North Central Regional Extension Publication No. 377

To Order Herbicide Mode of Action and Crop Injury Symptoms CD-ROM (Item #6893)

North Central Regional Publication 377

Herbicide Mode of Action
and Injury Symptoms

Jeffrey L. Gunsolus Extension Agronomist—Weed Science Department of Agronomy and Plant Genetics University of Minnesota

William S. Curran Extension Agronomist—Weed Science Department of Agronomy Pennsylvania State University

INTRODUCTION

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Herbicide Mode of Action

To be effective, herbicides must 1) adequately contact plants; 2) be absorbedby plants; 3) move within the plants to the site of action, without being deactivated; and 4) reach toxic levels at the site of action. The application method used, whether preplant incorporated, preemergence, or postemergence, determines whether the herbicide will contact germinating seedlings, roots, shoots, or leaves of plants.

The term mode of action refers to the sequence of events from absorption into plants to plant death. The mode of action of the herbicide influences how the herbicide is applied. For example, contact herbicides that disrupt cell membranes, such as acifluorfen (Blazer) or paraquat (Gramoxone Extra), need to be applied postemergence to leaf tissue in order to be effective. Seedling growth inhibitors, such as trifluralin (Treflan) and alachlor (Lasso), need to be applied to the soil to effectively control newly germinated seedlings.

Soil-Applied Herbicide Activity in Plants

Because the seeds of many weed species are quite small and germinate within 0.5 to 1.0 inch of the soil surface, it is important that soil- applied herbicides be positioned in the top 1 to 2 inches of soil to be effective. Herbicide positioning can be accomplished by mechanical incorporation or rainfall. Once a herbicide comes in contact with the plant, absorption through the roots or shoots is very important. A herbicide that is absorbed through the roots will be taken up as long as the herbicide-treated soil remains in contact with the absorbing region near the root tips. As the roots grow to greater soil depths, herbicide uptake declines. Therefore, weeds not killed before the root tips grow out of the herbicide-treated soil are likely to survive.

Many soil-applied herbicides are absorbed through plant shoots while they are still underground and may kill or injure the shoots before they emerge from the soil. Volatile herbicides such as the thiocarbamates (e.g., EPTC [Eradicane]) and the dinitroanilines (e.g., trifluralin [Treflan]) can penetrate the shoot as gases. Less volatile herbicides such as the acetanilides (e.g., alachlor [Lasso]) are absorbed into the shoot as liquids. Physical and environmental factors that promote rapid crop emergence reduce the length of time that a plant is in contact with a soil-applied herbicide and, therefore, reduce the possibility of crop injury.

Herbicides differ in their ability to translocate (i.e., move) within a plant. The soil-applied dinitroaniline herbicides (e.g., trifluralin [Treflan]) are not mobile within the plant. Therefore, their injury symptoms are confined to the site of uptake. Other herbicides are mobile within the plant. For example, soil-applied atrazine is absorbed by plant roots and moves upward within the water transport system of the plant (i.e., xylem) to be concentrated in the leaves. In general, injury symptoms will be most prominent at the site where the mobile herbicides concentrate.

Postemergence Herbicide Activity in Plants

Effective postemergence herbicide application is dependent upon adequate contact with above-ground plant shoots and leaves. Therefore, it is important that spray pressure and volume be adjusted for adequate plant coverage. Also, it is very important that the proper nozzles be used. Hollow-cone or flat-fan nozzles are generally recommended. Read the herbicide label for details.

For postemergence herbicides, the chemical and physical relationships between the leaf surface and the herbicide often determine the rate and amount of uptake. Factors such as plant size and age, water stress, air temperature, relative humidity, and herbicide additives can influence the rate and amount of herbicide uptake. Additives such as crop oil concentrates, surfactants, or liquid fertilizer solutions (e.g., UAN) can increase herbicide uptake by a plant. Application of herbicides under hot and dry conditions or application to older and larger weeds or weeds under water stress can decrease the amount of herbicide uptake. Differences in the rate and amount of herbicide uptake influence the potential for crop injury and weed control and often explain the year to year variation in the effectiveness of the herbicide. Also, the faster a herbicide is absorbed by a plant, the less likely it will be that rain will wash the herbicide off the plants.

Like soil-applied herbicides, postemergence herbicides differ in their ability to move within a plant. For adequate weed control, nonmobile postemergence herbicides must thoroughly cover the plant. Nonmobile herbicides are often called contact herbicides and include the bipyridylium, diphenylether, benzothiadiazole, and nitrile families. Other herbicides are mobile within the plant and can move from the site of application to their site of herbicidal activity. For example, growth regulator herbicides such as 2,4-D and dicamba (Banvel) move both upward and downward within a plant's food transport system (i.e., the phloem) to the growing points of the shoots and roots. In general, injury symptoms will be most prominent at the sites at which the mobile herbicides concentrate.

