| 2 | B |
Imidazolinones, pyrimidinylthiobenzoates, sulfonylaminocarbonyltriazolinones, sulfonylureas, and triazolopyrimidines are herbicides that inhibit acetolactate synthase (ALS), also called acetohydroxyacid synthase (AHAS), a key enzyme in the biosynthesis of the branched-chain amino acids isoleucine, leucine, and valine (LaRossa and Schloss 1984). Plant death results from events occurring in response to ALS inhibition and low branched-chain amino acid production, but the actual sequence of phytotoxic processes is unclear. Clicking on the Link will take you to a list of weeds resistant to this group of herbicides.
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| 106 | 68 | 174 |
| 5 | C1 C2 |
Ureas and amides are herbicides that inhibit photosynthesis by binding to the Q B-binding niche on the D1 protein of the photosystem II complex in chloroplast thylakoid membranes. Herbicide binding at this protein location blocks electron transport from Q A to Q B and stops CO 2 fixation and production of ATP and NADPH 2 which are all needed for plant growth. However, plant death occurs by other processes in most cases. Inability to reoxidize Q A promotes the formation of triplet state chlorophyll which interacts with ground state oxygen to form singlet oxygen. Both triplet chlorophyll and singlet oxygen can abstract hydrogen from unsaturated lipids, producing a lipid radical and initiating a chain reaction of lipid peroxidation. Lipids and proteins are attacked and oxidized, resulting in loss of chlorophyll and carotenoids and in leaky membranes which allow cells and cell organelles to dry and disintegrate rapidly. some compounds in this group may also inhibit carotenoid biosynthesis (fluometuron) or synthesis of anthocyanin, RNA, and proteins (propanil), as well as effects on the plasmalemma (propanil) (Devine et al. 1993). Clicking on the Link will take you to a list of weeds resistant to this group of herbicides.
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| 53 | 34 | 87 |
| 9 | G |
Glycines (glyphosate) are herbicides that inhibit 5-enolpyruvylshikimate-3-phosphate (EPSP) synthase (Amrhein 1980) which produces EPSP from shikimate-3-phosphate and phosphoenolpyruvate in the shikimic acid pathway. EPSP inhibition leads to depletion of the aromatic amino acids tryptophan, tyrosine, and phenylalanine, all needed for protein synthesis or for biosynthetic pathways leading to growth. The failure of exogenous addition of these amino acids to completely overcome glyphosate toxicity in higher plants (Duke and Hoagland 1978; Lee 1980) suggests that factors other than protein synthesis inhibition may be involved. Although plant death apparently results from events occurring in response to EPSP synthase inhibition, the actual sequence of phytotoxic processes is unclear. Clicking on the Link will take you to a list of weeds resistant to this group of herbicides.
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| 28 | 31 | 59 |
| 1 | A |
Aryloxyphenoxypropionate (FOPs) and cyclohexanedione (DIMs) herbicides inhibit the enzyme acetylCoA carboxylase (ACCase), the enzyme catalyzing the first committed step in de novo fatty acid synthesis (Burton 1989; Focke and Lichtenthaler 1987). Inhibition of fatty acid synthesis presumably blocks the production of phospholipids used in building new membranes required for cell growth. Broadleaf species are naturally resistant to cyclohexanedione and aryloxyphenoxy propionate herbicides because of an insensitive
ACCase enzyme. Similarly, natural tolerance of some grasses appears to be due to a less sensitive ACCase (Stoltenberg 1989). An alternative mechanism of action has been proposed involving destruction of the electrochemical potential of the cell membrane, but the contribution of this hypothesis remains in question. Clicking on the Link will take you to a list of weeds resistant to this group of herbicides.
