Sugarbeet is one of several crops within Beta vulgaris. Sugarbeet has evolved through time from a labor-intensive agricultural crop with static yield to one that is highly mechanized and with steadily improving yield.
Weeds have been a significant production challenge in sugarbeet since the crop first was cultivated in Europe in the late 1700s. Interference from uncontrolled weeds can suppress sugarbeet so severely that no crop is produced. Weeds that emerge within the first eight weeks after planting especially influence sugarbeet yield.
Herbicide application timing
Herbicides are applied alone or in mixtures before planting (preplant), immediately after planting (pre-emergence), after sugarbeet has emerged but before weeds have emerged (lay-by), and after sugarbeet and weed emergence (postemergence). Injury can occur from herbicides applied to sugarbeet for weed control, and from off-target movement of herbicides applied to other crops in adjacent fields or herbicide applied in previous years’ crops that carryover to sugarbeet.
How herbicides work
Herbicide efficacy depends on the morphology and anatomy of the plant and many physiological and biochemical processes that occur within the plant, including:
- Droplet retention.
- Herbicide deposition.
- Translocation (movement) of active herbicide within the plant.
- Toxic levels reaching the site of action, such as a specific enzyme, or the plant processes that are disrupted by the herbicide
The application method, whether preplant incorporated, pre-emergence or postemergence, largely determines when the herbicide will contact plants and the portion of the plant contacted.
Herbicide mode of action refers to how herbicides work and is the sequence of events beginning with herbicide contact and plant absorption until plant death. Herbicides with the same mode of action will have similar translocation patterns and produce similar injury symptoms.
Mode of herbicide action may determine the application method needed for best results. For example, herbicides that affect protein synthesis but have little soil residual, such as clopyralid (Stinger) or glyphosate (Roundup PowerMax), need to be applied postemergence and be in contact with leaf tissue.
Seedling growth inhibitors such as S-metolachlor (Dual Magnum) or cycloate (Ro-Neet SB) need to be applied to the soil to control newly germinating seedlings effectively.
The potential for a herbicide to kill certain plants without injuring others is called selectivity. Plants may degrade rapidly or deactivate a herbicide to escape that herbicide’s toxic effects.
For example, corn quickly deactivates atrazine by binding to naturally occurring plant chemicals. Soybean tolerance to metribuzin (Sencor/Dimetric) is at least partially due to the deactivation of the herbicide by conjugation (binding) to plant sugar molecules.
Desmedipham plus phenmedipham (Betamix) applied postemergence provides pigweed spp. control in sugarbeet. Sugarbeet avoids injury from Betamix partially through its rapid metabolism.
Effect of environmental stress
Situations may occur where a crop is injured by a herbicide that normally is not toxic to the crop. This often occurs because environmental stressors decrease a plant’s natural ability to reduce herbicide uptake or deactivate a herbicide. Stressors include:
- Hot or cold temperatures
- High relative humidity
Postemergence Betamix injury to sugarbeet under hot and wet weather conditions is a good example of environmentally induced herbicide injury.
An excessive amount of herbicide due to misapplication also can injure a tolerant crop by overwhelming the crop’s herbicide degradation and deactivation systems.
Seeds of many weed species are quite small and germinate only 0.5 to 1 inch below the soil surface, so soil-applied herbicides should be concentrated in the top 1 to 2 inches of soil for best weed control. Herbicide positioning can be accomplished by mechanical incorporation or precipitation.
Close contact between the herbicide and the plant is needed for absorption through the roots or shoots for effective weed control. Herbicide absorption through roots will continue if the absorbing region near the root tips remains in contact with the herbicide-treated soil.
Herbicide uptake declines as the roots grow deeper. Therefore, plants may survive if the root tips grow beyond the herbicide-treated soil before herbicide absorption is sufficient to kill the plants.
Many soil-applied herbicides are absorbed through unemerged plant shoots, and plants may be killed or injured before emergence.
