.
Weed characteristics that favor resistance
Weeds, by their nature, have a diverse genetic background that gives them the ability to adapt to many different environments. For example, the repeated mowing of a lawn selects for low growing plants that avoid or are not affected by repeated cutting. Therefore, it should not be surprising that weeds can adapt to certain herbicide programs. Weeds with a diverse genetic background may have a resistant biotype that has a 1 in 1 million chance of occurring within a weed population. Although these odds sound remote, a 1 in 1 million chance of occurrence can translate into a high probability of selecting for a herbicide resistant weed biotype unless proper methods to reduce selection intensity are used.
As a herbicide resistant biotype becomes more predominant in the weed population, two factors increase in importance:
- Weed reproductive capability.
- Weed seed dispersal mechanisms.
The greater the reproductive success of the resistant biotype, the greater its potential to spread and become a dominant part of the population. Due to the extended viability of most weed seeds, once established, a herbicide resistant biotype will be difficult to eliminate from the population, even if extensive remedial weed control measures are used. Weeds such as kochia can tumble for miles spreading seed onto previously uninfested land. As a result of the diverse seed dispersal mechanisms of weeds, it is apparent that a farm manager must always use good herbicide resistance management strategies to prevent resistant biotypes from developing on the land and prohibit the establishment of resistant weed biotypes spreading from adjacent lands or from custom harvesting equipment and other machinery.
Diagnosing herbicide resistant weeds
Before assuming that any weeds surviving a herbicide application are resistant, rule out other factors that might have affected herbicide performance. Several factors would be misapplication, unfavorable weather conditions, improper timing of herbicide application, and weed flushes after application of a non-residual herbicide. If resistance appears to be a likely possibility, check for the following:
- Are other weeds listed on the product label controlled satisfactorily? Chances are only one weed species will show herbicide resistance in any given field situation. Therefore, if several normally susceptible weed species are present, reconsider factors other than herbicide resistance as the cause of the lack of weed control.
- Did the same herbicide or herbicide with the same site of action fail in the same area of the field in the previous year?
- Do field histories indicate extensive use of the same herbicide or herbicide site of action year after year?
If one or more of these three situations apply, it is possible that the weeds are resistant to the herbicide. If resistance is suspected, control the weeds with a labeled herbicide having another site of action or use appropriate nonchemical weed control methods to prevent the weeds from going to seed. Next, contact your local crop consultant or extension agent, state weed specialist, and the appropriate chemical company to develop a comprehensive weed control program to manage the problem.
Herbicide resistant crops
Recent research efforts have been directed at breeding herbicide resistance into crops. For minor-use crops it may be more economical to breed herbicide resistance into a crop than to develop new selective herbicides for current crop varieties. For major-use crops such as corn, soybeans, and wheat, herbicide resistant crops may be useful where difficult to control weeds or environmental conditions dictate the use of specific herbicides to which the crop is normally susceptible.
The use of herbicide resistant crops could enhance the potential for selecting for herbicide resistant weeds unless careful management practices are followed. The key, once again, is selection intensity. Misuse of herbicide resistant crops could encourage the use of a single herbicide or herbicide family over several crop rotations, thereby enhancing the selection intensity for herbicide resistant weeds.
Herbicide resistant crop varieties or hybrids need to be carefully evaluated for other performance characteristics (e.g. yield) and these characteristics should be compared to all other suitable hybrids or varieties in the marketplace, whether they have herbicide resistance or not. This will ensure that crop producers are getting the best overall agronomic value for their money. It will also be very important that accurate records be kept of the exact planting location of the herbicide resistant crops to avoid herbicide misapplication.
Management strategies for avoiding and managing herbicide resistant weeds
The North Central Weed Science Society (NCWSS) Herbicide Resistance Committee has developed the following list of strategies for avoiding and managing problems with herbicide resistant weed biotypes. Keep in mind that reliance upon any one strategy is not likely to be effective. The crop producer must use the following strategies in carefully selected combinations if herbicide resistant weed problems are to be avoided or properly managed.
- Use herbicides only when necessary. Where available, herbicide applications should be based on economic thresholds. Continued development of effective economic threshold models should be helpful.
- Rotate herbicides (sites of action). Do not make more than two consecutive applications of herbicides with the same site of action to the same field unless other effective control practices are also included in the management system. Two consecutive applications could be single annual applications for two years, or two split applications in one year.
- Apply herbicides in tank-mixed, prepackaged, or sequential mixtures that include multiple sites of action. Both herbicides, however, must have substantial activity against potentially resistant weeds for this strategy to be effective. Remember that in the past, weeds that were selected for herbicide resistance often were not the primary target species. It may be expensive to apply herbicide combinations that duplicate a wide spectrum of weed control activity. Many of the more economical herbicide combinations may not be adequate. Table 10 is a cross reference list of package mixtures and their corresponding sites of action.