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| 0 | 51 | 51 |
| 4 | O |
Benzoic acids, phenoxycarboxylic acids, pyridine carboxylic acids, and quinoline carboxylic acids (O(4) and L(27)) are herbicides that act similar to that of endogenous auxin (IAA) although the true mechanism is not well understood. The specific cellular or molecular binding site relevant to the action of IAA and the auxin-mimicking herbicides has not been identified. Nevertheless, the primary action of these compounds appears to affect cell wall plasticity and nucleic acid metabolism. These compounds are thought to acidify the cell wall by stimulating the activity of a membrane-bound ATPase proton pump. The reduction in apoplasmic pH induces cell elongation by increasing the activity of enzymes responsible for cell wall loosening. Low concentrations of auxin-mimicking herbicides also stimulate RNA polymerase, resulting in subsequent increases in RNA, DNA, and protein biosynthesis. Abnormal increases in these processes presumably lead to uncontrolled cell division and growth, which results in vascular tissue destruction. In contrast, high concentrations of these herbicides inhibit cell division and growth, usually in meristematic regions that accumulate photosynthate assimilates and herbicide from the phloem. Auxin-mimicking herbicides stimulate ethylene evolution which may in some cases produce the characteristic epinastic symptoms associated with exposure to these herbicides. Clicking on the Link will take you to a list of weeds resistant to this group of herbicides.
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| 35 | 9 | 44 |
| 22 | D |
Bipyridyliums are examples of herbicides that accept electrons from photosystem I and are reduced to form an herbicide radical. This radical then reduces molecular oxygen to form superoxide radicals. Superoxide radicals then react with themselves in the presence of superoxide dismutase to form hydrogen peroxides. Hydrogen peroxides and superoxides react to generate hydroxyl radicals. Superoxides and, to a lesser extent, hydrogen peroxides may oxidize SH (sulfhydryl) groups on various organic compounds within the cell. Hydroxyl radical, however, is extremely reactive and readily destroys unsaturated lipids, including membrane fatty acids and chlorophyll. Hydroxyl radicals produce lipid radicals which react with oxygen to form lipid hydroperoxides plus another lipid radical to initiate a self-perpetuating chain reaction of lipid oxidation. Such lipid hydroperoxides destroy the integrity of cell membranes allowing cytoplasm to leak into intercellular spaces which leads to rapid leaf wilting and desiccation. These compounds can be reduced/oxidized repeatedly (Dodge 1982). Clicking on the Link will take you to a list of weeds resistant to this group of herbicides.
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| 23 | 10 | 33 |
| 14 | E |
Diphenylethers, N-phenylphthalimides, oxadiazoles, oxazolidinediones, phenylpyrazoles, pyrimidindiones, thiadiazoles, and triazolinones are herbicides that appear to inhibit protoporphyrinogen oxidase (PPG oxidase or Protox), an enzyme of chlorophyll and heme biosynthesis catalyzing the oxidation of protoporphyrinogen IX (PPGIX) to protoporphyrin IX (PPIX). Protox inhibition leads to accumulation of PPIX, the first light-absorbing chlorophyll precursor. PPGIX accumulation apparently is transitory as it overflows its normal environment in the thylakoid membrane and oxidizes to PPIX. PPIX formed outside its native environment probably is separated from Mg chelatase and other pathway enzymes that normally prevent accumulation of PPIX. Light absorption by PPIX apparently produces triplet state PPIX which interacts with ground state oxygen to form singlet oxygen. Both triplet PPIX and singlet oxygen can abstract hydrogen from unsaturated lipids, producing a lipid radical and initiating a chain reaction of lipid peroxidation. Lipids and proteins are attacked and oxidized, resulting in loss of chlorophyll and carotenoids and in leaky membranes which allows cells and cell organelles to dry and disintegrate rapidly (Duke 1991). Clicking on the Link will take you to a list of weeds resistant to this group of herbicides.