Herbicide Selectivity

Plants that can rapidly degrade or deactivate a herbicide can escape that herbicide's toxic effects. Corn is tolerant to the triazine herbicides because it quickly deactivates these herbicides by binding them to naturally occurring plant chemicals. Soybean tolerance to metribuzin (Sencor, Lexone) is at least partially due to the deactivation of the herbicide by conjugating (i.e., binding) to plant sugar molecules.

Situations may occur in which a crop may be injured by a herbicide to which it is normally tolerant. This often occurs because environmental stresses such as hot or cold temperatures, high relative humidity, or hail decrease a plant's natural ability to reduce herbicide uptake or deactivate a herbicide. Postemergence cyanazine (Bladex) injury to corn under cold and wet weather conditions is a good example of environmentally induced herbicide injury. An excessive application of herbicide, due to misapplication, can also injure a tolerant crop by overwhelming the crop's herbicide degradation and deactivation systems.

Herbicide Resistance

A number of weed species that were once susceptible and easily managed by certain herbicides have developed resistance. These weeds are no longer controlled by applications of previously effective herbicides. To date, at least 53 species of weeds are resistant to at least five different herbicide families. Some well-known herbicides and resistant species are presented in Table 1.

Herbicide resistance probably develops through the selection of naturally occurring biotypes of weeds exposed to a particular family of herbicides over a period of years. A biotype is a population of plants within the same species that has specific traits in common. Resistant plants survive, go to seed, and create new generations of herbicide resistant weeds.

Mechanisms for resistance vary depending on herbicide family. Resistant biotypes may have slight biochemical differences from their susceptible counterparts that eliminates sensitivity to certain herbicides. For example, in sulfonylurea susceptible plants, a herbicide attaching or binding to an enzyme (acetlactate synthase or ALS) is responsible for disrupting amino acid biosynthesis (see Figure 1). Sulfonylurea herbicide resistant plants have a modified ALS enzyme that prevents herbicide binding.

Also, while photosynthesis is inhibited in triazine herbicide susceptible biotypes, because of a slight change in a chloroplast protein, triazine resistant biotypes are able to continue normal photosynthesis upon exposure to triazine herbicides (see Figure 2). The potential for developing herbicide resistant biotypes is greatest when an herbicide has a single site of action (Figures 1 and 2).

Regardless of the mechanism for resistance, becoming familiar with the herbicide mode of action can help design programs that prevent the introduction and spread of herbicide resistant weeds. Management programs for herbicide resistance should emphasize an integrated approach that stresses prevention. Dependence on a single strategy or herbicide family for managing weeds will surely increase the likelihood of additional herbicide resistance problems in the future. Some guidelines for an integrated approach to managing herbicide resistant weeds are given below.

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• Practice crop rotation.

• Rotate herbicide families and use herbicides with different modes of action.

• Use herbicide mixtures with different modes of action.

• Control weedy escapes and practice good sanitation to prevent the spread of resistant weeds.

• Integrate cultural, mechanical, and chemical weed control methods.

Herbicide Families

An understanding of how herbicides kill weeds (i.e., herbicide mode of action) may be useful in selecting and applying the proper herbicide for a given weed control problem and for preventing herbicide resistance problems. Understanding herbicide mode of action is also very useful in diagnosing herbicide injury complaints. Although a large number of herbicides are available in the marketplace, several have similar chemical properties and herbicidal activity. Herbicides with a common chemistry are grouped into "families." Herbicide families are a convenient way of organizing information about herbicides. In addition, two or more herbicide families may have the same mode of action within the plant and thus express the same herbicide activity and injury symptoms. The following paragraphs describe the characteristics of widely used herbicide families grouped by their mode of action. These seven major modes of action are as follows: growth regulation, amino acid synthesis inhibition, lipid synthesis inhibition, seedling growth inhibition, photosynthesis inhibition, cell membrane disruption, and pigment inhibition.

1. Growth Regulators

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   The growth regulators include the following herbicide families: phenoxy acetic acids, benzoic acids, and the pyridines. Growth regulator herbicides can act at multiple sites in a plant to disrupt hormone balance and protein synthesis and thereby cause a variety of plant growth abnormalities. Growth regulator herbicides selectively kill broadleaf weeds; however, they are capable of injuring grass crops. Herbicides in this group can move in both the xylem and the phloem to areas of new plant growth. As a result, many herbicides in this group are effective on perennial and annual broadleaf weeds. Herbicide uptake is primarily through the foliage but root uptake is possible. Injury symptoms are most obvious on newly developing leaves.

