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Preventing and Managing Herbicide-Resistant Weeds in Turfgrass

Publication Number: P2844
Updated: March 15, 2018
View as PDF: P2844.pdf

Herbicide-resistant weeds are among the most troublesome issues facing the turfgrass industry. The loss of effective and economically viable herbicides results in lower quality turf and increases weed management budgets. Herbicide resistance is the inherited ability of a plant population to survive and reproduce following treatment with a normally lethal dose of herbicide.

This is not a new issue. Simazine- and atrazine-resistant groundsel (Senecio vulgaris) was reported as early as 1970 (Ryan, 1970). Simazine-resistant annual bluegrass (Poa annua) has plagued golf courses, sports fields, industrial turf, and sod production in the Southeast for more than two decades. As of 2014, more than 420 unique cases of herbicide-resistant weeds have been reported globally (Heap, 2014). That equates to 232 species having evolved resistance to 22 of 25 known herbicide sites of action and to 152 different herbicides. Table 1 lists herbicide-resistant turfgrass weeds of Mississippi as of 2014.

Table 1. Herbicide-resistant turfgrass weeds of Mississippi reported by the International Survey of Herbicide-Resistant Weeds (Heap, 2014).*

Resistant weed

Mode of action

Active ingredient

Trade name

State

goosegrass

mitotic inhibitors

pendimethalin

trifluralin

Pendulum

Treflan

MS

goosegrass

EPSP synthase inhibitors

glyphosate

Round-Up

MS

Poa annua

photosystem II inhibitors

atrazine

simazine

Aatrex

Princep

MS

*There likely are instances of resistance not yet reported.

Preventing and managing herbicide resistance is crucial to preserving key chemistries that turfgrass managers use to provide a playable and aesthetically pleasing turf surface. It is important to understand some basic terminology associated with herbicide resistance.

Mode of action (MOA) — Herbicides are active at one or more target sites within plants. Target sites are often enzymes that play a critical role in plant metabolism. The term “site of action” is used interchangeably with MOA; however, the terms have somewhat different connotations. The MOA is how a herbicide kills a plant. For instance, atrazine inhibits photosystem II, subsequently leading to a buildup of oxidative free radicals and a decrease in photosynthesis. Site of action is where the herbicide binds in order to kill a plant. Atrazine inhibits photosystem II by binding to a specific site of action, the quinone-B binding niche on the D1 protein.

Table 2 lists common turfgrass MOAs and example trade names. The fundamental principle for managing herbicide resistance is this: repeatedly relying upon a single MOA selects for populations that are resistant. Herbicides do not cause a mutation; they merely select for populations that tolerate a dose of herbicide. Subsequently, those populations expand in number.


Table 2. Modes of action commonly used by turfgrass managers.

Mode of action

WSSA

HRAC

Active ingredient

Trade name

acetyl CoA carboxylase (ACCase) inhibitors

1

A

diclofop
clethodim

Illoxan
Envoy

acetolactate synthase (ALS or AHAS) inhibitors

2

B

bispyribac-sodium
foramsulfuron

Velocity
Revolver

photosystem (PS) II inhibitors

5

C1

simazine

Princep

photosystem (PS) I inhibitors

22

D

diquat

Diquat

protoporphyrinogen oxidase (protox) inhibitors

14

E

oxadiazon
sulfentrazone

Ronstar
Dismiss

carotenoid biosynthesis inhibitors

28

F2

mesotrione
topramezone

Tenacity
Pylex

enolpyruvyl shikimate-3-phosphate (EPSP) synthase inhibitors

9

G

glyphosate

Round-up

glutamine synthase inhibitors

10

H

glufosinate

Finale

mitotic inhibitors

3

K1

prodiamine

Barricade

cellulose synthesis inhibitors

29

L

indaziflam

Specticle

fatty acid and lipid biosynthesis inhibitors

16

N

ethofumesate

Prograss

synthetic auxins

4

O

dicamba

Banvel

Preventing herbicide resistance requires rotating herbicide MOAs in order to avoid the expansion of resistant populations. Classification systems have been developed to help herbicide applicators alternate MOAs. The most common are those developed by the Weed Science Society of America (WSSA) and the Herbicide Resistance Action Committee (HRAC).

The WSSA system assigns each herbicide a number based on the MOA. The HRAC system assigns a letter based on an alphabetized list of herbicide MOAs. Inhibition of acetyl CoA carboxylase (ACCase) is assigned the HRAC grouping of A. HRAC further amends herbicide groupings with a subscript numbering system that indicates different binding behavior. In the case of photosystem II-inhibiting herbicides, subclasses C1, C2, and C3 indicate different behavior with a key binding protein.

