Abstract

Quinclorac (3,7-dichloro-quinoline-carboxylic acid) is a selective herbicide widely used to control annual grasses and certain broadleaf weeds. Echinochloa phyllopogon (Stapf) Koss. is the most noxious grass weed in California rice fields and has evolved resistance to multiple herbicides with different modes of action. A quinclorac-resistant (R) E. phyllopogon biotype found in a Sacramento Valley rice field where quinclorac has never been applied was investigated. Resistant to susceptible (S) GR(50) (herbicide rate for 50% growth reduction) ratios ranged from 6 to 17. The cytochrome P450 inhibitor malathion (200 mg L(-1)) caused R plants to become as quinclorac susceptible as S plants. Quinclorac rapidly (6 HAT) stimulated ethylene formation in S plants, but only marginally in R plants. Malathion pretreatment did not reduce ethylene formation by quinclorac-treated S and R plants. Activity of β-cyanoalanine synthase (β-CAS) in tissue extracts was 2-3-fold greater in R than in S plants, and incubation of shoot extracts with 1 mM malathion reduced β-CAS activity by 40% in both biotypes. Resistance to quinclorac in R E. phyllopogon involved at least two mechanisms: (a) insensitivity along the response pathway whereby quinclorac induces ethylene production; (b) enhanced β-CAS activity, which should enable greater HCN detoxification following quinclorac stimulation of ethylene biosynthesis. This unveils new resistance mechanisms for this multiple-resistant biotype widely spread throughout California rice fields.

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