Acetolactate Synthase (ALS) or Acetohydroxy Acid Synthase (AHAS) Inhibitors
HRAC GROUP: B
WSSA Group: 2
The acetolactate synthase (ALS) inhibiting herbicides, also called acetohydroxyacid synthase (AHAS), have a broad spectrum of selectivity and are used at low rates as soil-applied or postemergence treatments in many cropping systems, trees and vines, roadsides, range and pasture, turf, and vegetation management. ALS herbicides are readily absorbed by both roots and foliage and translocated in both the xylem and phloem to the site of action at the growing points. ALS has diverse herbicides belonging to different chemistries including: imidazolinones, pyrimidinylthiobenzoates, sulfonylaminocarbonyltriazolinones, sulfonylureas, and triazolopyrimidines. These herbicides inhibit acetolactate synthase, a key enzyme in the pathway of biosynthesis of the branched-chain amino acids isoleucine, leucine, and valine. Plant deaths result from events occurring in response to inhibition of branched-chain amino acids, but the actual sequence of phytotoxic processes is unclear.
Injury symptoms: Injury symptoms caused by ALS Inhibitors are generally similar. However, the intensity of ALS Inhibitor symptoms varies depending on the herbicide concerned, the rate of application, and the plant species receptor involved. It is not possible, by visual observation alone, to determine what particular ALS Inhibitors may have caused plant damage. It must also be noted that many symptoms that may on first inspection appear to be related to ALS Inhibitors might in fact be symptoms resulting from other biotic or abiotic causes that are entirely unconnected to ALS exposure. In general, injury symptoms caused by ALS inhibiting herbicides are not apparent until several days after treatment. Diagnostic symptoms arising from ALS Inhibitors generally begin with chlorosis. Chlorosis associated with such ALS exposure is shiny or mottled, sometimes with discolored foliage vein. The lower sides of the leaves usually develop a purplish/reddish color. Finally, leaves may die and become necrotic. Symptoms of ALS Inhibitor injury are usually minimal on leaves that are fully expanded before exposure. Fully expanded leaves will appear wilted, crinkled, and chlorotic. Leaves that develop after treatment are chlorotic, crinkled, stunted, and distorted. Affected plants also can exhibit interveinal chlorosis, chlorotic banding on grass leaves, red leaf venation, purpling, necrotic (brown) leaf margins, and gradual death. ALS Inhibitors may stop terminal and lateral growth and cause shoot tips to die. Stems may develop a dark red color with necrotic lesions and cracks.
Growth of ALS sensitive trees, shrubs, and vines usually slows or ceases one to three weeks after exposure (this period will fluctuate depending on the maturity of the tree concerned, plant species, herbicide, rate, and environmental conditions). Where there is high ALS herbicide uptake, the meristematic tip on the stem will die followed by stem dieback. The buds below the dead parts usually grow after a period of time forming new growth that is generally stunted or distorted. After a period of time the plant will resume growth; however, such new growth will have short internodes and multiple branching. At the end of the growing season, the tree may have a "Christmas tree-like" appearance. Several of these symptoms, such as general and interveinal chlorosis, yellow spotting, necrosis, and stem dieback, may result from other causes not ALS Inhibitor damage. If ALS damage is suspected, the progression of symptoms and the study of ALS Inhibitor symptomology, in its entirety, are critical.
Chemistry Group and Common Names of ALS Inhibitors
Used in the United States