Mode of Action Definitions
A(1), B(2), C(15), D(22), F1(12), F2(28), F3(11,13), G(9), H(10), I(18), K(13), L(20,21,26), M(24), N(8,18), O(4), P(19)A (1) Acetyl CoA Carboxylase (ACCase) Inhibitors –
inhibits long chain fatty acid biosynthesis in grasses with concurrent safety to broadleaf weeds and crops. Most of the herbicides that inhibit this site of action have little to no soil residual activity, so the majority of the activity comes from foliar applications. Activity generally appears within the first week of application with chlorosis and a loss of apical dominance in the meristem with concurrent reddening in certain leaf tissue. Complete control of susceptible species may require two to three weeks following applications. Many of these herbicides are systemic in nature and can have activity on both annual and perennial grass weeds. Antagonism (or reduced herbicidal activity) has been observed in certain weed species when applied in mixtures with auxin mimic- 1 (O) herbicides or ALS inhibitors- 2 (B). Currently, there are 35 different species in more than 120 locations that have demonstrated resistance to this herbicide site of action; some of those species of importance to Tennessee include Italian ryegrass and johnsongrass.
TopB(2)-Acetolactate Syntase (ALS) or Acetohydroxy Acid Synthase (AHAS) Inhibitors –
inhibits the formation of the branched chain amino acids valine, leucine and isoleucine. Five major classes of chemistry inhibit this enzyme and residual activity, crop selectivity and the spectrum of weeds controlled can vary greatly depending on the herbicide selected. Activity generally appears within the first week of application as chlorosis with the possibility of some purple leaf veins appearing on the leaves of some plants; roots may have a bottlebrush appearance in some species. Complete control of susceptible species may require two to three weeks following applications. Many of these herbicides are systemic in nature and can have activity on both annual and perennial weed species. Antagonism (or reduced herbicidal activity) has been observed in certain weed species when applied in mixtures with ACCase inhibitors- 1 (A) or HPPD inhibitors- 27 (F2). Synergism (or improved herbicidal activity) has been observed in certain weed species when applied in mixtures with inhibitors of EPSP synthase- 9 (G). Currently, there are 95 different species in more than 275 locations that have demonstrated resistance to this herbicide site of action; some of those species of importance to Tennessee include common cocklebur, common waterhemp and Palmer amaranth.
TopC1 (5)- Inhibitor of photosynthesis at photosystem II site A (PSII site A) –
inhibitors of photosystem II bind to one of two sites (A or B). Through this binding they prevent the orderly flow of electrons (free electrons are generated by plants through absorption of sunlight) out of photosystem II, causing cell membrane degradation and necrosis in plant tissue. Symptoms generally appear as yellow leaf tissue in between leaf veins (interveinal chlorosis) on older leaf tissue within one to three days after application and these symptoms progress to the new leaves (meristem) of plants as the herbicide moves upward from the roots with water and other nutrients (apoplastically) over time. This chlorotic tissue typically becomes necrotic quite rapidly, but symptoms and timing can differ among various inhibitors of photosystem II. PSII inhibitors that bind to site A (C1) generally provide selective residual control of several broadleaf weeds and certain grasses in a variety of crop and non-crop environments, but a majority of the herbicides that bind to this site are used in monocot crops (i.e., turf, rice, corn, cereals, sugarcane, etc.). Because of its apoplastic movement, the success of foliar activity is generally dependent on aggressive adjuvants and applications made to smaller weeds. Synergism (or improved herbicidal activity) has been observed in certain weeds species when applied in mixtures with inhibitors of PPO- 14 (E), HPPD- 27 (F2), Photosystem I electron diverters- 22 (D) and DOXP synthase- 13 (F4). Currently, there are 66 different species in nearly 400 locations that have demonstrated resistance to this specific herbicide site of action; one species of particular importance to Tennessee is common lambsquarters.
C2 (7)- Inhibitor of photosynthesis at photosystem II site A different binding behavior than C1 (PSII site A2) –
herbicides that bind at site A2- 7 (C2) in photosystem II are usually applied preemergence in crop and non-crop areas, but most also have some significant postemergence foliar activity. Typically, herbicides that bind at this site of action generally have less movement in soil in comparison to PSII inhibitors that bind at site A- 5 (C1). This usually impacts the spectrum of weeds controlled and the type of crop selectivity when comparing these two different herbicide sites of action. Synergism (or improved herbicidal activity) has been observed in certain weed species when applied in mixtures with inhibitors of PPO- 14 (E), HPPD- 27 (F2), Photosystem I electron diverters- 22 (D) and DOXP synthase- 13 (F4). Currently, there are 21 different species in more than 50 locations that have demonstrated resistance to this specific herbicide site of action; so far, no resistant biotypes to this mode of action have been discovered in Tennessee.