Volatile herbicides can move in the soil and penetrate plant shoots as gasses or liquids. Examples of volatile herbicides include:
- Thiocarbamates, such as cycloate (Ro-Neet SB)
- Dinitroanilines, such as trifluralin (Treflan)
Less volatile herbicides are absorbed into the shoots only as liquids. Chloroacetamides, such as S-metolachlor, dimethenamid-P (Outlook) or acetochlor (Warrant), are examples of less volatile herbicides.
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. This, in turn, reduces the possibility of crop injury.
Herbicides differ in translocation within a plant. The soil-applied dinitroaniline herbicides (such as trifluralin) are not mobile within the plant. Therefore, their primary injury symptoms mostly are confined to the site of uptake.
Other herbicides are mobile within the plant, and injury symptoms generally will be most prominent at the site where mobile herbicides concentrate. For example, soil-applied atrazine is absorbed by plant roots. It moves upward within the water transport system of the plant to the leaves, where symptoms occur.
Effective weed control from postemergence herbicides depends on adequate contact with above-ground plant shoots and leaves. Therefore, proper spray nozzle selection and the correct combination of spray nozzle pressure, spray volume and ground speed should be selected to optimize droplet size, plant coverage, retention and loss due to off-target movement.
Droplet size has minimal influence on weed control from readily translocated herbicides. That is, extremely coarse or ultracoarse spray droplets may provide less coverage, compared with a smaller droplet spectrum, but control between droplet spectrums should be equivalent.
Small spray droplets applied at high spray volume provide complete leaf coverage and are retained more than large droplets on hard-to-wet leaves such as vertical, waxy or small leaves. Small spray droplets uniformly covering the leaf surface provide better efficacy from contact herbicides than larger droplets or smaller droplets with insufficient leaf surface coverage.
Large spray droplets will better penetrate a spray canopy and drift less than small droplets. Droplet size is increased by:
- Reducing spray pressure
- Increasing nozzle orifice size
- Special drift reduction nozzles
- Adjuvants that increase spray viscosity
- Rearward nozzle orientation on aircraft.
Factors affecting uptake
The postemergence herbicide rate of uptake and amount absorbed often are determined by chemical and physical relationships between the leaf surface and the herbicide. Factors such as plant size and age, water stress, air temperature, relative humidity and adjuvants can influence the rate and amount of herbicide uptake.
Adjuvants such as petroleum oil concentrates or methylated seed oils, nonionic surfactants or liquid fertilizer solutions can increase a plant’s herbicide uptake.
Hot and dry conditions, mature weeds and weeds growing under drought stress all can reduce herbicide uptake.
The amount and rate of herbicide uptake influences the potential for crop injury and weed control, and often explains year-to-year variation in the effectiveness of herbicides. Also, rapid herbicide absorption by plants will reduce the time that rain or sunlight degradation can remove the herbicide.
Postemergence herbicides, like soil-applied herbicides, differ in their movement within a plant. For adequate weed control, nonmobile postemergence herbicides must cover plants thoroughly. Nonmobile herbicides often are called contact herbicides and include the bipyridylium, diphenyl-ether, 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 generally move upward and downward with the food transport system to the growing points of the shoots and roots. In general, injury symptoms will be most prominent at the sites where mobile herbicides accumulate.
Herbicide resistance is defined by the Weed Science Society of America as
“the inherited ability of a plant to survive and reproduce following exposure to a dose of herbicide normally lethal to the wild type. In a plant, resistance may be naturally occurring or induced by such techniques as genetic engineering or selection of variants produced by tissue culture or mutagenesis.”
Plants not controlled by herbicides before any selection pressure or genetic manipulation would be considered naturally tolerant but not herbicide resistant.
How resistance develops
Resistant weeds usually are selected from the existing field population through repeated treatment over time with a given herbicide or herbicides having the same site of action. Herbicide-resistant weed seed populations begin as a small percentage of the original population and consist of one or more rare variants within a species that resist a herbicide that usually kills the weed species.
