University of Missouri Extension

G4907, Revised May 2006

Herbicide Resistance in Weeds

Andrew Kendig
Department of Agronomy
Delta Center
Fred Fishel
Integrated Pest Management

In 1992 no known herbicide-resistant weeds existed in Missouri. In 1994 there were more than five sites. Herbicide-resistant weeds are populations that were previously controlled by a particular herbicide but are no longer controlled by a normal rate of application for that herbicide. Much time is spent arguing about terminology: Is johnsongrass resistant to atrazine? Is pigweed resistant to Assure, Bugle, Fusilade, Poast and Select? Johnsongrass always has been resistant to atrazine, and, likewise, pigweed always has been resistant to grass herbicides. Is "tolerant" a better word to describe johnsongrass's response to atrazine? Regardless of the terminology used, the problem this guide addresses is weeds that used to be controlled but are now tolerant to particular herbicides

Herbicide-resistant weeds were first discovered in the United States in the late 1960s in a pine nursery where triazine herbicides had been used repeatedly. There probably have been a few resistant weeds in Missouri over past years, but the first confirmed discovery of a problem did not occur until 1993. By 1994 Missouri had five cases of herbicide-resistant weeds.

Weed resistance is not unique. Insecticide-resistant insects, fungicide-resistant diseases and antibiotic-resistant bacteria were discovered long before herbicide-resistant weeds. These pests have two common traits: They have exceptionally large populations, and they reproduce rapidly. The reason that weeds were the last pest category to show resistance is that they reproduce (set seed) only once a year while insects reproduce several times a year. Some bacteria and fungi reproduce several times in a single hour. Exceptionally large populations also result in a wide variety of types, or genetic diversity, within the population. With most control measures (insecticides, herbicides or antibiotic drugs), small groups in the pest population (one in a million, billion, etc.) are tolerant.

Weeds typically become resistant to herbicides when the same herbicide is used repeatedly for several (4 to 10) years in a row. It often is thought that selection pressure forces the weeds to mutate and become resistant. However, biologists tell us that what most likely happens is:

Resistance makes some weeds less fit than normal weeds. However, other resistant weeds are just as vigorous as normal types. For example, triazine-resistant pigweed has a different photosynthesis metabolism, which is less efficient than that of the normal type. The "mutant" pigweed grows much slower than normal pigweed. But when atrazine is used, the normal pigweed is controlled, and the resistant pigweed thrives because of lessened competition. However, ALS-herbicide-resistant kochia grows just as fast and just as tall as normal kochia.

Look carefully for resistance

How to identify herbicide resistance: As farmers learn about herbicide resistance, an unfortunate side effect is that some herbicide failures from bad weather, weeds that are too large or improper applications are considered herbicide-resistance problems. Do not suspect herbicide resistance unless a herbicide failure fits the following traits:

Even if a control failure exhibits these traits, it is not an absolute diagnosis of herbicide resistance.

Resistance in Missouri and nearby states

Technical tidbit

It often is thought that weeds change or mutate to become resistant. Biologists, however, believe that weeds do not change at all. Instead, populations change. The resistant weeds always have been present in low populations. When a particular herbicide is used, it controls the normal-susceptible types. This makes room for the population of the resistant weeds to increase. Consequently, when growers say that their "weeds have become resistant," they really mean that the population of their resistant weeds has increased greatly and the population of their susceptible weeds has decreased.

ALS-resistant cocklebur
Several newer herbicides target the acetolactate synthase (or ALS) enzyme, which is found only in plants. A Scepter-resistant cocklebur was originally reported in Mississippi in 1993. This cocklebur also showed resistance to herbicides that are chemically related to Scepter (imidazolinone family), such as Arsenal, Cadre and Pursuit. Sulfonylurea (pronounced sulfo-neal- urea) herbicides, which also work by inhibiting ALS, were still effective against this cocklebur. At about the same time, a Missouri farmer also was failing to control cocklebur with Scepter. After the grower contacted MU, research determined that his cocklebur was cross resistant to chemicals from both the imidazolinone and the sul-fonylurea families of chemistry. It is noteworthy that this cocklebur was completely resistant to Classic, even though it had never been sprayed in the field, and was completely resistant to Broadstrike (another ALS inhibitor) before it was registered and sold.