C3 (6)- Inhibitor of photosynthesis at photosystem II site B (PSII site B) –
herbicides that bind to site B of the D1 protein in photosynthesis behave slightly different than those that bind to site A. Typically these compounds have little to no soil residual activity, and in general the majority of their activity is from foliar applications. In addition, susceptible weeds typically display rapid necrosis within one to two days after application, with plant death ensuing rapidly. Also, PSII site B inhibitors are generally only active against broadleaf weeds and have little to no activity on grasses. This is the reason why all are registered for use in corn and/or certain specialty crops. Synergism (or improved herbicidal activity) has been observed in certain weed species when applied in mixtures with inhibitors of PPO- 14 (E), HPPD- 27 (F2) and DOXP synthase- 13 (F4). Currently, there is only one weed (common groundsel) in only one location (Oregon) that has demonstrated resistance to this specific herbicide site of action; so far, no resistant biotypes to this mode of action have been discovered in Tennessee.
TopD (22)- Photosystem I Inhibitors –
accept free radicals near the ferrodoxin site in Photosystem I, which leads to the production of the highly oxidative compounds hydrogen peroxide, superoxide and various hydroxyl radicals that quickly peroxidize cell membranes leading to rapid cell degradation. Currently, paraquat and diquat are two bipyridylium herbicides that target this site of action. Symptoms from postemergence applications of these two herbicides can appear within one hour after application. Plants initially appear wilted and water-stressed but eventually rapid necrosis appears and plants can be completely dead in just a day or two following application. This rapid herbicidal response, coupled with no soil residual activity, has made these compounds ideal for rapid burndown of vegetation prior to planting, for use in between the rows of specialty crops or for use as a late-season crop desiccant. Antagonism (or reduced herbicidal activity) has been observed in certain weed species when applied in mixtures with EPSP synthase inhibitors- 9 (G). Synergism (or improved herbicidal activity) has been observed in certain weed species when applied in mixtures with inhibitors of PSII site A- 5 (C1), PSII site A2- 7 (C2) and glutamine synthetase- 10 (H). Currently, there are 23 different species in almost 40 locations that have demonstrated resistance to this herbicide site of action; so far, no resistant biotypes to this mode of action have been discovered in Tennessee.
E (14)- Protoporphyrinogen IX oxidase (PPG oxidase or Protox) Inhibitor –
cause cell membrane degradation by causing protoporphyrin IX to accumulate in the cytoplasm where it can react with oxygen and sunlight to create toxic oxygen species that lead to cell membrane degradation. In addition, PPO inhibitors also impair the production of chlorophyll in plants. Given these dual roles in membrane and chlorophyll degradation, it is not surprising that PPO inhibitors cause rapid burn in susceptible weeds and crops within one day after postemergence treatment. Certain PPO inhibitors also have some soil residual activity (i.e., sulfentrazone, flumioxazin, etc.), which causes susceptible weeds to germinate with yellow- to orange-colored foliage. Following exposure to sunlight, they turn necrotic quite rapidly. Many PPO inhibitors are applied for weed control in soybeans; however, more recent chemistry has established the use of PPO inhibitors in several grass and horticultural crops as well. PPO inhibitors are typically more active on broadleaf weeds in comparison to most grasses and are better on annual weeds as opposed to perennial weeds because they do not translocate well in plants. Antagonism (or reduced herbicidal activity) has been observed in certain weed species when applied in mixtures with EPSP synthase inhibitors- 9 (G). Synergism (or improved herbicidal activity) has been observed in certain weed species when applied in mixtures with PSII site B inhibitors- 6 (C3) or HPPD inhibitors- 27 (F2). Currently, there are three different species in five locations that have demonstrated resistance to this herbicide site of action; so far, no resistant biotypes to this mode of action have been discovered in Tennessee.