   1. Phenoxy Acetic Acids
      1. Use: 2,4-D for small grains, corn, grass pastures, and non- cropland. MCPA for small grains 2,4-DB for alfalfa and soybeans
      2. Injury Symptoms: Broadleaf plants exhibit stem twisting (epinasty), callus tissue formation, and leaf malformations (cupping, crinkling, parallel veins, leaf strapping). Corn plants exhibit rolled leaves (onion-leafing), fused brace roots, stalk bending and brittleness, and missing kernels. Small grains exhibit twisted flag leaves, sterile florets or multiple florets. See Photos 1 to 10.
      3. Site of Action: Specific site(s) unknown, believed to have multiple sites of action.

   2. Benzoic Acids
      1. Use: Dicamba (Banvel, Clarity) for corn, wheat, oats, sorghum, pastures, and noncropland
      2. Injury Symptoms: Banvel injury is similar to that caused by the phenoxy acetic acid herbicides; however, broadleaf plants may exhibit more cupping than strapping of leaf tissue.
      3. Site of Action: Specific site(s) unknown, believed to have multiple sites of action.

   3. Pyridines
      1. Use: Clopyralid (Stinger) for small grains, sugarbeets, corn, and grass pastures
         Picloram (Tordon) for noncropland, small grains, and grass pastures
         Triclopyr (Crossbow, see package mixtures, Table 11) for noncropland and grass pasture
      2. Injury Symptoms: Similar to the phenoxy acetic acids.
      3. Site of Action: Specific site(s) unknown, believed to have multiple sites of action.

2. Amino Acid Synthesis Inhibitors

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   The amino acid synthesis inhibitors include the following herbicide families: sulfonylureas, imidazolinones, sulfonamide, and amino acid derivatives. Amino acid synthesis inhibitors act on a specific enzyme to prevent the production of specific amino acids, key building blocks for normal plant growth and development. Sulfonylurea, imidazolinone, and sulfonamide herbicides prevent the production of three essential branch-chain amino acids by inhibiting one key plant enzyme. The amino acid derivative herbicides inhibit the production of three essential aromatic amino acids by inhibiting another key plant enzyme. In general, injury symptoms are slow to develop (1 to 2 weeks) and include stunting or slowing of plant growth and a slow plant death. Herbicides in the sulfonylurea, imidazolinone, and sulfonamide families can move in both the xylem and phloem to areas of new growth and can be taken up through plant foliage and roots. Herbicides in these three families may have activity on annual and perennial broadleaf or grass weeds and may be soil- or foliar-applied. The amino acid derivative herbicides are nonselective and the site of uptake is the plant foliage. Herbicides in this family move via the phloem to all parts of the plant; these are excellent perennial weed control herbicides and are active on annual weeds as well.

   1. Imidazolinones
      1. Use: Imazamethabenz (Assert) for wheat, barley, and sunflowers - Imazaquin (Scepter) for soybeans - Imazethapyr (Pursuit) for soybeans, dry beans, and peas.
      2. Injury Symptoms: Grass plants may be stunted, with interveinal yellowing (chlorosis) or purpling. Corn plants may be stunted and show symptoms of root inhibition such as pruning of lateral roots. Leaves emerging from the corn whorl may not unfurl properly and may be yellow to translucent in appearance. Broadleaf plants may be stunted and chlorotic or purple. Soybean injury can range from stunting to death of the terminal growing point. Soybean leaves may be yellow in appearance and leaf veination may appear red or purple in color. See Photos 11 to 18.
      3. Site of Action: Acetolactate synthase (ALS) enzyme. Also referred to as acetohydroxy acid synthase (AHAS).

   2. Sulfonylureas
      1. Use: Chlorimuron (Classic) for soybeans
         Chlorsulfuron (Glean) for small grains and the Conservation Reserve Program (CRP)
         Primisulfuron (Beacon) for corn
         Thifensulfuron (Harmony) for small grains (Pinnacle) for soybeans
         Triasulfuron (Amber) for small grains
         Nicosulfuron (Accent) for corn
         Metsulfuron (Ally) for small grains, grass pastures, and CRP
         Tribenuron (Express) for small grains
         
      2. Injury Symptoms: Same as the imidazolinone herbicides.
      3. Site of Action:Acetolactate synthase (ALS) enzyme. Also referred to as acetohydroxy acid synthase (AHAS).

   3. Sulfonamides
      1. Use: DE-498 (Broadstrike) experimental for corn and soybeans.
      2. Injury Symptoms: Same as the imidazolinone herbicides.
      3. Site of Action: Acetolactate synthase (ALS) enzyme. Also referred to as acetohydroxy acid synthase (AHAS).

   4. Amino Acid Derivatives
      1. Use: Glyphosate (Roundup, Ranger, Rodeo) nonselective weed control for burndown and spot treatments in corn, soybeans, small grains, pasture, and noncropland
      2. Injury Symptoms: Plant foliage, especially new growth, will first yellow and then turn brown and die within 10 to 14 days after herbicide application. See Photo 19
      3. Site of Action: 5-enolpyruvyl-shikimate-3 phosphate synthase (EPSP synthase) enzyme.