ACCase-resistant Johnsongrass, crabgrass
The post-emergence grass herbicides (Assure, Bugle, Fusilade, Option, Poast and Select) inhibit an enzyme called acetyl coenzyme A carboxylase, or "ACCase." In 1993, Johnsongrass resistant to post-emergence grass herbicides was reported in Mississippi. In subsequent research, the Johnsongrass tolerated normal-use rates of Assure, Fusilade and Poast. Labeled rates of Select were still killing the grass, but detailed studies showed that the grass was more resistant to low Select rates than was normal Johnsongrass. Crabgrass with similar resistance has been found in the northern United States. At the time of this publication, resistant Johnsongrass also has been found in Arkansas, but not in Missouri.

Glean-resistant prickly lettuce/kochia
The first cases of ALS-resistant weeds involved prickly lettuce, kochia and the wheat herbicide Glean. Glean made headlines as the first of the "ounce-per-acre" herbicides. However, after four to five years of use, growers began to observe prickly lettuce and kochia escaping Glean treatments. After four additional years, Glean-resistant weeds were widespread across the western United States.

Londax-resistant weeds — California rice. The rice herbicide Londax is another sulfonylurea, ALS-inhibiting herbicide. Approximately four years after its labeling, a resistant arrowhead was found. Recent estimates indicate that one in three California rice fields have at least one Londax-resistant weed.

MSMA/DSMA-resistant cocklebur
DSMA and MSMA are closely-related, arsenical herbicides that are commonly used in cotton and turfgrass. DSMA and MSMA are used primarily for grass control although they also provide a significant amount of broadleaf suppression. Although they often are considered "grass herbicides," they have good activity on cocklebur and are a particularly economical option for its control. Resistant cocklebur is difficult to identify in a field setting because the resistant types are injured by DSMA and MSMA just as the normal types of cocklebur are injured. The resistant types recover, however, and the susceptible types die. Resistant cocklebur has been discovered in cotton fields in Arkansas, Louisiana, Mississippi and Tennessee. At the time this guide was prepared, a preliminary field test indicated that arsenical-resistant cocklebur may exist in Missouri.

Propanil-resistant barnyardgrass
In the mid-South the most common rice weed is barnyardgrass, and the main herbicide for its control is propanil (Stam, others). In the late 1980s, growers in northeast Arkansas began reporting poor barnyardgrass control. In this area some fields had been in rice for upwards of 20 consecutive years. When barnyardgrass from these fields was tested, it tolerated as much as 20 times the normal use rate of propanil. A preliminary survey of farmers determined that a simple crop rotation greatly reduced the probability of resistance.

Dinitroaniline- (or DNA-) resistant goosegrass
Goosegrass is a common summer annual grass and is ranked among the 10 worst weeds in the United States. In the early 1980s, resistance was suspected in a South Carolina cotton field that had received Treflan applications for more than 10 consecutive years. Subsequent studies determined that the goosegrass was completely resistant to Balan, Basalin, Prowl, Sonolan, Surflan and Pursuit. These herbicides are all in the Dinitroaniline family of chemistry (or "DNAs"). It is now believed that DNA-resistant goosegrass can be found throughout the mid-South.

Triazine-resistant weeds
A number of Triazine-resistant weeds have been found across the United States. The first discovery was reported in early 1970 with groundsel. Within a few years, triazine resistance was reported with pigweed and lambsquarters. Now more than 50 species of triazine-resistant weeds exist. A triazine-resistant waterhemp (a member of the pigweed family) was discovered in Missouri in 1994.

Cross resistance

More than 100 different herbicides are on the market today. But many of these work in exactly the same way or, in other words, have the same mode of action. Fewer than 20 plant-growth mechanisms are affected by current herbicides. ALS-herbicide resistance is a good example of the problem of cross resistance. ALS herbicides exist for many crops. The Missouri-ALS-resistant cocklebur came from a field receiving only Scepter, but the cocklebur is cross resistant to Beacon, Broadstrike and Classic. It is even resistant to a number of experimental herbicides that have yet to be labeled.