TopF1(12)- Inhibitior of phytoene desaturase step (PDS) -
inhibits carotenoid production by blocking the conversion of phytoene to carotene. Plants treated with phytoene desaturase inhibitors typically develop bleaching symptoms in the new leaves (meristematic tissue) during the first week after application. These bleaching symptoms progress toward necrosis and susceptible plants generally die within two to three weeks after treatment. The phytoene desaturase inhibitor norflurazon provides preemergence control of grasses, yellow nutsedge, certain broadleaf weeds in several horticultural crops. Another common herbicides in this class, fluridone, provides broad-spectrum control of several weeds in aquatic environments. Synergism (or improved herbicidal activity) has been observed in certain weed species when applied in mixtures with inhibitors of PSII site A- 5 (C1), PSII site B- 6 (C3) and PPO- 14 (E). Currently, there are two different weed species in 3 locations that have demonstrated resistance to this herbicide site of action; so far no weeds have demonstrated resistance to this herbicide site of action in Tennessee.
F2 (28)- Inhibitor of 4-hydroxyphenyl-pyruvate-dioxygenase (HPPD –
inhibits carotenoid production by impeding the production of plastoquinone, a key co-factor in carotenoid biosynthesis. In addition, the inhibition of HPPD also prevents the production of the anti-oxidant α-tocopherol (vitamin E) in susceptible plants. Plants treated with HPPD inhibitors typically develop bleaching symptoms in the new leaves (meristematic tissue) during the first week after application. These bleaching symptoms progress toward necrosis and susceptible plants generally die within two to three weeks after treatment. Most HPPD inhibitors (F2) provide postemergence control of key broadleaf weeds and certain grasses in corn; however, other herbicides in this class also provide weed control in wheat, rice and certain horticultural crops. In addition, some HPPD inhibitors (F2) have some soil residual activity and can provide preemergence weed control (i.e., mesotrione, isoxaflutole, etc.). Antagonism (or reduced herbicidal activity) has been observed in certain weed species when applied in mixtures with ALS inhibitors (A). Synergism (or improved herbicidal activity) has been observed in certain weed species when applied in mixtures with inhibitors of PSII site A- 5 (C1), PSII site B- 6 (C3) and PPO- 14 (E). Currently, there are no weeds that have demonstrated resistance to this herbicide site of action.
F3(11,13) Inhibitor of 1-deoxy-D-xylulose-5-phosphate synthatase (DOXP synthase) ?
prevents carotenoid production by inhibition of the terpenoid pathway. Currently, clomazone is the only commercial product that targets this specific site of action. Following preemergence applications, susceptible weed seedlings emerge bleached or chlorotic in appearance. These plants then become necrotic and die within five to 14 days after emergence. Clomazone controls many broadleaf and grass weeds in several horticultural crops (i.e. pumpkins, peppers, cucumbers, sweet potato, etc.), tobacco and soybean, but must be applied carefully as it is extremely volatile and can cause damage to sensitive non-target plants if used improperly. Synergism (or improved herbicidal activity) has been observed in certain weed species when applied in mixtures with PSII site A inhibitors- 5 (C1). Currently, there are no weeds that have demonstrated resistance to this herbicide site of action.
TopG (9)- 5-enolpyruvyl-shikimate-3-phosphate synthase (EPSP synthase) Inhibitors –
inhibits the formation of the aromatic amino acids phenylalanine, tryptophan and tyrosine. Currently, glyphosate is the only commercial product that targets this specific site of action. Following postemergence treatment, susceptible plants become chlorotic and stunted within five to seven days after application. Complete plant death may take up to two to four weeks following application. Glyphosate is systemic and can therefore provide excellent control of both annual and perennial weeds. However, its lack of soil residual activity creates a need for tank mix partners or multiple applications for full-season weed control. Antagonism (or reduced herbicidal activity) has been observed in certain weed species when applied in mixtures with Photosystem I electron diverters- 22 (D) or PPO inhibitors- 14 (E). Synergism (or improved herbicidal activity) has been observed in certain weeds species when applied in mixtures with ALS inhibitors- 2 (B). Currently, there are 13 different species in more than 50 locations that have demonstrated resistance to this herbicide site of action; two species of particular importance to Tennessee are horseweed and Palmer amaranth.