Resistance can be either innate or evolved. Innate resistance is the ability of a plant to survive and reproduce following a herbicide application from the very first exposure. Innate resistance is also known as tolerance. Evolved resistance is a change in a specific weed species that was once susceptible to a herbicide but is now no longer controlled.

 

 

Both innate and evolved resistance can be due to either target-site or nontarget-site resistance. Target-site resistance is due to a change in the molecular structure of the intended biochemical target that prevents the herbicide from binding. In the case of resistance to photosystem II inhibitors (atrazine, simazine, diuron, and amicarbazone), a molecular change prevents the specific binding of herbicide to the quinone-B binding site of the D1 protein. Similar modes of target-site resistance are also known to cause resistance to acetolactate synthase inhibitors (bispyribac-sodium, foramsulfuron), acetyl-CoA carboxylase inhibitors (fluazifop, diclofop, fenoxaprop), and mitotic-inhibiting herbicides (prodiamine, pendimethalin, oryzalin).

Nontarget-site herbicide resistance is a change in the ability of the herbicide to be absorbed, translocate throughout the plant, or be metabolized by the plant. Nontarget-site resistance may develop due to structural and chemical changes in plant leaves, such as thicker wax on leaf surfaces. It may also be due to reduced movement of the herbicide throughout the plant. For example, glyphosate resistance in horseweed (Conyza canadensis) has occurred due to reduced translocation of the herbicide (Koger and Reddy, 2005).

 

Prevent and Manage Resistance

Herbicide resistance is real, but you can take steps to prevent resistance and control already-resistant populations. The WSSA and HRAC classification systems are tools for developing resistance management strategies, but they should not be relied upon solely. Principally, proper cultural management enhances turfgrass vigor and reduces the reliance upon chemical weed control. Mechanical weed removal and application of nonselective herbicides via spot spraying are also crucial elements of resistance prevention and management.

 

Rotate Modes of Action

Repeat applications of the same MOA will select for resistant plants within a population. The more frequently herbicides with the same MOA are used, the more quickly resistant weed populations will develop. Rotation from Brand A to Brand B does not slow resistance development if both herbicides have the same MOA. Not only do managers have to rotate different herbicides, but they also have to use different MOAs. For instance, using atrazine in rotation with simazine is a futile approach, as both are photosystem II inhibitors (Group 5 herbicides). See Table 3 for a more complete list of WSSA and HRAC classifications.

Table 3. Mode of action and classification of common turfgrass herbicides according to the Weed Science Society of America and the Herbicide Resistance Action Committee.

