Cooperative
Extension
Service


University of Illinois
at
Urbana-Champaign


No. 3/April 11, 1997

Weed Resistance to Herbicides--A Growing Concern

The development of herbicide-resistant weed biotypes continues to be a major concern among weed scientists. A simple definition of resistance could be that weeds are no longer controlled by previously effective herbicides. Instances of weed resistance continues to increase, and Illinois has not been immune to this problem. Some persons may not be overly concerned about weed resistance, but an attitude of "this could never happen to me" may only serve to expedite the problem.

Why be concerned about the occurrence of weed resistance? The reasons for concern probably vary depending upon one's position (producer, agrichemical retailer, crop consultant, etc.), but practically all reasons can find common economic grounds. If previously controlled weed species are no longer controlled by a particular herbicide, the return on the herbicide investment is greatly reduced. Agrichemical retailers and crop consultants may find themselves the recipients of producer frustration and anger should the problem develop in one of their customer's fields. This anger may lead to a lost account for the retailer. Weed resistance may dramatically reduce the effectiveness of a particular family of herbicide chemistry, thus reducing the useful life of these herbicides and adversely effecting the industry as a whole.

Before entering into a discussion of how weed resistance develops, we should first define some terms often encountered when discussing how herbicides work.

Herbicide mode of action may be defined as the metabolic or physiological process within the plant that is impaired or inhibited by the herbicide. Put into simpler terms, mode of action is how the herbicide controls the plant. Mode of action is distinctly different from herbicide site of action, which is the physical location within the plant where the herbicide acts. Mode of action is a "how," whereas site of action is a "where." A herbicide must successfully bind to its site of action within the plant before it can exert its mode of action. Are these differences in terminology really important when discussing weed resistance? In a word, "yes."

For a herbicide to work effectively, several events must successfully occur:

1. To inhibit plant growth, the herbicide must reach its site of action within the plant. For example, if rainfall occurs within minutes of applying a postemergence herbicide that has no soil activity, effective weed control most likely will not be realized because the herbicide is removed from the leaf surface by the rainfall, preventing it from reaching its site of action.

2. The degree of inhibition achieved by the herbicide depends upon the concentration of the active herbicide at its site of action. Application of a postemergence, translocated herbicide during periods of cool temperatures often results in poor weed control. Plants, in general, do not translocate materials (including herbicides) as rapidly or as extensively during cool periods as they do during warm periods. A translocated herbicide may be capable of reaching its site of action under cool conditions, but not in sufficient quantities to inhibit plant growth. A situation similar to this scenario often occurs during the spring when many burndown herbicides are applied to no-till fields during periods of cool (especially nighttime) temperatures.

3. The herbicide must remain bound to its site of action long enough for the inhibition of the particular plant process to be lethal to the plant. Many selective herbicides are selective to a particular crop because the crop is able to metabolize (break down) the herbicide to an "inactive" form faster than the weeds can.

What is the significance of these principles with respect to weed resistance? Many causes of poor weed control as well as weed resistance can be explained because one or more of these principles was not satisfied.

The key to avoiding the problem of weed resistance is to understand where the resistant weeds come from. Evidence indicates that herbicide-resistant weeds are naturally occurring biotypes that exist in very small numbers within the population of a particular weed species. Plants that possess certain traits or characteristics not common to the entire species are referred to as biotypes. When a particular herbicide effectively controls the majority of susceptible members of a species, only those plants that possess a resistance trait can survive and produce seed for future generations. This theory is often referred to as natural selection or survival of the fittest. Biological organisms (people, plants, animals, etc.) exhibit a wide range of diversity. The plants in a population that possess characteristics enabling them to survive under a wide range of environmental and other adverse conditions (such as herbicide applications) will be able to produce seed that maintains these survival characteristics. Plants less adapted generally do not survive, and hence only the fittest plants reproduce.

What, then, is meant by the term "selection pressure" in regards to herbicide-resistant weeds? Herbicides are used to control a wide spectrum of weeds. By controlling susceptible members of a weed population, we are essentially using herbicides as agents to select for biotypes that are naturally resistant to the herbicide. These resistant biotypes are better adapted to survive in the environment created by controlling susceptible members of the population. The seed produced by the resistant biotypes ensures that the resistance trait will carry into future generations. If the same or a similar herbicide is used repeatedly (year after year or several times during the growing season), the resistant biotypes continue to thrive, eventually outnumbering the normal (susceptible) population. In other words, relying on the same herbicide for weed control creates a selection pressure that favors the development of herbicide-resistant weeds.

