Quinclorac resistance: a concerted hormonal and enzymatic effort in Echinochloa phyllopogon.

BACKGROUND: 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. RESULTS: 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 ß-cyanoalanine synthase (ß-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 ß-CAS activity by 40% in both biotypes. CONCLUSION: 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 ß-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.

Mechanism of resistance to penoxsulam in late watergrass [ Echinochloa phyllopogon (Stapf) Koss.].

Late watergrass [ Echinochloa phyllopogon (Stapf.) Koss.] is a major weed of California rice that has evolved P450-mediated metabolic resistance to multiple herbicides. Resistant (R) populations are also poorly controlled by the recently introduced herbicide penoxsulam. Ratios (R/S) of the R to susceptible (S) GR(50) (herbicide rate for 50% growth reduction) ranged from 5 to 9. Although specific acetolactate synthase (ALS) activity was 1.7 higher in R than in S plants, the enzyme in R plants was about 6 times more susceptible to the herbicide. R plants exhibited faster (2.8 times) oxidative [(14)C]-penoxsulam metabolism than S plants 24 h after treatment. Addition of malathion (P450 inhibitor) enhanced herbicide phytotoxicity and reduced penoxsulam metabolism in R plants. Tank mixtures with thiobencarb (can induce P450) antagonized penoxsulam toxicity in R plants, suggesting penoxsulam may be broken down by a thiobencarb-inducible enzyme. These results suggest E. phyllopogon resistance to penoxsulam is mostly due to enhanced herbicide metabolism, possibly via P450 monooxidation.