How to manage herbicide resistance

Management of resistance, once it occurs, is simple: The grower must switch to an alternative method of control (be it an alternative herbicide or a cultural control method, such as cultivation). Some private-industry personnel have recommended that the grower continue to use the same herbicide in combination with another herbicide with a different mode of action (for example, Scepter followed by Basagran where resistant cocklebur exist). Their reasoning is that the Scepter will provide control of many other weeds and that Basagran will control cocklebur. Although little data supports it, weed scientists urge growers with resistance problems to avoid particular herbicides if they have resistant weeds and to switch to herbicides with a different action mechanism. In theory, this allows the weed populations some chance to shift back to predominantly susceptible types.

Although resistance management appears simple, it is better to prevent resistance from becoming a problem. Herbicide cross resistance renders many herbicides useless at once. With the example of the Scepter-resistant Missouri cocklebur, the use of Accent, Beacon, Canopy, Classic, Permit, Pursuit or Staple could be affected. And no one can predict if or when these fields will change back to an ALS-susceptible population.

If a field is infested with herbicide-cross-resistant weeds, the farmer may lose yield because a competitive weed isn't controlled. Growers also may have higher costs if they lose the use of several economical herbicides. The use of future herbicides may even be affected. As an example, the Missouri cocklebur was resistant to Broadstrike before it was available and is already resistant to a useful cotton herbicide that, at the time this guide was written, was still not registered for use.

If you suspect a resistance problem:

How to prevent herbicide resistance

Table 1 lists factors that promote resistance. Avoiding these factors is a good start to preventing resistance. Although Table 1 lists ALS herbicides as being prone to resistance, farmers still should use them when appropriate. However, they should avoid using ALS herbicides repeatedly without rotation

Table 1
When and why is herbicide resistance most likely?

Factor Explanation of effect
Lack of rotation. The same herbicide or environment year after year results in continual selection pressure, which kills susceptible populations while allowing resistant populations to grow.
A weed that is hypersensitive to a particular herbicide. The selection pressure is high. Very few of the susceptible types survive. Resistant types thrive and have no competition from susceptible types.
Herbicides with long residual periods. Again, high-selection pressure, continual control of susceptible types and continual release of resistant types.
Newer herbicide with a highly specific mode of action. The herbicide affects only one specific site in the plant; consequently, a resistant plant has to be different only in that one specific site. Older herbicides usually affect several sites, and thus, it is more unlikely for a plant to have resistance at all of the sites of action.
ALS-inhibiting herbicide. ALS-inhibiting herbicides often fit the previous four qualifications, and, in addition, resistant types of plants apparently aren't rare. A recurring tendency exists for ALS-resistant weeds to be discovered only four to five years after the introduction of an ALS-inhibiting herbicide.
Any herbicide or weed. Herbicide resistance does not necessarily occur when and where we expect it. It was thought that the extensive use of Accent, Beacon and Pursuit on shattercane would likely result in ALS-resistant shattercane. But a project specifically designed to investigate the probability of shattercane resistance instead discovered an ALS-resistant common waterhemp. This indicates that the overuse of any herbicide or mode of action could result in resistant weeds.

Table 2 can be used to cross-reference herbicides for their mechanism of action. Use this list to determine if you are using a resistance-prone herbicide program; that is, using same mode of action. Remember, this is primarily a problem when the herbicides target the same weed species. It's fine to use an ALS-inhibiting herbicide, such as Scepter, for cocklebur in Treflan-treated soybeans and then use another ALS-inhibiting herbicide, such as Accent, for Johnsongrass and shattercane control in atrazine-treated corn. The cocklebur are controlled by an ALS herbicide (Scepter) one year and by a photosynthetic inhibitor (Atrazine) the next year. Grasses are being controlled by a mitotic inhibitor (Treflan) one year and an ALS-inhibiting herbicide (Accent) the other year.

However, avoid using a program such as Pursuit (an ALS-inhibiting herbicide) for shattercane control in soybeans followed by Accent or Beacon (also ALS-inhibiting herbicides) for shattercane in corn.

Other recommendations for preventing resistance include the following practices:

Cultivation
There are no known cases of cultivator-resistant weeds. No-till farmers must exercise extra care in herbicide rotation because they rely more on herbicides and less on cultivation.