In Illinois, there are confirmed cases of triazine-resistant biotypes of common lambsquarters, kochia, and smooth pigweed (see Table 1 at the end of this document for a list of triazine herbicides). We also have identified biotypes of waterhemp demonstrating resistance to herbicides that inhibit the acetolactate synthase (ALS) enzyme (Table 2 at the end of this document). These herbicides are widely utilized for weed control in corn and soybean production systems. Because so many acres are treated with a herbicide having this mode of action, weed biotypes' developing resistance to this herbicide family could pose a significant problem to corn and soybean producers. Effectiveness of one or more of these herbicides could be decreased significantly.

Are all ALS herbicides the same? The imidazolinones, sulfonylureas, and sulfonamides all inhibit the ALS enzyme. These names (imidazolinone, sulfonylurea, sulfonamide) designate specific herbicide families based upon similar chemical structures. Numerous studies have shown that this is the common site of action for all these inhibitors. The specific binding site of a particular ALS-inhibiting herbicide on the enzyme may, however, be slightly different among the various inhibitors. Refer to Figure 4 for clarification of the following discussion.

Figure 4.

Within an ALS-inhibitor family, there is generally a large degree of overlap at the binding site of the enzyme. For example, the imidazolinones share a large degree of overlap, the sulfonylureas share a large degree of overlap, etc. That is not to say, however, that inhibitors within a family share a completely overlapping binding domain. The degree of overlap in binding domain between inhibitor families (imidazolinones vs. sulfonylureas for example) tends to be less than that for inhibitors within a family (two sulfonylureas, for example). This has strong implications for the potential of cross-resistance in weed biotypes. Cross-resistance may be defined as resistance to a herbicide that the plant has never been previously exposed to but which has a mode of action similar to the original herbicide that the resistant biotype was selected with. For example, if an ALS-resistant pigweed biotype was selected for with ALS-inhibitor A, it may or may not be cross-resistant to a different ALS-inhibitor. It is generally agreed that it is impossible to predict if an ALS-resistant biotype will be cross-resistant to a different ALS inhibitor.

For example, a change in the ALS enzyme at position A (Figure 4) will most likely diminish the effectiveness of an imidazolinone herbicide. A sulfonylurea herbicide will remain effective because this biotype has a change in the binding domain not common to sulfonylurea herbicides. If the change occurs at position B, the effectiveness of a sul˙fonylurea herbicide will be diminished, while an imidazolinone herbicide will remain effective. If, however, the resistant biotype has a change at position C, the effectiveness of both inhibitor families will be diminished because this change occurs at a portion of the binding domain common to both families. It becomes clear that because the location of the change in the ALS enzyme can vary, coupled with the fact that not all ALS herbicides share the same binding domain on the enzyme, being able to predict cross-resistance patterns is impossible. Theoretically, more than one resistant biotype could be present in a particular field, further complicating matters. We present these points because there is such an extremely wide variety of ALS inhibitors currently on the market, with others soon to follow.

We are aware that many claims by manufacturers of ALS herbicides are being made as sales points regarding how "different" their respective ALS herbicide is from all others on the market. "This herbicide is an ALS inhibitor, but it is so different from the others that you need not worry about developing resistant weeds if you have used a different ALS herbicide in the past." Statements such as this probably will do more to enhance further the development of ALS-resistant weeds than to prevent their spread. As was stated and illustrated previously, it is very difficult, if not impossible, to predict patterns of cross-resistance to ALS herbicides.

The best solution for the problem of weed resistance is to prevent their development. The following list of management strategies should be considered to deter the development of herbicide-resistant weeds. In all situations, incorporate as many of these management strategies as possible.

1. Scout fields on a regular basis throughout the growing season to identify resistant weeds. Respond quickly to changes in the weed population to restrict the spread of plants that may have developed resistance.

2. Rotate herbicides with different modes of action. Do not make more than two consecutive applications of herbicides with the same mode of action against the same weed unless other effective control practices are included in the management system. Consecutive applications can be single applications in 2 years or two split-applications in one year. Respraying a field with the same ALS herbicide that was previously applied is not recommended.

