ISU Weed Science Online - Herbicide Site of Action

Iowa State University

Herbicide Site of Action
Bob Hartzler
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March 17, 1998 - Knowing the site of action of a herbicide is necessary to plan an effective herbicide rotation scheme to delay the development of herbicide resistant weeds. Jamie Retzinger (American Cyanamid - Iowa) and Carol Mallory-Smith (Oregon State University) recently developed a classification system for identifying herbicide site of action (Retzinger, Jr., E.J. and C. Mallory-Smith. 1997. Classification of herbicides by site of action for weed resistance management strategies. Weed Technol. 11:384-393.). The following table is adapted from this publication and lists herbicides according to site of action and chemical family. Herbicides that are no longer being marketed are included in this table. Not all herbicides from certain families are included in this table. A partial list of tradenames is included, but is not meant to be all inclusive. Package mixes including the active ingredient are listed in italics.

A brief description of the different sites and modes of action follows the table.

Group	Site of Action	Family	Active Ingredient	U.S. Trade Name
1	ACC-ase inhibitor	Aryloxyphenoxy propionate Cyclohexanediones	diclofop fenoxaprop fluazifop quizalofop-p clethodim sethoxydim	Hoelon Whip, Acclaim, Fusion Fusilade 2000, Fusion Assure Select Poast, Poast Plus
2	ALS inhibitors	Sulfonylurea Imidazolinone	prosulfuron chlorimuron metsulfuron halosulfuron nicosulfuron primisulfuron rimsulfuron sulfometuron thifensulfuron foramsulam AC 299,263 imazapyr imazaquin imazethapyr flumetsulam chloransulam-methyl pyrithiobac	Peak, Exceed, Spirit Classic, Pinnacle, Canopy XL, Synchrony, Canopy Ally, Escort Permit Accent, Accent Gold, Basis Gold, Celebrity, Celebrity Plus Beacon Titus Oust Pinnacle Option Raptor Arsenal, Lightning Scepter, Detail, Backdraft, Squadron, TriScept, Steel Pursuit, Contour, Lightning, Pursuit Plus, Steel, Resolve Broadstrike,Python First Rate Staple
3	Microtubule inhibitors	Dinitroanilines Pyridazines	benefin ethalfluralin oryzalin pendimethalin trifluralin dithiopyr	Balan Sonalan Surflan Prowl, Pendimax, Pursuit Plus, Steel Treflan, TriScept, Treflan + Broadstrike Dimension
4	Synthetic auxins	Phenoxys Benzoic acids Carboxylic acids Quinoline carboxylic acid	2,4-D 2,4-DP dichlorprop; 2,4-DP MCPA MCPB MCPP dicamba clopyralid picloram triclopyr quinclorac	Various tradenames Banvel, Clarity, Resolve, Distinct, Celebrity, Celebrity Plus, Marksman, Northstar, Optill Reclaim, Stinger, Curtail, Hornet Tordon Garlon, Crossbow Facet
5	Inhibition of photosynthesis at PSII	Triazines Triazinones Uracils	ametryne atrazine cyanazine prometon simazine hexazinone metribuzin bromacil terbacil	Evik Aatrex, atrazine, many package mixes Bladex Pramitol Princep Velpar Sencor, Lexone Hyvar XL Sinbar
6	PSII inhibitor – different binding behavior than 5	Nitriles Benzothidiazole Phenyl-pyridazine	bromoxynil bentazon pyridate	Buctril, Buctril + Atrazine Basagran, Laddok Tough
7	PSII inhibitor – different binding behavior than 5 & 6	Ureas Amide	diuron linuron tebuthiuron propanil	Karmex Lorox Spike Stam
8	Inhibition of lipid synthesis	Thiocarbamates	butylate EPTC vernolate	Sutan + Eptam, Eradicane Vernam
9	Inhibition of EPSP	None	glyphosate	Roundup, Touchdown, many generic products
10	Inhibition of glutamine synthetase	None	glufosinate	Liberty, Liberty ATZ
11	Inhibition of carotenoid synthesis at unknown site (bleaching)	Triazole	amitrole	Amitrol T
12	Inhibition of carotenoid synthesis at phytoene desaturase (PDS)	Pyridazinone Others	norflurazon fluridone	Zorial Sonar
13	Inhibition of diterpenes (bleaching)	Isoxazolidinone	clomazone	Command, Commence
14	Inhibition of protoporphyrinogen oxidase (PPO)	Diphenylethers N-phenylphthalamides Triazolinone	acifluorfen fomesafen lactofen oxyfluorfen CGA-248757 flumiclorac sulfentrazone carfentrazone flumioxazin	Blazer, Status Reflex, Flexstar Cobra Goal Action Resource Authority, Canopy XL Aim Valor
15	Unknown	Chloroacetamides Oxyacetamides	acetochlor alachlor butachlor metolachlor pronamide proplachlor dimethenamid BAY FOE 5043	Harness, Surpass, Degree, Harness Xtra, Degree Xtra, FulTime, TopNotch, Surpass 100 Lasso Machete Dual, Dual Magnum, Bicep, Boundary Kerb Ramrod Frontier, Detail, Leadoff Axiom, Epic, Domain
16	Unknown	Benzofuran	ethofumesate	Nortran
17	Unknown	Organoarsenicals	DSMA MSMA	Various Various
18	Inhibition of DHP	Carbamate	asulam	Asulox
19	Inhibition of indoleacetic acid action	Phthalamate	naptalam	Alanap
20	Inhibition of cellulose synthase	Nitrile	diclobenil	Casoran
21	Inhibition of cell wall synthesis site-B	Benzamide	isoxaben	Gallery
22	Inhibition of photosystem I – electron diversion	Bipyridyliums	diquat paraquat	Diquat Gramoxone
23	Inhibition of mitosis	Carbamates	chlopropham propham
24	Uncoupling – membrane disrupters	Dinitrophenol	dinoseb
25	Unknown	Arylaminopropionic acid	flamprop-methyl
26	Unknown	None	TCA
27	Unknown	Various	bromobutide cinmethylin dymron flupoxam	Cinch
28	Inhibition of 4-HPPD	Triketone Isoxazole Pyrazole	sulcotrione isoxaflutole pyrazolynate mesotrione	Balance, Epic Callisto