- Rotate crops, particularly those with different life cycles (e.g. winter annuals such as winter wheat, perennials such as alfalfa, summer annuals such as corn or soybeans). At the same time, remember not to use herbicides with the same site of action in these different crops against the same weed unless other effective control practices are also included in the management system.
- Planting new herbicide resistant crop varieties should not result in more than two consecutive applications of herbicides with the same site of action against the same weed unless other effective control practices are also included in the management system.
- Combine, where feasible, mechanical weed control practices such as rotary hoeing and cultivation with herbicide treatments.
- Include, where soil erosion potential is minimal, primary tillage as a component of the weed management program.
- Scout fields regularly and identify weeds present. Respond quickly to changes in weed populations to restrict spread of weeds that may have been selected for resistance.
- Clean tillage and harvest equipment before moving from fields infested with resistant weeds to those that are not.
- Encourage railroads, public utilities, highway departments and similar organizations that use total vegetation control programs should be encouraged to use vegetation management systems that do not lead to selection of herbicide resistant weeds. Resistant weeds from total vegetation control areas frequently spread to cropland. Chemical companies, state and federal agencies, and farm organizations can all help in this effort.
The author would like to acknowledge the members of the 1991 and 1992 North Central Weed Science Society (NCWSS) Herbicide Resistance Committees who developed the ten management strategies for avoiding and managing herbicide resistant weeds listed in this publication and extensively reviewed this publication. The members are as follows: Thomas Bauman, T. Robert Dill, Ray Forney, R. Gordon Harvey (Chair-1991), Nick Jordan, Rex Liebl, Michael Owen, Jamie Retzinger, Dave Stoltenberg, G. Chris Weed, Phil Westra, Gail Wicks, and Bill Witt. It has been my pleasure to serve as Vice-chair and Chair of this committee in 1991 and 1992, respectively, and to work with these dedicated people.
The author would also like to thank the American Cyanamid Company for the use of Figures 3 and 5, B.D. Maxwell for Figure 4, and J.J. Kells for Figure 6.
Green, M.B., H.M. LeBaron, and W.K. Moberg (Editors), 1990. Managing Resistance to Agrochemicals: From Fundamental Research to Practical Strategies. American Chemical Society, Symposium Series No. 421. 496 pp.
Gressel, J. 1992. Addressing Real Weed Science Needs with Innovations. Weed Technology. Vol 6:509-525.
Gunsolus, J.L., and W.S. Curran. 1992 (revised). Herbicide Mode of Action and Injury Symptoms CD-ROM.
Maxwell, B.D., M.L. Roush, and S.R. Radesevich. 1990. Predicting the Evolution and Dynamics of Herbicide Resistance in Weed Populations. Weed Technology. Vol. 4:2- 13.
Table 1. Cross reference list of herbicide trade names and common names classified as growth regulators
|Trade * Name||Common Name||Trade * Name||Common Name|
|Butyrac||2,4-DB||Tordon 22K **||Picloram|
|Clarity||Dicamba||2,4-D Amine, others||2,4-D Amine|
|MCPA Amine, others||MCPA Amine||2,4-D Ester, others||2,4-D Ester|
|MCPA Ester, others||MCPA Ester||2,4-DB||2,4-DB|
Table 2. Cross reference list of herbicide trade names and common names classified as amino acid synthesis (ALS synthase enzyme) inhibitors.
|Trade * Name||Common Name||Trade *Name||Common Name|
|Assert||Imazamethabenz||Harmony Extra||Tribenuron + Thifensulfuron|
Table 3. Cross reference list of herbicide trade names and common names classified as amino acid synthesis (EPSP synthase enzyme) inhibitors.
|Trade * Name||Common Name||Trade * Name||Common Name|
Table 4. Cross reference list of herbicide trade names and common names classified as lipid (Acetyl-CoA carboxylase enzyme) inhibitors.
|Trade * Name||Common Name||Trade * Name||Common Name|
|Assure II||Quizalofop||Option II||Fenoxaprop|
|Fusilade DX||Fluazifop||Poast Plus||Sethoxydim|
|Fusion||Fluazifop + Fenoxaprop||Select||Clethodim|
Table 5. Cross reference list of herbicide trade names and common names classified as seedling root (tubulin protein) inhibitors.
|Trade * Name||Common Name||Trade * Name||Common Name|
Table 6. Cross reference list of herbicide trade names and common names classified as seedling shoot inhibitors.
