Herbicide Mode of Action and Sugarbeet Injury Symptoms (continued)

A-1085, August 1994

Table of Contents

IV. Seedling Growth Inhibitors
V. Photosynthesis Inhibitors
VI. Cell Membrane Disrupters
VII. Pigment Inhibitors
VIII. Non-Herbicidal Injury Symptoms
Glossary

IV. Seedling Growth Inhibitors

The seedling growth inhibitors include the dinitroanilines, acetanilides, and thiocarbamates. All of these herbicides must be used preplant incorporated or preemergence to the weeds to be effective. In some uses, the herbicides are applied after crop emergence but before weed emergence.

Seedling growth inhibitors interfere with new plant growth, thereby reducing the ability of seedlings to develop normally in the soil. 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 the action of seedling root inhibiting herbicides than seedling shoot inhibitor herbicides. 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. Present evidence suggests that these herbicides can affect multiple sites within a plant, primarily interfering with lipid and protein synthesis.

A. Root Inhibitors

1. Dinitroanilines

1. Use:
   Ethalfluralin (Sonalan) for soybean, sunflower and dry bean.
   Pendimethalin (Prowl) for corn (preemergence only) soybean, dry bean, and sunflower.
   Trifluralin (Treflan) for soybean, dry bean, sunflower, alfalfa, small grain, Canola (rapeseed), mustard and pea.
   
2. Injury Symptoms: Dinitroaniline residual in soil may cause sugarbeet to be severely stunted with small leaves that are more erect than normal (Photo 22). The roots of damaged sugarbeet seedlings may turn brown and die starting at the point where the root joins the hypocotyl, about 1 to 1.5 inches below the soil surface (Photo 23). Plants with dead roots may die or they may survive by producing secondary roots from the hypocotyl (Photo 24). Identical symptoms on roots of seedling sugarbeet also can be caused by imidazolinone, sulfonylurea or sulfonamide herbicides and by Aphanomyces, a fungal disease. Affected plants will be smaller than unaffected plants. Plant regrowth by secondary root production would be prevented by drought in the surface 2 inches of soil and injured plants would die. Imidazolinone, sulfonylurea and sulfonamide herbicides also can cause similar seedling root death.
   
3. Site of Action. Tubulin protein involved in cell division.

Photo 22. Stunted sugarbeet with abnormally erect leaves caused by Sonalan residual in soil. (24KB color photo)

Photo 23. Sugarbeet tap root has shriveled below the point where the hypocotyl joins the root, caused by trifluralin residue in soil. (15KB color photo)

Photo 24. Stunted plant on left from trifluralin residue in soil, undamaged plant on the right. The tap root on the damaged plant had died but the plant started secondary root growth from the living hypocotyl above the tap root. (23KB color photo)

B. Shoot Inhibitors

1. Acetanilides

1. Use:
   Alachlor (Lasso) for corn, dry bean, sorghum, sunflower and soybean.
   Acetochlor (Harness Plus, Surpass) for corn.
   Metolachlor (Dual) for corn, dry bean, sorghum, potato and soybean.
   Propachlor (Ramrod) for corn, flax, and sorghum.
   Dimethenamid (Frontier) for corn.
   
2. Injury Symptoms: Acetanilides cause no distinctive symptoms on sugarbeet. Some plants may die before emergence. Emerged but injured plants are normal in appearance but stunted.
   
3. Site of Action: Specific site(s) unknown, believed to have multiple sites of action.

2. Thiocarbamates

1. Use.
   EPTC (Eptam) for alfalfa, potato, dry bean, flax, safflower, sugarbeet and sunflower.
   EPTC plus safener (Eradicane) for corn.
   Butylate plus safener (Sutan+) for corn.
   Triallate (Far-Go) for wheat barley, lentils and pea.
   Cycloate (Ro-Neet) for sugarbeet.
   