3. Lipid Synthesis Inhibitors

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   The lipid synthesis inhibitors include the following herbicide families: aryloxyphenoxypropionates and cyclohexanediones. These herbicides prevent the formation of fatty acids, components essential for the production of plant lipids. Lipids are vital to the integrity of cell membranes and to new plant growth. The lipid synthesis inhibitor herbicides inhibit a single key enzyme involved in fatty acid biosynthesis (Figure 1). Broadleaf plants are tolerant to these herbicide families, however, almost all perennial and annual grasses are susceptible. Injury symptoms are slow to develop (7 to 14 days) and appear first on new leaves emerging from the whorl of the grass plant. These herbicides are taken up by the foliage and move in the phloem to areas of new growth.

   1. Cyclohexanediones
      1. Use: Sethoxydim (Poast, Poast Plus) for soybeans and alfalfa Clethodim (Select) for soybeans
      2. Injury Symptoms: Injury is seen on grass plants only. Newer leaf tissue will be yellow (chlorotic) or brown (necrotic) and the leaves in the leaf whorl can be easily separated from the rest of the plant. See Photos 20 to 23.
      3. Site of Action: Acetyl-CoA carboxylase enzyme.

   2. Aryloxyphenoxypropionates
      1. Use: Diclofop (Hoelon) for small grains Fluazifop (Fusilade) for soybeans Fenoxaprop (Whip, Option) for soybeans Quizalofop (Assure II) for soybeans
      2. Injury Symptoms: Same as the cyclohexanedione herbicides.
      3. Site of Action: Acetyl-CoA carboxylase enzyme.

4. Seedling Growth Inhibitors

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   The seedling growth inhibitors include the following herbicide families: dinitroanilines, acetanilides, and thiocarbamates. Seedling growth inhibitors interfere with new plant growth, thereby reducing the ability of seedlings to develop normally in the soil. Herbicides in these families must be soil-applied. Plants can take up these herbicides after germinating until the seedling emerges from the soil. Therefore, these herbicides are only effective on seedling annual or perennial weeds. Plants that have emerged from the soil uninjured are likely to remain unaffected. Seedling growth inhibitors are active at two main sites, the developing shoot and the root. Much more is known about how seedling root inhibiting herbicides work than about how seedling shoot inhibitors work. The root inhibitors stop plant cells from dividing, which inhibits shoot elongation and lateral root formation. Uptake is through developing roots and shoots. Because herbicide movement within the plant is limited, herbicide injury is confined primarily to plant roots and shoots. Shoot inhibiting herbicides are taken up by developing roots and shoots and can move via the xylem to areas of new growth. There is evidence to suggest that these herbicides can affect multiple sites within a plant, primarily interfering with lipid and protein synthesis.

   1. Root Inhibitors
      1. Dinitroanilines
         1. Use: Benefin (Balan) for alfalfa Ethalfluralin (Sonalan) for soybeans Pendimethalin (Prowl) for corn (preemergence only), soybeans, dry beans, and sunflowers Trifluralin (Treflan) for soybeans, dry beans, and sunflowers
         2. Injury Symptoms: General symptoms include stunted plants that do not fully emerge from the soil and short, thick lateral roots. Grass shoots are short and thick and may appear red or purple in color.
            Broadleaf plants may have swollen and cracked hypocotyls (the area below the cotyledons). Following preemergence treatments, callus tissue may appear at the base of soybean stems. See Photos 24 to 27.
         3. Site of Action: Tubulin protein involved in cell division.

   2. Shoot Inhibitors
      1. Acetanilides
         1. Use: Alachlor (Lasso) for corn, dry beans, sorghum, sunflowers, and soybeans
            Acetochlor an experimental for corn
            Metolachlor (Dual) for corn, dry beans, sorghum, and soybeans
            Propachlor (Ramrod) for corn, flax, and sorghum
            
         2. Injury Symptoms: General symptoms include stunting of shoots that result in abnormal seedlings that do not emerge from the soil. Grasses may leaf-out underground or leaves may not properly unfurl. Broadleaves may have crinkled leaves and/or a shortened mid-vein, which produces a "drawstring" effect. See Photos 28 to 31.
         3. Site of Action: Specific site(s) unknown, believed to have multiple sites of action.

      2. Thiocarbamates
         1. Use: EPTC (Eptam) for alfalfa, dry beans, flax, sugarbeets, and sunflowers
            EPTC plus safener (Eradicane, Eradicane Extra) for corn
            Butylate plus safener (Sutan+) for corn
            Triallate (Far-Go) for wheat and barley
         2. Injury Symptoms: General symptoms include stunting of shoots and poor emergence from the soil. Grasses may fail to emerge from the coleoptile or leaf-out underground. Leaf tips may not unfurl from the coleoptile properly, which results in the "buggy whip" effect. Broadleaves may have crinkled or puckered leaves or leaf buds may not open.
         3. Site of Action: Specific site(s) unknown, believed to have multiple sites of action.