Tank mixes, package mixes and sequential applications
Combinations of herbicides with different mechanisms of action, which control on the same species, also help prevent resistance. However, this strategy may only delay herbicide resistance rather than prevent it. In addition, the selection of the wrong combinations (sequentials or mixtures) of herbicides (where only one of the herbicides works on a particular weed) can cause resistant populations to build up just as rapidly as overusing a single herbicide.

Avoiding repeat or sequential applications of the same herbicide (or active ingredient)
For example Squadron followed by Scepter or Canopy followed by Classic results in two applications of the same active ingredient in one year.

Technical tidbit

More often than not, a lack of crop and herbicide rotation causes the species of weeds to change rather than the build-up of resistant varieties of weeds. For example, if you use nothing but Treflan for several years in a row, cocklebur is more likely to increase than is Treflan-resistant goosegrass. But, if you think about it, it is actually the same mechanism occurring — selection pressure causes susceptible types to decline while resistant types increase. The only difference is that the species of weeds shift in the typical case versus different types of the same weed species shifting in resistance cases.

Table 2
Herbicide products, active ingredients, chemical family and mechanism of action

Product Active ingredient Chemical family Mechanism of action
AAtrex (others) atrazine triazine photosynthetic inhibitor
Accent nicosulfuron sulfonyl-urea ALS inhibitor
Arrosolo molinate (Ordram)
propanil (Stam)
thiocarbamate
chloroacetamide
growth inhibitor
photosynthetic inhibitor
Assure quizalofop aryl-oxy-phenoxy ACCase inhibitor
Banvel dicamba benzoic hormone initiator
Basagran bentazon no family photosynthetic inhibitor
Battalion halosulfuron sulfonyl-urea ALS inhibitor
Beacon primisulfuron sulfonyl-urea ALS inhibitor
Benefit dimethenamid (Frontier)
pendimethalin (Prowl)
chloroacetamide
dinitroaniline
growth inhibitor
mitotic inhibitor
Bicep atrazine
metolachlor (Dual)
triazine
chloroacetamide
photosynthetic inhibitor
growth inhibitor
Bladex cyanazine triazine photosynthetic inhibitor
Blazer aciflourfen diphenyl ether PPO membrane disrupter
Bolero thiobencarb thiocarbamate growth inhibitor
Broadstrike (several package mixes) flumetsulam similar to sulfonyl-urea ALS inhibitor
Bronco glyphosate (Roundup)
alachlor (Lasso)
amino acid analog
chloroacetamide
EPSP synthase inhibitor
growth inhibitor
Bronate bromoxynil (Buctril) nitrile photosynthetic inhibitor
Buctril bromoxynil nitrile photosynthetic inhibitor
Bugle fenoxaprop aryl-oxy-phenoxy ACCase inhibitor
Bullet (or Lariat) atrazine
alachlor (Lasso)
triazine
chloroacetamide
photosynthetic inhibitor
growth inhibitor
Butyrac 2,4-DB phenoxy hormone imitator
Canopy (or Preview) chlorimuron (Classic)
metribuzin (Lexone, Sencor)
sulfonyl-urea
triazine
ALS-inhibitor
photosynthetic inhibitor
Caparol prometryn no family photosynthetic inhibitor
Clarity (or Banvel) dicamba benzoic hormone imitator
Classic chlorimuron sulfonyl-urea ALS inhibitor
Conclude B (Storm) bentazon (Basagran)
aciflourfen (Blazer)
no family
diphenyl ether
photosynthetic inhibitor
PPO membrane disrupter
Conclude G (Poast) sethoxydim
 