2. Injury Symptoms: Thiocarbamates reduce the formation of epicuticular wax on leaves, which can cause leaves to stick together rather than unfold normally (Photo 25). Affected plants may be stunted, leaves may be shortened and thickened, or true leaf development may be inhibited (Photo 26). Some severely stunted plants may die while others will start producing new leaves and will produce a nearly normal-sized root at harvest. Severely stunted plants may grow very little for two or more weeks after emergence and then make a complete or nearly complete recovery.
   
3. Site of Action: Specific site(s) unknown, believed to have multiple sites of action.

Photo 25. Sugarbeet leaves stuck together from Eptam at 5 lb/A. (22KB color photo)

Photo 26. Severely stunted sugarbeet plants from Eptam at 5 lb/A. (21KB color photo)

V. Photosynthesis Inhibitors

The photosynthesis inhibitors include triazines, phenylureas, uracils, benzothiadiazoles, nitriles, carbamate and dicarboxylic acid. Photosynthesis inhibitors shut down the photosynthetic (food producing) process in susceptible plants by binding to specific sites within the plant chloroplast. Inhibition of photosynthesis could result in a slow starvation of the plant; however, in many situations rapid death occurs perhaps from 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. Foliar applied photosynthetic inhibitors generally remain in the foliar portions of the treated plant and movement from foliage to roots is negligible.

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, soybean, potato, pea and lentil.
   Hexazinone (Velpar) for alfalfa.
   
2. Injury Symptoms: Residual of photosynthesis inhibitors in soil does not prevent seedlings from germinating or emerging. Injury symptoms occur after emergence and the speed of appearance of symptoms will be more rapid with sunny days than with cloudy weather. Also, symptoms will be more severe and more rapid as the level of herbicide in the soil increases. Sugarbeet plants may be in the two- to four-leaf stage before symptoms become noticeable but plants can die in the early two-leaf stage. Initial symptoms include browning of the cotyledonary leaves and yellowing of the true leaf margins (Photo 27). Browning of leaves will increase with time (Photos 28, 29) and total desiccation may result (Photo 30). Older and larger leaves are affected before younger leaves. Postemergence triazines cause an initial yellowing followed by desiccation and leaf browning.
   
3. Site of Action: D-1-quinone-binding protein of photosynthetic electron transport.

Photo 27. Early symptoms from atrazine residual in soil. Cotyledon leaves are brown and the leaf tips and margins are yellowing. (25KB color photo)

Photo 28. Later symptoms from atrazine residual in soil. Leaf tips and margins are brown. (30KB color photo)

Photo 29. Later symptoms from atrazine residual in soil. Browning has spread from old leaves to new leaves. (28KB color photo)

Photo 30. Sugarbeet killed by atrazine residual in soil. (28KB color photo)

2. Phenylureas

1. Use:
   Linuron (Lorox) for soybean 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.

4. Benzothiadiazoles

1. Use: Bentazon (Basagran) for soybean, corn, dry bean and grain sorghum.
   
2. Injury Symptoms: Leaves become chlorotic and later turn brown and die (Photo 31). The older leaves die first. All the older leaves can turn brown while the growing point remains green. Sugarbeet can recover, produce new leaves and produce a nearly normal-size root at harvest if the growing point survives.
   
3. Site of Action: D-1-quinone-binding protein of photosynthetic electron transport.

Photo 31. Sugarbeet injury from Basagran at 0.25 lb/A. Older leaf blades are brown but the growing point is alive. (25KB color photo)

5. Nitriles

1. Use: Bromoxynil (Buctril) for wheat, barley, oats, rye, flax, corn and alfalfa.
   
2. Injury Symptoms: Leaves become chlorotic and later turn brown and die (Photo 32). Contact with isolated spray droplets may cause a spotting or speckling of the leaves. The older sugarbeet leaves will be affected more than the young leaves. Sugarbeet can produce new leaves and a harvestable root if the growing point survives.
   