5. Photosynthesis Inhibitors

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   The photosynthesis inhibitors include the following herbicide families: triazines, phenylureas, uracils, benzothiadiazoles, and nitriles. Photosynthesis inhibitors shut down the photosynthetic (food producing) process in susceptible plants by binding to specific sites within the plant's chloroplasts. Inhibition of photosynthesis could result in a slow starvation of the plant; however, the plant experiences a more rapid death that is believed to be due to the production of secondary toxic substances. Injury symptoms include yellowing (chlorosis) of leaf tissue followed by death (necrosis) of the tissue. Three of the herbicide families (triazines, phenylureas, and uracils) are taken up into the plant via the roots or foliage and move in the xylem to plant leaves. As a result, injury symptoms will first appear on the older leaves, along the leaf margin. After foliar application, triazine, phenylurea, and uracil herbicides are less mobile and do not move out of the leaf tissue. The nitrile and benzothiadiazole herbicide families are not mobile in plants and are classified as postemergence contact herbicides. These herbicides have no soil activity. Contact herbicides must thoroughly cover a susceptible plant's foliage if complete control is to be achieved. Photosynthetic inhibitors may control annual or perennial grass or broadleaf weeds.

   1. Mobile Herbicides
      1. Triazines
         1. Use: Ametryn (Evik) for corn
            Atrazine for corn and sorghum
            Cyanazine (Bladex) for corn
            Simazine (Princep) for corn
            Metribuzin (Lexone, Sencor) for alfalfa and soybeans
            Hexazinone (Velpar) for alfalfa
            
         2. Injury Symptoms: Photosynthesis inhibitors do not prevent seedlings from germinating or emerging. Injury symptoms only occur after the cotyledons and first leaves emerge. Initial injury symptoms include yellowing of the leaf margins or tips. In broadleaf plants, yellowing between the leaf veins (interveinal chlorosis) may occur. Older and larger leaves will be affected first because they take up more of the herbicide-water solution and they are the primary photosynthetic tissue of the plant. Injured leaf tissue will eventually turn brown and die. Due to the chemical nature of the herbicide/soil relationship, injury symptoms are likely to increase as the soil pH increases (higher than pH 7.2). See Photos 32 to 34.
         3. Site of Action: D-1 quinone-binding protein of photosynthetic electron transport.

      2. Phenylureas
         1. Use: Linuron (Lorox) for soybeans and corn
            Tebuthiuron (Spike) for grass pasture and noncropland
         2. Injury Symptoms: Same as for the triazine herbicides.
         3. Site of Action: D-1 quinone-binding protein of photosynthetic electron transport.

      3. Uracils
         1. Use: Terbacil (Sinbar) for alfalfa
         2. Injury Symptoms: Same as for triazine herbicides.
         3. Site of Action: D-1 quinone-binding protein of photosynthetic electron transport.

   2. Nonmobile Herbicides
      1. Benzothiadiazoles
         1. Use: Bentazon (Basagran) for soybeans, corn, dry beans, and grain sorghum
         2. Injury Symptoms: Plant injury is confined to foliage that has come in contact with the herbicide. Affected leaves will become yellow or bronze in color and eventually turn brown and die. Injury symptoms can look similar to the injury caused by cell membrane disrupters. Crop oil concentrate and other additives may increase weed control and crop injury symptoms. See Photos 35 and 36.
         3. Site of Action: D-1 quinone-binding protein of photosynthetic electron transport.

      2. Nitriles
         1. Use: Bromoxynil (Buctril) for wheat, barley, oats, rye, flax, corn, and alfalfa
         2. Injury Symptoms: Plant injury is confined to foliage that has come in contact with the herbicide. Foliage that has been thoroughly covered with the herbicide will turn yellow, then turn brown and die. Contact of a low rate of herbicide with leaves may result in spotting or speckling of the leaf surface. Crop oil concentrates and other additives may intensify injury symptoms.
         3. Site of Action: D-1 quinone-binding protein of photosynthetic electron transport.

6. Cell Membrane Disrupters

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   The cell membrane disrupters include the diphenylether and bipyridylium herbicide families. These herbicides are postemergence contact herbicides that are activated by exposure to sunlight to form oxygen compounds such as hydrogen peroxide. These oxygen compounds destroy plant tissue by rupturing plant cell membranes. Destruction of cell membranes results in a rapid browning (necrosis) of plant tissue. On a bright and sunny day, herbicide injury symptoms can occur in 1 to 2 hours. Because these are contact herbicides, they are excellent for burndown of existing foliage and postemergence control of annual weeds. Perennial weeds usually regrow because there is no herbicide movement to underground root or shoot systems. These herbicides have little soil activity.