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| 12 | 4 | 16 |
| 15 | K3 N |
Acetamide, chloroacetamide, oxyacetamide, and tetrazolinone herbicides are examples of herbicides that are currently thought to inhibit very long chain fatty acid (VLCFA) synthesis (Husted et al. 1966; Böger et al. 2000). These compounds typically affect susceptible weeds before emergence, but do not inhibit seed germination. Clicking on the Link will take you to a list of weeds resistant to this group of herbicides.
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| 2 | 11 | 13 |
| 3 | K1 |
Benzamide, benzoic acid (DCPA), dinitroaniline, phosphoramidate, and pyridine herbicides are examples of herbicides that bind to tubulin, the major microtubule protein. The herbicide-tubulin complex inhibits polymerization of microtubules at the assembly end of the protein-based microtubule but has no effect on depolymerization of the tubule on the other end (Vaughn and Lehnen 1991), leading to a loss of microtubule structure and function. As a result, the spindle apparatus is absent, thus preventing the alignment and separation of chromosomes during mitosis. In addition, the cell plate can not be formed. Microtubules also function in cell wall formation. Herbicide-induced microtubule loss may cause the observed swelling of root tips as cells in this region neither divide nor elongate. Clicking on the Link will take you to a list of weeds resistant to this group of herbicides.
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| 2 | 10 | 12 |
| 34 | F3 |
Recent evidence suggests that clomazone is metabolized to the 5-keto form of clomazone which is herbicidally active. The 5-keto form inhibits 1-deoxy-D-xyulose 5-phosphate synthase (DOXP), a key component to plastid isoprenoid synthesis. Clomazone does not inhibit geranylgeranyl pyrophosphate biosynthesis (Croteau 1992; Weimer 1992).
Amitrole inhibits accumulation of chlorophyll and carotenoids in the light (Ashtakala, 1989), although the specific site of action has not been determined. Precursors of carotenoid synthesis, including phytoene, phytofluene, carotenes, and lycopene accumulate in amitrole-treated plants (Barry and Pallett 1990), suggesting that phytoene desaturase, lycopene cyclase, imidazoleglycerol phosphate dehydratase, nitrate reductase, or catalase may be inhibited. Other research (Heim and Larrinua 1989), however, indicates that the histidine, carotenoid, and chlorophyll biosynthetic pathways probably are not the primary sites of amitrole action. Instead, amitrole may have a greater effect on cell division and elongation than on pigment biosynthesis.
Aclonifen appears to act similar to carotenoid inhibiting/bleaching herbicides; but the exact mechanism of action in unknown. Clicking on the Link will take you to a list of weeds resistant to this group of herbicides.
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| 1 | 5 | 6 |
| 10 | H |
Phosphinic acids (glufosinate and bialophos) inhibit activity of glutamine synthetase (Lea 1984), the enzyme that converts glutamate and ammonia to glutamine. Accumulation of ammonia in the plant (Tachibana 1986) destroys cells and directly inhibits photosystem I and photosystem II reactions (Sauer 1987). Ammonia reduces the pH gradient across the membrane which can uncouple photophosphorylation. Clicking on the Link will take you to a list of weeds resistant to this group of herbicides.
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| 1 | 5 | 6 |
| 6 | C3 |
Benzothiadiazinones, nitriles, and phenylpyridazines are herbicides that inhibit photosynthesis by binding to the Q B-binding niche on the D1 protein of the photosystem II complex in chloroplast thylakoid membranes. Herbicide binding at this protein location blocks electron transport from Q A to Q B and stops CO 2 fixation and production of ATP and NADPH 2 which are all needed for plant growth. However, plant death occurs by other processes in most cases. Inability to reoxidize Q A promotes the formation of triplet state chlorophyll which interacts with ground state oxygen to form singlet oxygen. Both triplet chlorophyll and singlet oxygen can abstract hydrogen from unsaturated lipids, producing a lipid radical and initiating a chain reaction of lipid peroxidation. Lipids and proteins are attacked and oxidized, resulting in loss of chlorophyll and carotenoids and in leaky membranes which allow cells and cell organelles to dry and disintegrate rapidly. some compounds in this group may also inhibit carotenoid biosynthesis (fluometuron) or synthesis of anthocyanin, RNA, and proteins (propanil), as well as effects on the plasmalemma (propanil) (Devine et al. 1993). Clicking on the Link will take you to a list of weeds resistant to this group of herbicides.