cyclohexendione
 
ACCase inhibitor
Cobra lactofen diphenyl ether PPO membrane disrupter
Command clomazone no family carotenoid-inhibiting bleacher
Commence clomazone (Command)
trifluralin (Treflan)
no family
dinitroaniline
carotenoid-inhibiting bleacher
mitotic inhibitor
Concert (or Synchrony) chlorimuron (Classic)
thifensulfuron (Pinnacle)
sulfonyl-urea
sulfonyl-urea
ALS inhibitor
ALS inhibitor
Contour imazethapyr (Pursuit)
atrazine
imidazolinone
triazine
ALS inhibitor
photosynthetic inhibitor
Cotoran fluometuron urea photosynthetic inhibitor
Cotton Pro prometryn no family photosynthetic inhibitor
Detail dimethenamid (Frontier)
imazaquin (Scepter)
chloroacetamide
imidazolinone
growth inhibitor
ALS inhibitor
Direx (or Karmex) diuron urea photosynthetic inhibitor
Dual metolachlor chloroacetamide growth inhibitor
Eradicane/Epta EPTC thiocarbamate growth inhibitor
Exceed prosulfuron (Peak)
primisulfuron (Beacon)
sulfonyl-urea
sulfonyl-urea
ALS inhibitor
ALS inhibitor
Extrazine atrazine
cyanazine (Bladex)
triazine
triazine
photosynthetic inhibitor
photosynthetic inhibitor
Facet quinclorac no family hormone imitator
Flexstar (or Reflex) fomesafen diphenyl ether PPO membrane disrupter
Freedom alachlor (Lasso)
trifluralin (Treflan)
chloroacetamide
dinitroaniline
growth inhibitor
mitotic inhibitor
Frontier dimethenamid chloroacetamide growth inhibitor
Fusilade fluazifop aryl-oxy-phenoxy ACCase inhibitor
Fusion fluazifop (Fusilade)
fenoxaprop (Whip, Bugle)
aryl-oxy-phenoxy
aryl-oxy-phenoxy
ACCase inhibitor
ACCase inhibitor
Galaxy bentazon (Basagran)
aciflourfen (Blazer)
no family
diphenyl ether
photosynthetic inhibitor
PPO membrane disrupter
Gemini linuron (Lorox)
chlorimuron (Classic)
urea
sulfonyl-urea
photosynthetic inhibitor
ALS inhibitor
Genate butylate thiocarbamate growth inhibitor
Goal oxyflourfen diphenyl ether PPO membrane disrupter
Gramoxone Extra paraquat bipyridilium Ps membrane disrupter
Guardsman atrazine
dimethenamid (Frontier)
triazine
chloroacetamide
photosynthetic inhibitor
growth inhibitor
Harmony extra thifensulfuron (Harmony)
tribenuron (Express)
sulfonyl-urea
sulfonyl-urea
ALS inhibitor
ALS inhibitor
Harness (or Surpass) acetochlor chloroacetamide growth inhibitor
Karmex diuron urea photosynthetic inhibitor
Laddok bentazon (Basagran)
atrazine
no family
triazine
photosynthetic inhibitor
photosynthetic inhibitor
Landmaster glyphosate (Roundup)
2,4-D
amino acid
phenoxy
EPSP inhibitor
hormone imitator
Lasso alachlor chloroacetamide growth inhibitor
Lariat alachlor (Lasso)
atrazine
chloroacetamide
triazine
growth inhibitor
photosynthetic inhibitor
Lexone metribuzin (same as Sencor) triazine photosynthetic inhibitor
Linex linuron (Lorox) urea photosynthetic inhibitor
Londax bensulfuron sulfonyl-urea ALS inhibitor
Lorox linuron urea photosynthetic inhibitor
Lorox plus linuron
chlorimuron (Classic)
urea
sulfonyl-urea
photosynthetic inhibitor
ALS inhibitor
Marksman dicamba (Banvel)
atrazine
benzoic acid
triazine
hormone imitator
photosynthetic inhibitor
MCPA (many brands) MCPA phenoxy hormone imitator
Meturon fluometuron (Cotoran) urea photosynthetic inhibitor
Micro-Tech alachlor (Lasso) chloroacetamide growth inhibitor
Option II fenoxaprop (Whip, Bugle) aryl-oxy-phenoxy ACCase inhibitor
Ordram molinate thiocarbamate growth inhibitor
Passport imazethapyr (Pursuit)
trifluralin (Treflan)
imidazolinone
dinitroaniline