   Bipyridyliums
   1. Use: Paraquat (Gramoxone Extra) for nonselective weed control in corn, soybeans, small grains, and dormant alfalfa
      Difenzoquat (Avenge) for barley, winter wheat, and some spring and durum wheat varieties
   2. Injury Symptoms: Plant leaves will have a limp, water-soaked appearance, which is followed by browning (necrosis) of the plant tissue. Drift injury will appear as speckling on leaf tissue. See Photo 37 and 38.
   3. Site of Action: Activated by photosystem I (PSI).
   1. Diphenylethers
      1. Use: Acifluorfen (Blazer) for soybeans
         Lactofen (Cobra) for soybeans
         Fomesafen (Reflex) for soybeans
      2. Injury Symptoms: Plant leaves will yellow and then turn brown and die. Reddish-colored spotting on the leaf surface may appear shortly after the herbicide is applied. Plants that do not die may be stunted for a week or more. Crop oils and other additives, as well as extremely cool or warm temperatures, may increase plant injury.
      3. Site of Action: Inhibition of protoporphyrinogen oxidase (Protox).

7. Pigment Inhibitors

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   Pigment inhibitors prevent plants from forming photosynthetic pigments. As a result, the affected plant parts become white to translucent. Clomazone (Command), a soil-applied herbicide, is the only member of the isoxazolidinone family in use at this time. Command is taken up by plant roots and shoots and can move in the xylem to plant leaves. The newly developed foliage of many plant species is so sensitive to Command that very small amounts can whiten new plant growth. Norflurazon (Zorial), a soil-applied herbicide, is the only member of the pyridazinone family in use at this time. Zorial is taken up by plant roots and moves to the growing points of susceptible plants. Susceptible weeds will emerge as white plants before dying.

   1. Isoxazolidinones
      1. Use: Clomazone (Command) for soybeans
      2. Injury Symptoms: Plants turn white, often becoming translucent at the leaf tips. In corn, if more than 75% of the plant is white it will likely die. See Photos 39 to 41.
      3. Site of Action: Specific site(s) unknown but is different than the pyridazinones.

   2. Pyridazinones
      1. Use: Norflurazon (Zorial) for soybeans and cotton grown in the southern U.S.A. only.
      2. Injury Symptoms: Plants turn white, often becoming translucent.
      3. Site of Action: Phytoene and phytofluene desaturase enzymes of the terpenoid pathway.

Table 2. Cross Reference list of herbicide trade names and common names classified as growth regulators.

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Trade1 Name Common Name Trade Name Common Name Trade Name Common Name Banvel Dicamba MCPA Ester, others MCPA Ester 2,4-D Amine, others 2,4-D Amine Butyrac 2,4-DB Stinger Clopyralid 2,4-D Ester, others 2,4-D Ester Clarity Dicamba Tordon 22K2 Picloram 2,4-DB 2,4-DB MCPA Amine, others MCPA Amine

Table 3. Cross Reference list of herbicide trade names and common names classified as amino acid synthesis (ALS synthase enzyme) inhibitors.

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Trade1 Name Common Name Trade Name Common Name Trade Name Common Name Accent Nicosulfuron Broadstrike Flumetsulam Harmony Extra Tribenuron+ Ally Metsulfuron Classic Chlorimuron Thifensulfuron Amber Trisulfuron Express Tribenuron Pinnacle Thifensulfuron Assert Imazamethabenz Glean Chlorsulfuron Pursuit Imazethapyr Beacon Primisulfuron Harmony Thifensulfuron Scepter Imazaquin

Table 4. Cross Reference list of herbicide trade names and common names classified as amino acid synthesis (EPSP synthase enzyme) inhibitors.

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Trade1 Name Common Name Trade Name Common Name Trade Name Common Name Honcho Glyphosate Rattler Glyphosate Ruler Glyphosate Jury Glyphosate Rodeo Glyphosate Show-Off Glyphosate Mirage Glyphosate Roundup Glyphosate Silhouette Glyphosate Ranger Glyphosate

Table 5. Cross Reference list of herbicide trade names and common names classified as lipid (Acetyl-CoA carboxylase enzyme) inhibitors.

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Trade1 Name Common Name Trade Name Common Name Trade Name Common Name Assure II Quizalofop Hoelon2 Diclofop Poast Plus Sethoxydim Fusilade 2000 Fluazifop Option II Fenoxaprop Select Clethodim Fusilade DX Fluazifop Poast Sethoxydim Whip Fenoxaprop Fusion Fluazifop+ Fenoxaprop

Table 6. Cross Reference list of herbicide trade names and common names classified as seedling root (tubulin protein) inhibitors.

