The Status of Plant-Growth Substances and Herbicides in 1945.

Gilbert, Francis

doi:10.1021/cr60123a001

Cited by 12 publications

(7 citation statements)

References 28 publications

(30 reference statements)

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“…There is broad consensus in the literature that this great imbalance in auxin homeostasis and interactions with other hormones in the tissue provide the basis of auxin herbicide action in susceptible dicots. Since Gilbert's statement from 1946 [17] that auxin herbicides cause susceptible plants "to grow themselves to death", the hypothesis prevailing until recently mainly seized on the observed growth abnormalities, while the ultimate cause of death remained open [2, 3,4,5,18]. A continuous overreaction and stimulation of plant metabolism, including nucleic acid and protein synthesis, was thought to elicit a deregulation of growth through distorted cell division and expansion, leading to the collapse of the correlating plant growth structure.…”

Section: The Phenomenon Of Deregulation Of Plant Growthmentioning

confidence: 99%

News from Old Compounds: The Mode of Action of Auxin Herbicides

Großmann

2002

Chemistry of Crop Protection

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Section: The Phenomenon Of Deregulation Of Plant Growthmentioning

confidence: 99%

News from Old Compounds: The Mode of Action of Auxin Herbicides

Großmann

2002

Chemistry of Crop Protection

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“…The species selectivity of most auxin herbicides and the relatively low application rates suggest a specific mode of action. However, in spite of extensive research following Gilbert's statement that auxin herbicides cause susceptible plants "to grow themselves to death" (Gilbert 1946), clear concepts of the direct and specific molecular interaction leading to their phytotoxicity have yet to emerge (Coupland 1994;Devine et al 1993;Pallett 1991;Sterling and Hall 1997). Extensive affinity for auxin-binding sites or interactions with intracellular signal transduction processes involving ion channel regulation, rapid fluctuations in cytosolic Ca"2+ -concentration, an~ ~hanges in plasma membrane potential, triggered by the activity of plasma membrane H + -ATPase, have been discussed as the primary mechanism of action (Devine et al 1993;Estelle 1992;Sterling and Hall 1997;Wang et al 1997).…”

Section: Conceptions On the Mode Of Action Of Auxin Herbicidesmentioning

confidence: 99%

Quinclorac belongs to a new class of highly selective auxin herbicides

Großmann¹

1998

Weed sci.

127

105

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Substituted quinolinecarboxylic acids, including quinclorac (BAS 514H), are a new class of highly selective auxin herbicides, which are chemically similar to naturally occurring compounds isolated from plants and soils. Quinclorac is used in rice to control important dicot and monocot weeds, particularly barnyardgrass. The herbicide has also been developed for application in turfgrass areas, spring wheat, and chemical fallow. Quinclorac is readily absorbed by germinating seeds, roots, and leaves and is translocated in the plant both acropetally and basipetally. By mimicking an auxin overdose, quinclorac affects the phytohormonal system in sensitive plants. The compound stimulates the induction of 1-aminocyclopropane-1-carboxylic acid (ACC) synthase activity and thus promotes ethylene biosynthesis. In susceptible dicots, increased levels of ethylene trigger an accumulation of abscisic acid (ABA), which, as part of the intrinsic auxin activity of quinclorac, plays a major role in growth inhibition and the induction of epinasty and senescence. In sensitive grasses, such as barnyardgrass species, large crabgrass, broadleaf signalgrass, and green foxtail, quinclorac leads particularly to an accumulation of tissue cyanide, formed as a co-product during increased ACC and ethylene synthesis. This causes phytotoxicity characterized by the inhibition of root and particularly shoot growth with tissue chlorosis and subsequent necrosis. These effects were not observed in tolerant rice and a resistant biotype of barnyardgrass. No significant differences in uptake, translocation, or metabolism of quinclorac between resistant and sensitive grasses were found. Hence, a target-site-based mechanism of selectivity is suggested. The induction process of the ACC synthase activity plays the primary role in the selective herbicide action of quinclorac. This is a common effect of auxin herbicides and auxins, which lead to the accumulation of cyanide and/or ABA depending on the plant species and tissues, the compound concentration in the tissue, and their biological activity.

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“…This phenomenon has been described as an auxin overdose or as an effect of supraoptimal endogenous auxin concentrations which lead to an imbalance in auxin homeostasis and interactions with other hormones in the tissue. However, since Gilbert's statement from 194613 that auxin herbicides cause susceptible plants ‘to grow themselves to death’, the hypothesis prevailing until recently mainly seized on the observed growth abnormalities and a subsequent catastrophe scenario. Here, a continuous stimulation of plant metabolism was thought to elicit a deregulation of growth through distorted cell division and expansion, leading to the collapse of the correlating plant growth structure 14.…”

Section: Introductionmentioning

confidence: 99%

Auxin herbicides: current status of mechanism and mode of action

Großmann¹

2009

Pest Management Science

562

486

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Synthetic compounds that act like phytohormonal 'superauxins' have been among the most successful herbicides used in agriculture for more than 60 years. These so-called auxin herbicides are more stable in planta than the main natural auxin, indole-3-acetic acid (IAA), and show systemic mobility and selective action, preferentially against dicot weeds in cereal crops. They belong to different chemical classes, which include phenoxycarboxylic acids, benzoic acids, pyridinecarboxylic acids, aromatic carboxymethyl derivatives and quinolinecarboxylic acids. The recent identification of receptors for auxin perception and the discovery of a new hormone interaction in signalling between auxin, ethylene and the upregulation of abscisic acid biosynthesis account for a large part of the repertoire of auxin-herbicide-mediated responses, which include growth inhibition, senescence and tissue decay in sensitive dicots. An additional phenomenon is caused by the quinolinecarboxylic acid quinclorac, which also controls grass weeds. Here, the accumulation of phytotoxic levels of tissue cyanide, derived ultimately from quinclorac-stimulated ethylene biosynthesis, plays a key role in eliciting the herbicidal symptoms in sensitive grasses.

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The Status of Plant-Growth Substances and Herbicides in 1945.

Cited by 12 publications

References 28 publications

News from Old Compounds: The Mode of Action of Auxin Herbicides

News from Old Compounds: The Mode of Action of Auxin Herbicides

Quinclorac belongs to a new class of highly selective auxin herbicides

Auxin herbicides: current status of mechanism and mode of action

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