ALS inhibitor
mitotic inhibitor
Peak prosulfuron sulfonyl-urea ALS inhibitor
Pentagon (or Prowl) pendimethalin dinitroaniline mitotic inhibitor
Permit halosulfuron sulfonyl-urea ALS inhibitor
Pinnacle thifensulfuron sulfonyl-urea ALS inhibitor
Poast sethoxydim cyclohexendione ACCase inhibitor
Preview metribuzin (Lexone, Sencor)
chlorimuron
triazine
sulfonyl-urea
photosynthetic inhibitor
ALS inhibitor
Princep simazine triazine photosynthetic inhibitor
Prowl pendimethalin dinitroaniline mitotic inhibitor
Pursuit imazethapyr imidazolinone ALS inhibitor
Pursuit Plus imazethapyr (Pursuit)
pendimethalin (Prowl)
imidazolinone
dinitroaniline
ALS inhibitor
mitotic inhibitor
Ramrod propachlor chloroacetamide growth inhibitor
Ramrod Atrazine propachlor (Ramrod)
atrazine
chloroacetamide
triazine
growth inhibitor
photosynthetic inhibitor
Reflex fomesafen diphenyl ether PPO membrane disrupter
Rescue naptalam (Alanap)
2,4-DB (Butyrac)
chloroacetamides
phenoxy
growth inhibitor
hormone imitator
Resolve imazethapyr (Pursuit)
dicamba (Banvel)
imidazolinone
benzoic
ALS inhibitor
hormone imitator
Resource flumiclorac no family PPO membrane disrupter
Rezult B (or Basagran) bentazon no family photosynthetic inhibitor
Rezult G (or Poast Plus) sethoxydim cyclohexendiones ACCase inhibitor
Roundup glyphosate amino acid EPSP inhibitor
Salute metribuzin (Lexone, Sencor)
trifluralin (Treflan)
triazine
dinitroaniline
photosynthetic inhibitor
mitotic inhibitor
Scepter imazaquin imidazolinone ALS inhibitor
Scepter OT imazaquin (Scepter)
acifluorfen (Blazer)
imidazolinone
diphenyl ether
ALS inhibitor
PPO membrane disrupter
Select clethodim cyclohexendione ACCase inhibitor
Sencor metribuzin (same as Lexone) triazine photosynthetic inhibitor
Sonolan ethalfluralin dinitroaniline mitotic inhibitor
Squadron imazaquin (Scepter)
pendimethalin (Prowl)
imidazolinone
dinitroaniline
ALS inhibitor
mitotic inhibitor
Stam propanil chloroacetamide photosynthetic inhibitor
Staple pyrithiobac similar to sulfonyl-urea ALS inhibitor
Storm bentazon (Basagran)
aciflourfen (Blazer)
no family
diphenyl ether
photosynthetic inhibitor
PPO membrane disrupter
Surpass (or Harness) acetochlor chloroacetamide growth inhibitor
Surpass 100 atrazine
acetochlor (Harness)
triazine
chloroacetamide
photosynthetic inhibitor
growth inhibitor
Sutan butylate thiocarbamate growth inhibitor
Sutazine butylate (Sutan)
atrazine
thiocarbamate
triazine
growth inhibitor
photosynthetic inhibitor
Synchrony chlorimuron (Classic)
thifensulfuron (Pinnacle)
sulfonyl-urea
sulfonyl-urea
ALS inhibitor
ALS inhibitor
Topnotch (or Surpass) acetochlor chloroacetamide growth inhibitor
Tornado/Typhoon fluazifop (Fusilade)
fomesafen (Reflex)
aryl-oxy-phenoxy
diphenyl ether
ACCase inhibitor
PPO membrane disrupter
Tough pyridate no family photosynthetic inhibitor
Treflan trifluralin dinitroaniline mitotic inhibitor
Trific trifluralin (Treflan) dinitroaniline mitotic inhibitor
Trilin trifluralin (Treflan) dinitroaniline mitotic inhibitor
TriScept imazaquin (Scepter) imidazolinone ALS inhibitor
Turbo metribuzin (Lexone, Sencor)
metolachlor (Dual)
triazine
chloracetamide
photosynthetic inhibitor
growth inhibitor
Vernam vernolate thiocarbamate growth inhibitor
Whip fenoxaprop (Bugle) aryl-oxy-phenoxy ACCase inhibitor
Zorial norflurzon no family carotenoid-inhibiting bleacher
2,4-D 2,4-D phenoxy hormone imitator