Timing

Mode of action

WSSA group

HRAC group

Common name

Trade name

pre

mitotic inhibition

3

K1

dithiopyr

Dimension

pre

mitotic inhibition

3

K1

pendimethalin

Pendulum

pre

mitotic inhibition

3

K1

prodiamine

Barricade

pre

lipid biosynthesis inhibition

8

N

bensulide

Bensumec

pre

photosystem II inhibition

7

C2

siduron

Tupersan

pre

protoporphyrinogen oxidase (PPO) inhibition

14

E

oxadiazon

Ronstar

pre/post

mitotic inhibition

15

K3

dimethenamid

Tower

pre/post

mitotic inhibition

3

K1

pronamide

Kerb

pre/post

mitotic inhibition

15

K3

metolachlor

Pennant Magnum

pre/post

photosystem II inhibition

5

C1

amicarbazone

Xonerate

pre/post

photosystem II inhibition

5

C1

atrazine

Aatrex

pre/post

photosystem II inhibition

5

C1

metribuzin

Sencor

pre/post

photosystem II inhibition

5

C1

simazine

Princep

pre/post

cellulose synthesis inhibition

29

L

indaziflam

Specticle

pre/post

lipid biosynthesis inhibition

16

N

ethofumesate

Prograss

pre/post

carotenoid biosynthesis inhibition

28

F2

mesotrione

Tenacity

pre/post

protoporphyrinogen oxidase (PPO) inhibition

14

E

flumioxazin

SureGuard

post

synthetic auxin

4

O

2,4-D

multiple

post

synthetic auxin

4

O

dicamba

Banvel

post

synthetic auxin

inhibition of cell wall (cellulose) synthesis

4

27

O

L

quinclorac

Drive

post

acetolactate synthase (ALS) inhibition

2

B

bispyribac-sodium

Velocity

post

acetolactate synthase (ALS) inhibition

2

B

foramsulfuron

Revolver

post

acetolactate synthase (ALS) inhibition

2

B

imazaquin

Image

post

acetolactate synthase (ALS) inhibition

2

B

metsulfuron

Manor

post

acetolactate synthase (ALS) inhibition

2

B

rimsulfuron

TranXit

post

acetolactate synthase (ALS) inhibition

2

B

sulfosulfuron

Certainty

post

acetolactate synthase (ALS) inhibition

2

B

trifloxysulfuron

Monument

post

acetyl CoA carboxylase (ACCase) inhibitors

1

A

diclofop

Illoxan

post

acetyl CoA carboxylase (ACCase) inhibitors

1

A

clethodim

Select

post

enolpyruvyl shikimate-3 phosphate (EPSP) synthase inhibition

9

G

glyphosate

Roundup

post

glutamine synthetase inhibition

10

H

glufosinate

Finale

post

photosystem II inhibition

6

C3

bentazon

Basagran

post

photosystem I inhibition

22

D

diquat

Reward

post

photosystem I inhibition

22

D

paraquat

Gramoxone

 

Use Tank Mixtures

If you use herbicide tank mixtures with different MOAs that are active on the same species, the weedy population would need to have tolerance to two different MOAs at the same time in order to survive. This may decrease the potential for resistance, but there are differences of opinion surrounding the issue. It is, however, likely that multiple MOAs improve the spectrum of weeds controlled, simultaneously reducing plants that need follow-up applications.

 

Use Both Pre- and Post-Emergence Herbicides

Integrating both pre- and post-emergence herbicides into a weed management plan will diversify MOAs and eliminate weeds before they mature and develop seed. In such a plan, it would also be necessary to rotate both the pre- and post-emergence MOAs used each year. Atrazine followed by simazine would again be futile, because they have the same MOA. See Mississippi State University Extension Publication 1532 Weed Control Guidelines for Mississippi.

 

Maximize Control and Minimize Escapes

It is important that herbicide applicators use the maximum labeled application rates in order to maximize control. Plants that escape control should be removed manually or chemically using a high-rate or nonselective spot spray application, according to label recommendations.

 

Optimize the Environment for Turf Plants

As always, the most important approach for weed management is to simply optimize the environment for the desired turf species. This will decrease the number of weeds that are actually treated by herbicides, thus decreasing the potential for resistance development.

 

Summary

Herbicide-resistant weeds are an increasing problem. An effective cultural and chemical management plan is required to achieve maximum weed control in turfgrass systems; however, emphasis should be placed on rotating herbicide modes of action and eliminating escaped weeds after herbicidal treatments have been applied. The Weed Science Society of America has developed a five-part training module on herbicide resistance awareness and education. Those modules can be accessed online at http://wssa.net/weed/resistance/.

Figure 1. Many agro-chemical companies have adopted a strategy of clearly labeling modes of action on the product label. Quinclorac (Drive) is a WSSA classified group 4 herbicide, which means it is a synthetic auxin.

References

Heap, I. 2014. The international survey of herbicide-resistant weeds. Available online at www.weedscience.org.

HRAC Website. 2014. Herbicide resistance action committee. Available online at www.hracglobal.com.

Koger, C.H. & K.N. Reddy. 2005. Role of absorption and translocation in the mechanism of glyphosate in horseweed (Conyza canadensis). Weed Science, 53: 84-89.

Ryan, G.F. 1970. Resistance of common groundsel to simazine and atrazine. Weed Science, 18: 614-616.

Weed Control Guidelines for Mississippi. 2014. Mississippi State Extension Service, Publication 1532. Available online at http://extension.msstate.edu/publications/publications/weed-control-guidelines-for-mississippi.

Weed Science Society of America. 2014. Herbicide resistance training modules. Available online at http://wssa.net/weed/resistance/.

 

Publication 2844 (POD-03-18)

By Jay McCurdy, PhD, Assistant Professor, Plant and Soil Sciences. Some ideas and concepts for this publication originate from an article that appeared in the November 2012 issue of Golf Course Management, written by Dr. Scott McElroy.
 

 

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Authors

Assistant Professor
Turfgrass Extension Specialist/Weed Scientist/Weed Control-Turf and Ornamentals

Your Extension Experts

Extension/Research Professor
Weed control in agronomic crops
Extension/Research Professor
Weed Scientist/Weed Control - Agronomic and Horticultural Crops and noncropland
Assistant Professor
Turfgrass Extension Specialist/Weed Scientist/Weed Control-Turf and Ornamentals
Associate Professor

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