TopH (10)- Glutamine synthetase Inhibitors –
inhibits the conversion of the amino acid glutamate plus ammonia to the amino acid glutamine. This leads to an impairment of nitrogen metabolism and an accumulation of toxic levels of ammonia in susceptible plants, which in turn inhibits photosynthesis causing lipid peroxidation of cell membranes in the presence of sunlight. Currently, glufosinate is the primary commercial product that targets this specific site of action. This herbicide only has postemergence activity (no soil residual activity) and since it does not translocate effectively, it must be evenly applied to sufficiently control most target plants. In addition, glufosinate is very sensitive to extremes in temperature and humidity, which can impact its performance. While glufosinate is considered a non-selective herbicide, it does tend to provide more consistent control of most annual broadleaf weeds in comparison to certain grass species. Following postemergence application of glufosinate, susceptible plants tend to become chlorotic/necrotic within one to three days after application; total plant death generally occurs within five to 10 days after application. Synergism (or improved herbicidal activity) has been observed in certain weed species when applied in mixtures with inhibitors of Photosystem I electron diverters- 22 (D). Currently, there are no weeds that have demonstrated resistance to this herbicide site of action.
TopI (18)- Dihydropterate Synthetase Inhibitors –
inhibits cell division and expansion in plant meristems, perhaps by interfering with microtubule assembly or
function. Dihyropteroate synthase is an enzyme involved in folic acid synthesis which is needed for purine nucleotide biosynthesis. Asulam is the only
commercial product that targets this site of action. There are no known cases of weed resistance to inhibitors of this site of action.
K1 (3)- Inhibitor of microtubule assembly –
inhibits tubulin formation in cells, which blocks the completion of cell division (mitosis) and in turn prevents shoot elongation and the lateral root development in emerging weeds. In general, chemicals that inhibit microtubule assembly are volatile and susceptible to photolytic degradation, so the activity of many of these herbicides can be enhanced by immediate incorporation following preemergence applications. These herbicides typically control many annual grasses and certain small seeded broadleaf weeds in several grass or broadleaf crops. Weed seedlings that absorb inhibitors of microtubule assembly generally emerge abnormally with rapid cessation of vertical shoot growth. Seedlings appear stunted and roots appear club-shaped. Complete plant death occurs within one to two weeks after seedling emergence. Even though these herbicides are readily absorbed by plants, they are not systemic and therefore are only effective for preemergence control of annual weeds. Crop selectivity to inhibitors of microtubule assembly can generally be attributed to three different things: 1) the herbicide is placed in the soil where it can come in contact with emerging weed seedlings, but not emerging crop seedlings 2) crop seeds are generally larger with more energy reserves than many smaller seeded weed species and this difference allows them to better withstand the herbicidal activity of inhibitors of microtubule assembly 3) herbicide safeners are incorporated with these herbicides to improve crop safety by enhancing metabolism of the herbicide. Currently, there are 10 different species in more than 25 locations that have demonstrated resistance to this herbicide site of action; one species of particular importance to Tennessee is goosegrass.
K2 (23) - Mitosis Inhibitors -
The carbamate herbicides, carbetamide, chlorpropham, and propham, are examples of herbicides that inhibit cell division and microtuble organization and polymerization.
K3 (15) – Very Long Chain Fatty Acid (VLCFA) synthesis inhibitors –
inhibit cell growth and cell division by impairing membrane formation, which leads to inhibition of shoot and root growth in seedling weeds. In general, preemergence applications either prevent seedlings from emerging through the soil surface or seedlings emerge stunted with either very dark green or sometimes chlorotic foliage. Inhibitors of very long chain fatty acids generally provide preemergence control of many annual grasses, sedges and some small-seeded broadleaf weeds (i.e., pigweed). Herbicides in this group are registered in a number of grass and broadleaf crops; however, much of the safety afforded with many of these products in grass crops is due to the incorporation of a herbicide safener into their formulation. Currently, there are three different species in six locations that have demonstrated resistance to this herbicide site of action; so far, no resistant biotypes to this mode of action have been discovered in Tennessee.
TopL (20,21,26)- Cellulose Inhibitors –
inhibits cellulose production which prevents the proper formation of the cell wall during mitosis. Most inhibitors of cellulose synthase- 21 (L) prevent weeds from emerging above the soil surface, but those that do are often stunted, club-like in appearance and often have cracked stems. Inhibitors of cellulose synthase are generally active on a broad range of annual grasses and broadleaf weeds. Selectivity of these herbicides to certain plants is due to applications made after the target plant (i.e., crop, turf, ornamental, tree, etc.) has emerged or established and prior to the germination of weed species. Currently, there is one weed in one location that has demonstrated resistance to this herbicide site of action; so far, no resistant biotypes to this mode of action have been discovered in Tennessee.