|Trade * Name||Common Name||Trade * Name||Common Name|
|Confidence **||Alachlor||Harness Plus **||Acetochlor + Safener|
|Cropstar **||Alachlor||Judge **||Alachlor|
|Eradicane||EPTC + Dichlormid||Ramrod||Propachlor|
|Eradicane Extra||EPTC + Dichlormid + Dietholate||Stall **||Alachlor|
|Far-Go||Triallate||Surpass **||Acetochlor + Dichlormid|
|Sutan||Butylate + Dichlormid|
Table 7. Cross reference list of herbicide trade names and common names classified as photosynthesis (D-1 quinone-binding protein) inhibitors.
|Trade * Name||Common Name||Trade * Name||Common Name|
|Buctril-Atrazine **||Bromoxynil + Atrazine||Sencor||Metribuzin|
|Extrazine II **||Cyanazine + Atrazine||Spike||Tebuthiuron|
|Laddok **||Bentazon + Atrazine||Velpar||Hexazinone|
Table 8. Cross reference list of herbicide trade names and common names classified as cell membrane disrupters.
|Trade * Name||Common Name||Trade * Name||Common Name|
|Activated by Photosystem I||Inhibit Protoporhyrinogen Oxidase|
|Gramoxone Extra **||Paraquat||Reflex||Fomesafen|
Table 9. Cross reference list of herbicide trade names and common names classified as pigment inhibitors.
|Trade * Name||Common Name||Trade * Name||Common Name|
Table 10. Cross reference list of package mixture trade names and common names and their corresponding sites of action.
|Trade * Name||Common Name||Reference Table||Trade * Name||Common Name||Reference Table|
|Bicep **||Atrazine + Metolachlor||7 + 6||Galaxy||Bentazon + Acifluorfen||7 + 8|
|Broadstrike + Dual||Flumetsulam + Metolachlor||2 + 6||Gemini||Linuron + Chlorimuron||7 + 2|
|Broadstrike + Treflan||Flumetsulam + Trifluralin||2 + 5||Harmony Extra||Tribenuron + Thifensulfuron||2 + 2|
|Bronate||Bromoxynil + MCPA||7 + 1||Laddok **||Bentazon + Atrazine||7 + 7|
|Bronco **||Alachlor + Glyphosate||6 + 3||Landmaster||Glyphosate + 2,4-D||3 + 1|
|Buckle||Triallate + Trifluralin||6 + 5||Lariat **||Alachlor + Atrazine||6 + 7|
|Buctril-Atrazine **||Bromoxynil + Atrazine||7 + 7||Lasso + Atrazine **||Alachlor + Atrazine||6 + 7|
|Bullet **||Alachlor + Atrazine||6 + 7||Lorox Plus||Linuron + Chlorimuron||7 + 2|
|Cannon **||Alachlor + Trifluralin||6 + 5||Marksman **||Dicamba + Atrazine||1 + 7|
|Canopy||Chlorimuron + Metribuzin||2 + 7||Passport||Trifluralin + Imazethapyr||5 + 2|
|Cheyenne TP **||Fenoxaprop + MCPA ester + Thifensulfuron + Tribenuron||4 + 1 + 2 +2||Preview||Metribuzin + Chlorimuron||7 + 2|
|Commence||Clomazone + Trifluralin||9 + 5||Prozine **||Pendimethalin + Atrazine||5 + 7|
|Concert||Chlorimuron + Thifensulfuron||2 + 2||Pursuit Plus||Imazethapyr + Pendimethalin||2 + 5|
|Crossbow||Triclopyr + 2,4-D ester||1 + 1||Ramrod + Atrazine **||Propachlor + Atrazine||6 + 7|
|Curtail||Clopyralid + 2,4-D amine||1 + 1||Salute||Trifluralin + Metribuzin||5 + 7|
|Curtail M||Clopyralid + MCPA ester||1 + 1||Squadron||Imazaquin + Pendimethalin||2 + 5|
|Cycle **||Metolachlor + Cyanazine||6 + 7||Storm||Acifluorfen + Bentazon||8 + 7|
|Dakota TP||Fenoxaprop + MCPA ester||4 + 1||Sutazine **||Butylate + Atrazine||6 + 7|
|Extrazine II **||Cyanazine + Atrazine||7 + 7||Synchrony STS||Chlorimuron + Thifensulfuron||2 + 2|
|Fallow Master||Glyphosate + Dicamba||3 + 1||Tiller||Fenoxaprop + 2,4-D + MCPA||4 + 1 +1|
|Finesse||Chlorsulfuron + Metsulfuron||2 +2||Tornado||Fluazifop + Fomesafen||4 + 8|
|Freedom **||Alachlor + Trifluralin||6 + 5||Tri-Scept||Imazaquin + Trifluralin||2 + 5|
|Fusion||Fluazifop + Fenoxaprop||4 + 4||Turbo||Metolachlor + Metribuzin||6 + 7|
* Reference to commercial products or trade names is made with the understanding that no discrimination is intended and no endorsement by the University of Minnesota Extension is implied.
** Restricted Use Herbicide