Inhibition of Lipid Synthesis by Diclofop-Methyl Is Age Dependent in Roots of Oat and Corn

DiTomaso, Joseph M.; Stowe, A.E.; Brown, Patrick H.

doi:10.1006/pest.1993.1023

Cited by 7 publications

(5 citation statements)

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“…A large body of evidence indicates that the postemergence graminicides inhibit lipid biosynthesis in leaves (5,37,52), roots (19,36,38), isolated chloroplasts (39,43,46,52), and etioplasts (44,45). The inhibitory effect on biosynthesis of lipids, primarily polar lipids and triglycerides (5,19), has been shown to occur within 0.5 to 4 h after treatment in leaves of com (Zea mays L.), bamyardgrass (Echinochloa crus-galli (L.) Beauv. ), wild oat (Avena fatua L.), and wheat (Triticum aestivum L.) (37), with concentrations inhibiting activity by 50% (I 50 ) 4 ranging between 4 nM and 3 pM in sensitive grasses (Table 1).…”

Section: Mechanism Of Action Of the Graminicidesmentioning

confidence: 99%

Evidence Against a Direct Membrane Effect in the Mechanism of Action of Graminicides

Tomaso

1994

Weed sci.

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The aryloxyphenoxypropionate and cyclohexanedione herbicides, which inhibit acetyl-coenzyme A carboxylase (EC 6.4.1.2), have also been hypothesized to act at specific sites on the plasmalemma. An impermeant sulfhydryl binding agent was reported to block the diclofop acid-induced depolarization of the membrane potential (Em) in rigid ryegrass. A correlation between the antagonistic interaction with auxin herbicides both in the field and in the Emresponse, and the repolarization of Emin herbicide-resistant rigid ryegrass following removal of diclofop acid also provide support for this hypothesis. However, similar membrane responses in resistant grasses and broadleaf species suggest that the membrane response may not be important in the phytotoxic activity of the postemergence graminicides under field conditions. In addition, an antagonistic interaction was not observed in roots of susceptible grasses exposed to combinations of diclofop-methyl and 2,4-D. Furthermore, the repolarization of the Emin diclofop-resistant rigid ryegrass was correlated to differential acidification of the external solution and an increase in the protonated form of diclofop acid, rather than a site-specific interaction at the plasmalemma. Although the membrane response is probably not involved in herbicide phytotoxicity in agricultural systems, a higher extracellular pH in the resistant biotypes of rigid ryegrass may inhibit the movement of these weak-acid herbicides across the plasmalemma, and possibly contribute to increased herbicide tolerance.

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Section: Mechanism Of Action Of the Graminicidesmentioning

confidence: 99%

Evidence Against a Direct Membrane Effect in the Mechanism of Action of Graminicides

Tomaso

1994

Weed sci.

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“…Fluazifop-P-butyl inhibits the conversion of acetyl-CoA to malonyl-CoA by blocking the enzyme ACCase, which is the initial step in fatty acid synthesis (Burton et al 1989;Devine et al 1993a;Di Tomaso 1993;Rendina and Felts 1988;Secor and Cseke 1988). ACCase herbicides stop the production of phospholipids that are required for cell membrane production, cell membrane maintenance, and a variety of hormonal signaling agents throughout the plant.…”

Section: Introductionmentioning

confidence: 99%

Characterization of Fluazifop-P-butyl Activity on Bristly Starbur (Acanthospermum hispidum)

et al. 2006

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During routine use of fluazifop-P-butyl for grass control, county extension agents in Georgia observed control of bristly starbur in grower fields. Experiments to characterize the activity of fluazifop-P-butyl on bristly starbur were conducted under greenhouse conditions in Gainesville, FL, during 2001 and 2002. Fluazifop-P-butyl activity was characterized as a function of herbicide rate and time after application. Commercially available fluazifop-P-butyl was compared to technical fluazifop-P-butyl as a function of herbicide rate and bristly starbur height. Finally, injury to bristly starbur was evaluated when clethodim, diclofop, fluazifop-P-butyl, haloxyfop, quizalofop-p, and sethoxydim were applied at two growth stages. Fluazifop-P-butyl caused >90% injury to bristly starbur with all other post graminicides displaying <8% injury. Nonlinear regression revealed a sigmoidal response of bristly starbur injury to fluazifop-P-butyl. Estimates for 50 and 90% bristly starbur injury (I50and I90) were 0.07 and 0.14 kg ai/ha, respectively. There was no difference in activity of technical and commercial fluazifop-P-butyl formulations. There was a differential response of bristly starbur to fluazifop-P-butyl over time as a function of plant height at the time of treatment. However, 14 days after treatment (DAT) all treatments displayed >89% injury. Bristly starbur response to fluazifop-P-butyl was similar to injury associated with contact-type herbicides.

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“…The selectivity of the herbicides is basically based on their effects at the herbicide target site, acetyl‐CoA carboxylase (ACCase) in plastids in which de novo fatty acid synthesis takes place (Rendina & Felts 1988; Secor & Cséke 1988; Burton et al . 1989; Di Tomaso et al . 1993).…”

Section: Introductionmentioning

confidence: 99%

Susceptibility of a broad‐leaved weed, Acanthospermum hispidum, to the grass herbicide fluazifop‐butyl

Luo¹,

Matsumoto

2002

Weed Biology and Management

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Broad‐leaved plants are generally resistant to aryloxyphenoxypropionate (AOPP) and cyclohexanedione (CHD) herbicides. In laboratory experiments, however, we confirmed that Acanthospermum hispidum, a Compositae weed, was susceptible to one of the AOPP herbicides, fluazifop‐butyl, but tolerant to other AOPP herbicides (quizalofop‐ethyl and fenoxaprop‐ethyl) and a CHD herbicide (sethoxydim). The symptoms induced by fluazifop‐butyl in A. hispidum (wilting and necrosis) were distinctly different from those induced in oat (chlorosis). The period required to cause seedling death of A. hispidum (48–72 h) was shorter than that of oat (ca 15 days). The (R)‐enantiomer of fluazifop‐butyl was more active on this weed. In oat, lipid biosynthesis and acetyl‐CoA carboxylase (ACCase) activity were inhibited, and electrolyte leakage from the shoots was increased by fluazifop‐butyl and sethoxydim. In the case of A. hispidum, the membrane permeability increased and the lipid biosynthesis was inhibited only by fluazifop‐butyl. These results indicate that A. hispidum is particularly sensitive to fluazifop‐butyl, and its mechanism of action in the plant may be different from its mechanism of action in oat.

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Inhibition of Lipid Synthesis by Diclofop-Methyl Is Age Dependent in Roots of Oat and Corn

Cited by 7 publications

References 0 publications

Evidence Against a Direct Membrane Effect in the Mechanism of Action of Graminicides

Evidence Against a Direct Membrane Effect in the Mechanism of Action of Graminicides

Characterization of Fluazifop-P-butyl Activity on Bristly Starbur (Acanthospermum hispidum)

Susceptibility of a broad‐leaved weed, Acanthospermum hispidum, to the grass herbicide fluazifop‐butyl

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