Susceptible biotypes are reduced in the seed bank through repeated use of the herbicide or herbicides with the same site of action, while resistant biotypes increase until the weed population is no longer controlled effectively with that group of herbicides.
Herbicide resistance may be based on many different factors:
- Differential absorption.
- An altered site of action.
- Sequestration of the herbicides.
- Overexpression of the target protein.
Herbicide resistance can result from a single gene mutation or a combination of multiple gene changes.
Single-gene mutation resistance often confers a relatively high level of resistance, and population shifts occur rapidly. Multiple gene resistance often is a lower level of resistance that gradually increases through time and is more difficult to confirm.
An understanding of the way herbicides act to kill weeds (herbicide mode of action) is useful in selecting and applying the proper herbicide for a given weed control problem. Herbicide mode of action information also is useful in diagnosing injury from herbicides.
Although many herbicides are available, they can be categorized into groups with similar chemical and phytotoxic (plant injury) properties. The Weed Science Society of America (WSSA) has developed a numbered classification system based on the herbicide site of action or the specific plant process disrupted by the herbicide.
Knowledge of herbicide sites of action allows proper selection and rotation of herbicides to reduce the risk of developing herbicide-resistant weeds.
The following webpages describe the characteristics of widely used herbicide families grouped by mode of action and the WSSA classification number (in parentheses). These eight major modes of action are:
Growth regulators (SOAs 4 & 19)
Amino acid synthesis inhibition (SOAs 2 & 9)
Lipid synthesis inhibition (SOA 1)
Seedling growth inhibition (SOAs 3, 8 & 15)
Photosynthesis inhibition (SOAs 5, 6 & 7)
Nitrogen metabolism inhibition (SOA 10)
Pigment inhibition (SOAs 13 & 27)
Cell membrane disruption (SOAs 14 & 22)
Nonherbicide injury symptoms
Sugarbeet is sensitive to temperatures of 28 degrees F or less until true leaves have developed. Plants develop a water-soaked appearance as they thaw (Photo 66). Frosted tissues later turn brown and desiccate (Photo 67). Frost injury is erratic and a plant may be killed next to another plant that appears uninjured.
Evidence indicates nurse crops planted with sugarbeet may provide some protection against frost. Sugarbeet canopies serve as a short-term insulating barrier to help minimize freeze damage to roots in the fall (Photo 68).
Close contact between insecticide and sugarbeet root can blacken or constrict root growth. Insect damage, including stand loss, can mimic stand loss caused by herbicides such as amino acid synthesis inhibitors or seedling growth inhibitors (Photo 69).
Seepage of blackened exudate from Lygus bug feeding on petiole also mimics damage caused by amino acid synthesis inhibitor (Photo 70). Yellowing and discoloration of older leaves and leaf tips mimic photosynthesis inhibitors (Photo 71).
Saturated soil can cause sugarbeet to become a bright yellow with leaves that are more erect than normal.
Root rots may occur due to excessive wet conditions and the lack of oxygen movement into root tips when soils are saturated for several days, especially when soil temperatures are high (Photo 72). Root rots and the odor of fermentation can be confused with effect of other root-rotting pathogens such as Rhizoctonia solani, Aphanoymces cochlioides or Pythium spp. (Photos 73, 74).
Water damage can cause sugarbeet to become more susceptible to postemergence herbicides. Water stress plus herbicide cause more sugarbeet injury than water stress or herbicide alone. Excessive water causes fangy roots at harvest. Fangy roots indirectly increase tare due to the amount of soil lodged between roots (Photo 75).
Water stress causes plant leaves to wilt, especially during afternoon hours when temperatures are high (Photo 76). Leaves in contact with hot soil surfaces can become scorched and eventually dry.
Water stress is relieved and leaves return to an upright position following precipitation or overnight cooler temperatures.
Leaf scorch may be confused with foliar diseases, including bacterial leaf spot (Photo 77). Leaf wilting also may be a symptom associated with root pathogens such as aphanomyces or rhizomania. These problems can be distinguished by making evaluations during morning hours.