Group

The ACC-ase inhibitors block the activity of an enzyme (Acetyl-CoA Carboxylase) involved in fatty acid biosythesis. Resistance to these herbicides is confirmed in Iowa.
ALS (acetolactate synthase) is an enzyme involved in the sythesis of several amino acids. This enzyme is also referred to as acetohydroxy acid synthase (AHAS). Resistance to these herbicides is confirmed in Iowa.
The dinitroaniline and other herbicides in this class interfere with the organization of microtubules. They prevent polymerization of the protein tubulin into microtubules. Micotubules are involved in cell division and cell wall structure.
The synthetic auxins interfere with plant growth by disrupting hormone balance and protein synthesis. The exact mode of action is unclear, and it is believed these herbicides have several sites of action.
Several classes of herbicides disrupt photosynthesis by blocking electron transfer in Photosystem II (PSII). Herbicides in Classes 5, 6 and 7 bind to the same protein in PSII, but the herbicides exhibit different binding characteristics. For example, resistance to the triazine herbicides usually is due to a modification of the binding site. This modification usually provides resistance to herbicides in class 5, but not for herbicides in classes 6 and 7. Because of this, Basagran and Buctril will control triazine resistant weeds, even though the binding site for these herbicides has been modified. Resistance to these herbicides is confirmed in Iowa.
See 5.
See 5.
The thiocarbamate herbicides inhibit lipid synthesis, but the exact site and mode of action is unclear. These herbicides may have multiple sites of action.
Glyphosate inhibits EPSP synthase (5-enolpyruvyl-shikimate-3 phosphate synthase), an enzyme involved in the production of several amino acids. Both class 2 and class 9 herbicides inhibit amino acid synthesis, but their target sites are different enzymes and they disrupt the synthesis of different amino acids.
Glufosinate inhibits glutamine synthetase, a key enzyme in incorporating ammonium into amino acids. Blockage of this enzyme allows a buildup of phytotoxic ammonia.
The triazole herbicides block synthesis of caretenoid pigments, but the site of action is unknown. A primary role of carotenoids is to protect chlorophyll from photooxidation. These herbicides are known as bleachers because sensitive plants turn white due to the loss of chlorophyll.
These herbicides block caratenoid synthesis by inhibiting PDS (phytoene desaturase). (See 11.)
Clomozone inhibits the synthesis of all diterpenes, resulting in the loss of carotenoids and other compounds. (See 11.)
These herbicides inhibit PPO (protoporphyrinogen oxidase). Inhibition of this enzyme results in the accumulation of Proto IX, a molecule that generates singlet oxygen. Singlet oxygen is highly reactive and disrupts membranes, resulting in rapid degeneration of plant tissues.
The site of action for these herbicides is unknown; they are believed to have multiple sites of action.
Unknown site and mode of action.
The site of action is unknown, but the rapid destruction of tissue suggest that membranes are disrupted by some mechanism.
Inhibition of DHP (dihydropteroate synthase), an enzyme in folic acid synthesis, a precursor of DNA components.
Exact mechanism of action is unclear, but evidence suggests this herbicide inhibits auxin (indoleacetic acid) transport.
Diclobenil inhibits cellulose synthase, an enzyme involved in the synthesis of components of the cell wall.
Inhibits cell wall synthesis site B.
These herbicides intercept electrons moving through Photosystem I (PSI). These electrons are then passed on to other compounds, resulting in the formation of hydrogen peroxide which disrupts cellular integrity.
These herbicides inhibit mitosis, the process of cell division.
Dinoseb is believed to block enzymes involved in the transfer of energy released during respiration, resulting in disruption of membranes.
Unknown
Unknown
Unknown
Inhibit the enzyme 4-HPPD (4-hydroxyphenyl-pyruvate-dioxygenase), an enzyme involved in the synthesis of carotenoids (See 11).

Terminology:

Site of action: Primary biochemical site that is affected by the herbicide, ultimately resulting in death of the plant.

Mode of action: The sequence of events form absorption of the herbicide into the plant through plant death.

Prepared by Bob Hartzler, extension weed management specialist, Department of Agronomy, Iowa State University

For more information contact:
ISU Extension Agronomy
2104 Agronomy Hall
Ames, Iowa 50011-1010
Voice: (515) 294-1923
Fax: (515) 294-9985
http://www.weeds.iastate.edu

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Common chemical and trade names are used in this publication. The use of trade names is for clarity by the reader. Inclusion of a trade name does not imply endorsement of that particular brand of herbicide and exclusion does not imply nonapproval.