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Herbicide Mode of Action and Injury Symptoms

Herbicide Mode of Action

To be effective, herbicides mush 1) adequately contact plants; 2) be absorbed by 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 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.

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 reventing herbicide resistance problems. Understanding herbicide mode of action is also very useful in diagnosing herbicide injury complaints. Although a place, 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.

I. Growth Regulators

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 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. (2,4-D, MCPA Dicamba's such as Banvel®, Clarity® and Stinger™ )

II. Amino Acid Synthesis Inhibitors

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, imidazolinon, and sulfanamide families can move in both 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. (Pursuit®, Scepter®, Accent®, Broadstrike®, Beacon®, Roundup®, and Ranger®)

III. Lipid Synthesis Inhibitors

The lipid synthesis inhibitors include the following herbicide families: aryloxyphenoxypropionates and cyclohexanediones. These herbicides prevent the formation of fatty acids, components essential to the production of plant lipids. Lipids are vital to the integrity of cell membrane and to new plant growth. The lipid synthesis inhibitor herbicides inhibit a single key enzyme involved in fatty acid biosynthesis. 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. (Poast®, Select®, Assure® II, Fusilade® DX, and Fusilade® 2000)

IV. Seedling Growth Inhibitors

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 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. (Prowl®, Treflan®, Sonalan®, Lasso®, Harness® Xtra, Frontier®, Dual Magnum®)

V. Photosynthesis Inhibitors

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 issue 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 ,trizine, 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. (Triazines such as Atrazine, Bladex®, Princep®, Sencor®, Basagran®, Buctril®)

VI. Cell Membrane Disrupters

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. (Paraquat, Blazer®, Cobra®, Gramoxone Max®)

VII. Pigment Inhibitors

Pigment inhibitors prevent plants from forming photosynthetic pigments. As a result, the affected plant parts become white to translucent. The chemical is taken up by plant roots and moves to the growing points of susceptible plants. Susceptible weeds will emerge as white plants before dying. (Command®, Zorial®)