3. Site of Action: D-1-quinone-binding protein of photosynthetic electron transport.

Photo 32. Sugarbeet injury from Buctril at 0.06 lb/A. Older leaf blades are brown but the growing point is still alive. (30KB color photo)

6. Carbamate

1. Use:
   Desmedipham (Betanex) for sugarbeet.
   Desmedipham+Phenmedipham (Betamix) for sugarbeet.
   
2. Injury Symptoms: Desmedipham and phenmedipham are registered for sugarbeet but injury sometimes occurs, most often in a hot and moist environment. Symptoms from desmedipham and phenmediham are very similar to symptoms from bentazon and bromoxynil. Injured leaves may turn brown and die. The older leaves die first and the growing point may remain green and alive even when most leaves are dead (Photos 33,34). Sugarbeet plants with a surviving growing point will produce new leaves and a nearly normal size root at harvest.
   
3. Site of Action: D-1-quinone-binding protein of photosynthetic electron transport.

Photo 33. Sugarbeet injury from Betanex at 1.5 lb/A. Older leaves are brown, but cotyledons and growing point are injured very little. (25KB color photo)

Photo 34. Sugarbeet injury from Betamix at 3 lb/A. Older leaves are brown and new leaf growth has started from these severely injured plants. (28KB color photo)

7. Dicarboxylic Acid

1. Use: Endothall (H-273) for sugarbeet.
   
2. Injury Symptoms: Endothall is registered for sugarbeet but injury sometimes occurs, most often in a hot and moist environment. Symptoms from endothall are very similar to symptoms from bentazon, bromoxynil, desmedipham and phenmedipham. Injured leaves turn brown and die. The older leaves die first and the growing point may remain green and alive even when most leaves are dead (Photo 35). Sugarbeet plants with a surviving growing point will produce new leaves and a nearly normal size root at harvest.
   
3. Site of Action: D-1-quinone-binding protein of photosynthetic electron transport.

Photo 35. Sugarbeet injury from Herbicide 273 at 4 lb/A. Older leaves are brown and new leaf growth has started from these severely injured plants. (27KB color photo)

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 one to two 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 the herbicides do not move to underground root or shoot systems. These herbicides have little pytotoxicity through the soil.

1. Bipyridyliums

1. Use:
   Paraquat (Gramoxone Extra) for nonselective weed control in corn, soybean, dry bean, sunflower, sugarbeet, small grains and dormant alfalfa and for desiccation of potato and sunflower.
   Difenzoquat (Avenge) for barley, winter wheat and some spring and durum wheat varieties.
   
2. Injury Symptoms: Drift on sugarbeet often will appear as spotting of leaf tissue (Photo 36). High amounts of drift or an accidental application may cause patches of brown tissue on leaves (Photo 37). Spots from bipyridylium drift (Photo 38) have been confused with foliar diseases such as Cercospora or bacterial blight. Generally the pattern of injury in a field can be used to distinguish between disease and drift. If in doubt, samples should be taken to a diagnostic laboratory for disease identification.
   
3. Site of Action: Activated by photosystem I (PSI).

Photo 36. Diquat caused spotting of sugarbeet leaves from drift. (21KB color photo)

Photo 37. Brown patches on sugarbeet leaves caused by an accidental direct application of diquat. (35KB color photo)

Photo 38. Paraquat caused circular brown spots which could be confused with sugarbeet foliar diseases. (17KB color photo)

2. Diphenylethers

1. Use:
   Acifluorfen (Blazer) for soybean.
   Lactofen (Cobra) for soybean.
   Fomesafen (Reflex) for soybean.
   
2. Injury Symptoms: Affected leaves will exhibit dessication where the herbicide contacted the plant (Photo 39). Drift generally will not kill sugarbeet but the plants may be severely stunted. New leaf growth will appear normal.
   