TopM (24) - Oxidative Phosphorylation Uncouplers -
Dinitrophenols (dinoterb) are herbicides that cause near immediate membrane necrosis and disruption by uncoupling the process of oxidative phosphorylation.
TopN (8,16)-Fatty Acid and Lipid Biosynthesis Inhibitors –
thiocarbamates are the only class of chemistry that function as lipid synthesis inhibitors, but the specific site(s) of action that these herbicides target is/are not fully understood. These herbicides not only decrease the production of lipids (leading to destabilization of cell membranes and cessation of cell division or enlargement) but have also been found to inhibit the production of the plant hormone gibberellic acid (leading to plant growth reductions) and can affect chromosome and general nuclei development in the shoot cells of susceptible seedlings. In addition, many of the herbicides that target this mode of action are extremely volatile and are therefore incorporated immediately after application. Lipid synthesis inhibitors provide broad-spectrum control of many grasses and broadleaf weeds and often get their selectivity to target crops through the use of safeners or through specific placement of the herbicide in the soil profile to avoid contact with emerging crop shoots (similar to inhibitors of microtubule assembly). Typical symptoms from lipid synthesis inhibitors include stunting, dark green leaf tissue, puckered leaves (broadleaf weeds) and a special symptom called “buggy whipping” whereby the leaves of certain grasses have trouble releasing from the protective sheath of the shoot tip (coleoptile). Currently, there are eight different species in more than 15 locations that have demonstrated resistance to this specific herbicide site of action; so far, no resistant biotypes to this mode of action have been discovered in Tennessee.
TopO (4)- Synthetic auxins –
herbicides that mimic the internal plant hormone indole-3-acetic acid (IAA or auxin). These herbicides cause uncontrolled plant growth that leads to twisting, leaf cupping, stem cracking and ultimately plant death in susceptible annual and perennial broadleaf weeds and crops. Grass weeds and crops are generally safe to standard use rates of auxin herbicides due to an extra layer of specialized cells (schlerenchyma) that protect the vascular transport system (xylem and phloem) from closure due to stem twisting (epinasty). With few exceptions (i.e., picloram), auxin herbicides typically have only moderate to low residual activity, with the majority of their activity coming from foliar absorption. Symptoms typically appear within one day after application; however, susceptible plants may take up to two to four weeks to completely die. Many of these herbicides are systemic in nature and can have activity on both annual and perennial broadleaf weed species. Antagonism (or reduced herbicidal activity) has been observed in certain weed species when applied in mixtures with ACCase inhibitors- 1 (A). Synergism (or improved herbicidal activity) has been observed in certain weeds species when applied in mixtures with inhibitors of indoleacetic acid transport- 19 (P). Currently, there are 25 different species in more than 35 locations that have demonstrated resistance to this herbicide site of action; so far, no resistant biotypes to this mode of action have been confirmed in Tennessee.
TopP (19)- Auxin Transport Inhibitors –
inhibit a transport protein on the plasmalemma of cells that prevents internal plant auxins from moving out of the cells. This leads to a build-up of internal plant auxin in cells that creates symptoms similar to those caused by auxin mimic- 1 (O) herbicides. There are only two commercial compounds that inhibit this site of action 1) naptalam (Alanap) – a preemergence specialty crop herbicide (i.e., pumpkins, etc.) 2) diflufenzopyr – an auxin synergist that is currently only sold in combinations with dicamba (Distinct, Overdrive, Status). As diflufenzopyr demonstrates, inhibitors of indoleacetic acid transport- 19 (P) can be used to synergize the activity of auxin mimic- 1 (O) herbicides because they prevent these herbicides from leaving plant cells, just as they prevent internal plant auxins from doing the same thing. In addition to improving the control of certain broadleaf weeds in combinations with auxin herbicides (O) (i.e., dicamba), combinations of diflufenzopyr plus dicamba also improve herbicidal activity on certain annual grasses. Currently, there are no weeds that have demonstrated resistance to this herbicide site of action.