3. Apply herbicides in tank-mixed, prepackaged, or sequential mixtures that include multiple modes of action. Both herbicides in the mixture must have substantial activity against potentially resistant weeds, as well as similar persistence, if they possess soil activity. For example, if one is concerned about potentially ALS-resistant pigweed, a tank mixture of Basagran with an ALS inhibitor would be a poor choice because Basagran has very little activity on pigweed. A couple of guidelines may help with tank-mix or premix selection: (a) when applied alone at the rate that will be used in the tank-mixture, does the tank-mix or premix partner control the weed species that I am concerned may develop resistance?; and (b) if I apply the tank-mix or premix partner alone at the rate that will be used in the tank-mix, will it have similar residual activity to the other component?

4. As new herbicide-tolerant/-resistant crops become available, their use should still not result in more than two consecutive applications of herbicides with the same mode of action against the same weed species unless other effective practices are included in the management system.

5. Combine mechanical control practices such as rotary hoeing and cultivation with herbicide treatments whenever possible.

6. Clean tillage and harvest equipment before moving from fields infested with resistant weeds to those fields that are not infested. This approach may not be practical, but it can help prevent the spread of resistant weed seed that is present in soil which adheres to the equipment.

Several criteria may be used to correctly diagnose a herbicide-resistant weed problem:

1. All other causes of herbicide failure have been eliminated. This requires that the three principles of herbicide action described earlier have all been satisfied.

2. Other weeds on the herbicide label (other than the one in question) were controlled effectively.

3. The field has a history of continuous use of the same herbicide or herbicides with the same mode of action.

4. The weed species that now demonstrates potential resistance was controlled effectively in the past by the herbicide.

For additional information concerning weed resistance to herbicides, consult chapter 21 of the 1997 Illinois Agricultural Pest Management Handbook.

Aaron Hager and Marshal McGlamery, Department of Crop Sciences, (217)333-4424

Table 1. Triazine herbicides.

Herbicide family Common name* Trade name
 Triazine  atrazine  AAtrex
  atrazine + metolachlor  Bicep II, Bicep Lite II
  atrazine + bromoxynil  Buctril + atrazine
  atrazine + alachlor Bullet, Lariat
  atrazine + imazethapyr Contour
  atrazine + cyanazine  Extrazine II
  atrazine + dimethenamid Guardsman
  atrazine + acetochlor  Surpass 100, Harness Xtra,
FulTime
  atrazine + bentazon Laddok S-1
  atrazine + dicamba Marksman
  atrazine + 2,4-D Shotgun
  simazine Princep
  cyanazine  Bladex
  metribuzin Sencor, Lexone
  metribuzin + metolachlor Turbo
  metribuzin + chlorimuron Canopy


 *Herbicides in italics have a differentmode of action.

Table 2. ALS inhibitors.

Herbicide familyCommon name*Trade name
ImidazolinoneimazethapyrPursuit
imazethapyr + pendimethalinPursuit Plus
imazethapyr + imazaquin + pendimethalinSteel
imazethapyr + atrazineContour
imazethapyr + dicambaResolve
imazethapyr + imazapyrLightning
imazaquinScepter
imazaquin + pendimethalinSquadron
imazaquin + acifluorfenScepter O.T.
imazaquin + dimethenamidDetail
imazaquin + trifluralinTri-Scept
imazapyrArsenal, Chopper, Contain
SulfonylureaschlorimuronClassic, Skirmish
chlorimuron + thifensulfuronConcert, Synchrony STS
chlorimuron + metribuzinCanopy
chlorimuron + sulfentrazoneCanopy XL, Authority, Broadleaf
thifensulfuronPinnacle
thifensulfuron + chlorimuronConcert, Synchrony STS
thifensulfuron + tribenuronHarmony Extra
thifensulfuron + rimsulfuronBasis
metsulfuronAlly
nicosulfuronAccent
nicosulfuron + rimsulfuron + atrazineBasis Gold
primisulfuronBeacon
sulfometuronOust
halosulfuronPermit
prosulfuronPeak
prosulfuron + primisulfuronExceed
tribenuronExpress
chlorsulfuronGlean, Telar
Sulfonamidesflumetsulam + metolachlorBroadstrike + Dual
flumetsulam + clopyralidHornet
flumetsulam + clopyralid + 2,4-DScorpion III
flumetsulam + trifluralinBroadstrike + Treflan
cloransulamFirstRate
*Herbicides in italics have a different mode of action.