3. Site of Action: Inhibition of photoporphyrinogen oxidase (Protox).

Photo 39. Sugarbeet injury from Cobra at 0.2 lb/A. Older leaves have speckled burn but growing point appears healthy. (27KB color photo)

VII. Pigment Inhibitors

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. Clomazone 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 very susceptible to clomazone and very small amounts can whiten new plant growth. Susceptible weeds will emerge as white plants before dying.

1. Isoxazolidinones

1. Use: Clomazone (Command) for soybean.
   
2. Injury Symptoms: All or portions of the true leaves will turn white (Photo 40). Sugarbeet is relatively tolerant of clomazone residual in soil and generally plants with symptoms will live, turn green, and produce a nearly normal-size root at harvest.
   
3. Site of Action: Specific sites unknown.

Photo 40. Sugarbeet with white leaves from Command residual in soil. (24KB color photo)

VIII. Non-Herbicidal Injury Symptoms

1. Frost: Plants develop a watersoaked appearance as they thaw. Frosted tissues later turn brown and desiccate. Frost injury is erratic and a plant may be killed next to another plant that appears uninjured (Photo 41).

Photo 41. Dead sugarbeet plant on the right from frost while the adjacent plant was uninjured. (34KB color photo)

2. Insecticides: Close contact between insecticide and sugarbeet root can blacken or constrict root growth. The injury in Photo 42 was caused by an in-furrow application of chlorpyrifos (Lorsban).

Photo 42. Constriction and blackening of sugarbeet root caused by Lorsban granules applied in-furrow. (19KB color photo)

3. Water: Saturated soil can cause sugarbeet to become a bright yellow with leaves that are more erect than normal (Photo 43). Water damage can cause sugarbeet to become more susceptible to postemergence herbicides. In Photo 44, the center two rows were not herbicide treated; the four rows of injured sugarbeet on each side of the center two rows were treated with postemergence sugarbeet herbicides. The relatively healthy sugarbeet at the rear of the plots beyond the signs was less water stressed than the area in front of the signs. Water stress plus herbicide caused more sugarbeet injury than water stress alone or herbicides alone.

Photo 43. Yellow and abnormally erect sugarbeet leaves caused by excess water. (26KB color photo)

Photo 44. The center two rows were not herbicide treated, the four rows of injured sugarbeet on each side of the center two rows were treated with postemergence sugarbeet herbicides. The relatively healthy sugarbeet at the rear of the plots beyond the signs was less water stressed than the area in front of the signs. Thus, water stress plus herbicide caused more sugarbeet injury than water stress alone or herbicides alone. (36KB color photo)

4. Diseases and Insects: Many diseases and insects affect sugarbeet. The "Compendium of Beet Diseases and Insects" published by the American Phytopathological Society, 3340 Pilot Knob Road, St. Paul, MN 55121 has an extensive description and pictures of symptoms of diseases and insect damage as well as nutritional disorders, drought, hail, lightning, crusting, salt injury and others.

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).

Chlorsis - 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 or 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 after a 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 I 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 to serve as a conduit for the upward movemet (translocation) of water from the roots to above-ground plant parts.

Betaseed, Inc. 1788 Marschall Road Shakopee, MN 55379 1-800-428-8455 Betaseed, Inc. has funded this publication as part of our ongoing tradition of commitment to the North American Sugarbeet Industry.

Photo Credits

Alan G. Dexter: Photos 1-3, 5-8, 10-43.
Allan W. Cattanach: Photos, 4, 9, 44

Site of Action References

Duke, S.O., 1990. Overview of Herbicide Mechanisms of Action. Environmental Health Perspectives. Vol.87:263-271.
Gronwald, J.W.,USDA/ARS, Plant Science Research Unit, University of Minnesota, St. Paul. Personal communication.
Weimer, M.R., Dept. of Agronomy and Plant Genetics, University of Minnesota, St.Paul. Personal communication

[ Table of Contents ]

A-1085, August 1994