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Trade1 Name Common Name Trade Name Common Name Trade Name Common Name Balan Benefin Prowl Pendimethalin Treflan Trifluralin Basalin Fluchloralin Sonalan Ethalfuralin Trific Trifluralin Trillin Trifluralin

Table 7. Cross Reference list of herbicide trade names and common names classified as seedling shoot inhibitors.

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Trade1 Name Common Name Trade Name Common Name Trade Name Common Name Arena2 Alachlor Eradicane EPTC+ Judge2 Alachlor Confidence2 Alachlor Dichlormid Lasso2 Alachlor Cropstar2 Alachlor Eradicane Extra EPTC+ Partner2 Alachlor Dual Metolachlor Dichlormid+ Ramrod Propachlor Eptam EPTC Dietholate Stall Alachlor Far-Go Triallate Surpass2 Acetochlor+ Frontier Dimethenamid Dichormid Harness Plus2 Acetochlor+ Sutan Butylate+ Safener Dichlormid

Table 8. Cross Reference list of herbicide trade names and common names classified as photosynthesis (D-1 quinone-binding protein) inhibitors.

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Trade1 Name Common Name Trade Name Common Name Trade Name Common Name Atrazine2 Atrazine Exrazine II2 Cyanazine+ Linex Linuron Basagran Bentazon Atrazine Lorox Linuron Bladex2 Cyanazine Hyvar XL Bromacil Princep Simazine Buctril Bromoxynil Laddok2 Bentazon+ Sencor Metribuzin Buctril-Atrazine2 Bromoxynil+ Atrazine Sinbar Terbacil Atrazine Lexone Metribuzin Spike Tebuthiuron Evik Ametryn Tough Pyridate Velpar Hexazinone

Table 9. Cross Reference list of herbicide trade names and common names classified as cell membrane disrupters.

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Trade1 Name Common Name Trade Name Common Name Activated by Photosystem I Inhibit Protoporhyrinogen Avenge Difenzoquat Blazer Acilfluorfen Cyclone2 Paraquat Cobra Lactofen Gramoxone Extra2 Paraquat Reflex Fomesafen

Table 10. Cross Reference list of herbicide trade names and common names classified as pigment inhibitors.

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Trade1 Name Common Name Trade Name Common Name Command Clomazone Zorial Norflurazon

Table 11. Cross reference list of package mixture trade names and common names and their sites of action.

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Trade1 Name Common Name Reference Table Trade1 Name Common Name Reference Table Bicep2 Atrazine+ 8+ Galaxy Bentazon+ 8+ Metolachlor 7 Acifluorfen 9 Broadstrike+ Flumetsulam+ 3+ Gemini Linuron+ 8+ Dual Metrolachlor 7 Chlorimuron 3 Broadstrike+ Flumetsulam+ 3+ Harmony Extra Tribenuron+ 3+ Treflan Trifluralin 6 Thifensulfuron 3 Bronate Bromoxynil 8+ Laddok2 Bentazon+ 8+ MCPA 2 Atrazine 8 Bronco2 Alachlor+ 7+ Landmaster Glyphosate 4+ Glyphosate 4 2,4-D 2 Buckle Triallate+ 7+ Lariat2 Alachlor+ 7+ Trifluralin 6 Atrazine 8 Buctril-Atrazine2 Bromoxynil+ 8+ Lasso+Atrazine2 Alachlor+ 7+ Atrazine 8 Atrazine 8 Bullet2 Alachlor+ 7+ Lorox Plus Linuron+ 8+ Atrazine 8 Chrlorimuron 3 Cannon2 Alachlor+ 7+ Marksman2 Dicamba+ 2+ Trifluralin 6 Atrazine 8 Canopy Chlorimuron+ 3+ Passport Trifluranlin+ 6+ Metribuzin 8 Imazethapyr 3 Cheyenne TP2 Fenoxaprop+ 5+ Preview Metribuzin+ 8+ MCPA ester+ 2+ Chlorimuron 3 Thifensulfuron+ 3+ Prozine2 Pendimethalin+ 6+ Tribenuron 3 Atrazine 8 Commence Clomazone+ 10+ Pursuit Plus Imazethapyr+ 3+ Trifluralin 6 Pendimethalin 6 Concert Chlorimuron 3+ Ramrod+Atrazine2 Propachlor+ 7+ Thifensulfuron 3 Atrazine 8 Crossbow Triclopyr+ 2+ Salute Trifluralin+ 6+ 2,4-D ester 2 Metribuzin 8 Curtail Clopyralid+ 2+ Squadron Imazaquin+ 3+ 2,4-D amine 2 Pendimethalin 6 Curtail M Clopyralid+ 2+ Storm Acifluorfen+ 9+ MCPA ester 2 Bentazon 8 Cycle2 Metolachlor+ 7+ Sutazine2 Butylate 7+ Cyanazine 8 Atrazine 8 Dakota TP Fenoxaprop+ 5+ Synchrony STS Chlorimuron+ 3+ MCPA ester 2 Thifensulfuron 3 Extrazine II2 Cyanazine+ 8+ Tiller Fenoxaprop+ 5+ Atrazine 8 2,4-D+ 2+ Fallow Master Glyphosate+ 4+ MCPA 2 Dicamba 2 Finesse Chlorsulfuron 3+ Tornado Fluazifop+ 5+ Metsulfuron 3 Fomesafen 9 Freedom2 Alachlor+ 7+ Tri-Scept Imazaquin 3+ Trifluralin 6 Trifluralin 6 Fusion Fluazifop+ 5+ Turbo Metolachlor+ 7+ Fenoxaprop 5 Metribuzin 8