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| 4 | 1 | 5 |
| 12 | F1 |
Amides, anilidex, furanones, phenoxybutan-amides, pyridiazinones, and pyridines are examples of compunds that block carotenoid biosynthesis by inhibition of phytoene desaturase (Bartels and Watson 1978; Sandmann and Böger 1989). Carotenoids play an important role in dissipating the oxidative energy of singlet O 2 ( 1O 2). In normal photosynthetic electron transport, a low level of photosystem II reaction center chlorophylls in the first excited singlet state transform into the excited triplet state ( 3Chl). This energized 3Chl can interact with ground state molecular oxygen (O 2) to form 1O 2. In healthy plants, the energy of 1O 2 is safely quenched by carotenoids and other protective molecules. Carotenoids are largely absent in fluridone-treated plants, allowing 1O 2 and 3Chl to abstract a hydrogen from an unsaturated lipid (e.g. membrane fatty acid, chlorophyll) producing a lipid radical. The lipid radical interacts with O 2 yielding a peroxidized lipid and another lipid radical. Thus, a self-sustaining chain reaction of lipid peroxidation is initiated which functionally destroys chlorophyll and membrane lipids. Proteins also are destroyed by 1O 2. Destruction of integral membrane components leads to leaky membranes and rapid tissue desiccation. Clicking on the Link will take you to a list of weeds resistant to this group of herbicides.
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| 4 | 1 | 5 |
| 27 | F2 |
Callistemones, isoxazoles, pyrazoles, and triketones are examples of herbicides that inhibit phydroxyphenyl pyruvate dioxygenase (HPPD), which converts p-hydroxymethyl pyruvate to homogentisate. This is a key step in plastoquinone biosynthesis and its inhibition gives rise to bleaching symptoms on new growth. These symptoms result from an indirect inhibition of carotenoid synthesis due to the involvement of plastoquinone as a cofactor of phytoene desaturase. Clicking on the Link will take you to a list of weeds resistant to this group of herbicides.
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| 4 | 1 | 5 |
| 29 | L |
Benzamides (WSSA Group 21), and nitriles (Group 20) are herbicides that inhibits cell wall biosynthesis (cellulose) in susceptible weeds (Heim et al. 1990). Clicking on the Link will take you to a list of weeds resistant to this group of herbicides.
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| 0 | 4 | 4 |
| 13 | F4 |
Clicking on the Link will take you to a list of weeds resistant to this group of herbicides.
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| 0 | 3 | 3 |
| 0 | Z |
Several herbicides have been identified as having an unknown mode of action including the arylaminopropionic acids. Clicking on the Link will take you to a list of weeds resistant to this group of herbicides.
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| 0 | 3 | 3 |
| 23 | K2 |
The carbamate herbicides, carbetamide, chlorpropham, and propham are examples of herbicides that inhibit cell division and microtubule organization and polymerization. Clicking on the Link will take you to a list of weeds resistant to this group of herbicides.
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| 0 | 1 | 1 |
| 0 | Z |
Several herbicides have been identified as having an unknown mode of action including the organic arsenicals. Clicking on the Link will take you to a list of weeds resistant to this group of herbicides.
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| 1 | 0 | 1 |
| 0 | Z |
These herbicides have not been classified herbicides. Clicking on the Link will take you to a list of weeds resistant to this group of herbicides.
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| 0 | 1 | 1 |
| 0 | Z |
Several herbicides have been identified as having an unknown mode of action including the pyrazoliums. Clicking on the Link will take you to a list of weeds resistant to this group of herbicides.
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| 0 | 1 | 1 |