Hail storms may occur at any time during the growing season (Photo 78). Hail reduces tonnage and sugar quality but is dependent on timing and intensity.
In general, damage to foliage later in the season has greater impact on tonnage than damage earlier in the season. Intensity of defoliation also impacts sugar quality.
The greatest potential for damage from wind occurs in the early stages of growth. Damage often is associated with soil particles blown across the soil surface (Photo 79).
Portions of the root system may be exposed as soil is removed, or small plants may be buried by soil deposits in extreme cases (Photo 80).
Many diseases and insects affect sugarbeet. The Compendium of Beet Diseases and Pests, Second Edition, published by the American Phytopathological Society, provides extensive descriptions and pictures of disease symptoms and insect damage as well as nutritional disorders, drought, hail, lighting, crusting, salt injury and others.
Images of important diseases in sugarbeet can be seen in Photos 81 and 82.
Terms and Herbicide Classification
Callus tissue – a mass of plant cells that forms at a wounded surface.
Chimera – tissue that is a mixture of two or more genetically diverse types of cells. Chimeras also may arise by a mutation in cells of a growing region. The new kind of tissue may be conspicuously different from the old (as when it is bleached instead of green).
Chloroplast – a membrane-enclosed structure that contains the green pigment molecule (chlorophyll) essential for photosynthesis (food production).
Contact herbicides – 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 (for example, stems or leaf petioles) downward 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 generally are dark brown.
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 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 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, herbicide and other soluble materials from one plant part to another.
Translucent – an absence of leaf tissue pigments that results in the diffusion of light, making the plant appear off-white.
Xylem – plant tissue that functions as a conduit for the upward movement (translocation) of water from the roots to above-ground plant parts
Table 1. WSSA classification number, site of action abbreviation and full description for herbicides.
|Number||Site of action (abbrev.)||Site of action (full)|
|1||ACCase||acetyl-CoA carboxylase inhibitor|
|2||ALS||acetolactate synthase inhibitor|
|3||MT||microtubule assembly inhibitor|
|5||PSII(A)||photosystem II inhibitor, binding site A (binding behavior is different than group 7)|
|6||PSII(B)||photosystem II inhibitor, binding site B|
|7||PSII(A)||photosystem II inhibitor, binding site A (binding behavior is different than group 5)|
|8||LS||lipid synthesis inhibitor, not ACCase|
|9||EPSPS||enolpyruvyl-shikimate-phosphate synthase inhibitor|
|10||GS||glutamine sythetase inhibitor|
|12||PDS||phytoene desaturase synthesis inhibitor|
|13||DOXP||deoxyxylulose phosphate synthatase inhibitor|
|14||PPO||protoporphyrinogen oxidase inhibitor|
|15||VLCFA||very long chain fatty acid synthesis inhibitor|
|19||ATI||auxin transport inhibitor|
|22||ED||photosystem I electron diverter|
|27||HPPD||hydroxyphenylpyruvate dioxygenase inhibitor|
Gunsolus, J.L., and W.S. Curran. 2002. Herbicide mode of action and injury symptoms. North Central Regional Extension Publication 377.
Harveson, R.M., and C.D. Yonts. 2011. Abiotic Disease of Sugarbeets in Nebraska. Institute of Agriculture and Natural Resources, University of Nebraska-G2045.
Harveson, R.M., L.E. Hanson and G.L. Hein., ed. 2009. Compendium of Beet Diseases and Pests, Second Addition. American Phytopathological Society, St. Paul, Minn. 140 pp.
Klingman, G.C., and F.M. Ashton. 1975. Weed Science Principles and Practices. Wiley Interscience, New York, N.Y. 431 pp.
Shaner, D.L., ed. 2014. Herbicide Handbook. Weed Science Society of America, Champaign, Ill. 513 pp.
CAUTION: Mention of a pesticide or use of a pesticide label is for educational purposes only. Always follow the pesticide label directions attached to the pesticide container you are using. Remember, the label is the law.
Reviewed in 2018