Glossary Callus tissue— A mass of plant cells that form at a wounded surface. Chloroplast— A membrane-enclosed structure that contains the green pigment molecules (chlorophyll) essential for photosynthesis (i.e., food production). Chlorosis— A yellowing in plant color due to a decline in chlorophyll levels. Contact Herbicide— A general classification for herbicides that are unable to move within a plant. A contact herbicide's effectiveness is highly dependent upon uniform coverage of treated soil or plant tissue. Epinasty— A bending of plant parts (e.g., stems of leaf petioles) downwards due to increased growth on the upper side of an affected plant part. Often associated with the plant growth regulator herbicides. Herbicide mode of action— The sequence of events from absorption of the herbicide into the plant through plant death. Refers to all plant-herbicide interactions. Herbicide site of action— The primary biochemical site that is affected by the herbicide, ultimately resulting in the death of the plant. Also referred to as herbicide mechanism of action. Necrosis— The death of specific plant tissue while the rest of the plant is still alive. Necrotic areas are generally dark brown in color. Phloem— Plant tissue that functions as a conduit for the movement (translocation) of sugars and other plant nutrients. Postemergence application— A time of herbicide application occurring after the crop and weeds emerge from the soil. Also referred to as a foliar application. Preemergence application— A time of herbicide application occurring before the crop is planted but before the crop or weeds emerge from the soil. Preplanting application— A time of herbicide application occurring before the crop is planted. Often followed by an incorporation (mechanical mixing) into the top 1 to 2 inches of soil. Often referred to as a preplant incorporation treatment. Systemic herbicide— A general classification for herbicides that are able to move away from the site of absorption to other parts of the plant. Translocation— The movement of water, plant sugars, and nutrients, herbicides, and other soluble materials from one plant part to another. Translucent— An absence of leaf tissue pigments that results in the diffusion of light, giving the plant an off-white color. Xylem— Plant tissue that functions as a conduit for the upward movement (translocation) of water from the roots to above-ground plant parts.

North Central Regional Extension Publications are subject to peer review and prepared as a part of the Cooperative Extension activities of the thirteen land-grant universities of the 13 North Central States, in cooperation with the Extension Service — U.S. Department of Agriculture, Washington, D.C. The following states cooperated in making this publication available: ILLINOIS Ag. Publication Office 69 Mumford Hall University of Illinois Urbana, IL 61801 217-333-2007 oacepubs@idea.ag.uiuc.edu *MINNESOTA Distribution Center 20 Coffey Hall 1420 Eckles Ave. University of Minnesota St. Paul, MN 55108-6069 612-625-8173 jwb@dc.mes.umn.edu OHIO Publications Office 385 Kottman Hall 2021 Coffey Rd. Ohio State University Columbus, OH 43210-1044 614-292-1607 cripe.2@osu.edu IOWA Publications Distribution Printing & Pub. Bldg. Iowa State University Ames, IA 50011-3171 515-294-5247 pubdist@exnet.iastate.edu SOUTH DAKOTA Ag. Comm. Center Box 2231 South Dakota State University Brookings, SD 57007 605-688-5628 am02@sdsumus.sdstate.edu WISCONSIN Coop. Ext. Pub. Distribution Room 245 30 N. Murray St. University of Wisconsin Madison, WI 53715-2609 608-262-3346 MICHIGAN Bulletin Office 10B Ag. Hall Michigan State University East Lansing, MI 48824-1039 517-355-0240 bulletin@msuces.canr.msu.edu NEBRASKA IANR Comm. and Computing Services University of Nebraska Lincoln, NE 68583 402-472-3023 NORTH DAKOTA Ag. Communications Box 5655, Morrill Hall North Dakota State University Fargo, ND 58105-5655 701-237-7881 dctr@ndsuext.nodak.edu *Publishing State For copies of this and other North Central Regional Extension Publications, write to: Publications Office, Cooperative Extension Service, in care of the University listed above for your state. If they do not have copies or your state is not listed above, contact the publishing state as marked with an asterisk.

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