Identifying herbicides with the same mode of action

Because of the great variety of trade names and package mixes of herbicides, it is difficult for growers to keep track of which modes of action they use. Some identical active ingredients actually have multiple product names. Some package mixes deter resistance while others do not. Use Table 2 to identify herbicides that have the same mechanism of action. However some traits may be useful for identification of a herbicide's mechanism of action without having to refer to a large table:

ALS-inhibiting herbicides include many of those used at extremely low (ounce per acre) rates. This trait correctly identifies herbicides such as Accent, Beacon, Classic, Pursuit and Scepter. The "ounce per acre" feature is lost with package mixes such as Squadron, TriScept and Broadstrike plus Dual. Another trait of ALS-inhibiting herbicides is that they act relatively slowly, stunting weeds first followed by a gradual death of the weeds.

Post-emergence grass herbicides (Assure, Bugle, Fusilade, Option, Poast, Select and Whip) have the same mechanism of action. They inhibit the ACCase enzyme. At this time, these are the only herbicides that provide post-emergence grass control with no broadleaf activity. Identifying a herbicide from this group is not difficult.

Photosynthetic inhibitors (Atrazine, Bladex, Cotoran, Lexone, Lorox, Sencor and others) include triazine, urea and uracil types of herbicide chemistry as well as some miscellaneous herbicides, such as Basagran and Stam. With some notable exceptions, these tend to be pre-emergence herbicides that control broadleaf weeds. They allow weeds to germinate and emerge, but a fairly rapid burn starts at the edge of the leaves and moves inward. Large-seeded weeds may continue to grow as the "burn" follows the growing point up the plant. All photosynthetic inhibitors do not affect the same site of action in the plant; consequently, complete cross resistance is not likely.

Dinitroanilines (Prowl, Treflan and others) are almost always yellow or orange. They usually are (but not always) pre-plant incorporated herbicides that control annual grasses and small-seeded broadleaves.

Diphenyl ethers (Blazer, Cobra, Goal and Reflex) are almost exclusively post-emergence soybean herbicides. They cause a rapid bronze-colored burn on weeds and soybeans, but soybeans recover.

Technical tidbit

Why are crops resistant? Why are weeds resistant? Most herbicides are selective. They control weeds but have little effect on the crop. The usual reason that a crop tolerates herbicides is that it "digests" or metabolizes the herbicide into non-poisonous compounds before they can kill the plant. Weeds cannot metabolize the herbicide, so the herbicide remains in its original form and kills the weeds. Although it makes sense that resistant weeds are metabolizing and deactivating the herbicide, what happens in most cases is that the actual site of action within the weed is "immune" to the herbicide. For example, with the ALS-resistant cocklebur in Missouri, it is possible to apply a high-enough rate of Classic to injure soybeans, although it will have no effect on the cocklebur. This is because the high rate overloads the soybeans' ability to metabolize the herbicide, and there is enough unmetabolized herbicide to affect the ALS enzyme. In the cocklebur, none of the Classic is metabolized, but the ALS enzyme is "immune" to the Classic.

Exceptions to this rule exist. Some resistant weeds can metabolize the herbicide to nontoxic chemicals instead of having a modified binding site. Sometimes the crop has a modified, "immune" herbicide binding site. A unique type of cross resistance has been found in Australia, where certain ryegrass types have the ability to metabolize and deactivate a wide variety of herbicides. This is the worst case of cross resistance because rotating to a different mechanism of action may have no effect.

Conclusion

Herbicide resistance is a complicated subject. Many weed scientists warn of hidden dangers in rotating modern herbicides. Because so many modern herbicides have the same mechanism of action, a grower could rotate crops and herbicides but still wind up with a resistance problem. The mode of action may not change even when crops and chemicals are rotated. But so far, the resistance cases in Missouri have come about from the same crop and same herbicide being used year after year
Growers should keep the hidden danger of modern herbicides in the back of their minds, but the major problem in Missouri has been the violation of one of the simplest rules of good farming — rotation.

MU does not warrant herbicide performance and regrets any errors or omissions in this publication. Trade names may be used to help audiences recognize commonly used materials. The use of a trade name does not constitute recommendation of one product over other products of a similar nature.

G4907, reviewed May 1996

G4907 Herbicide Resistance in Weeds | University of Missouri Extension

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