Diclofop-methyl Cross-Resistance in a Chlorotoluron-Resistant Biotype ofAlopecurus myosuroides

Abstract

A chlorotoluron-resistant biotype ofAlopecurus myosuroidesfound in Spain exhibited cross-resistance to the acetyl-CoA carboxylase (ACCase)-inhibiting herbicide diclofop-methyl. Herbicide rates that inhibited shoot growth by 50% (ED50values) were determined for five aryloxyphenoxypropionates (diclofop-methyl, haloxyfop-methyl, propaquizafop, clodinafop-propargyl, and fluazifop-p-butyl) and three cyclohexanediones (cycloxydim, sethoxydim, and tralkoxydim), all of them ACCase inhibitors. Diclofop-methyl was the only herbicide with an ED50value in the resistant biotype higher than the recommended field rates. However, this biotype also displayed a significant increase in tolerance to tralkoxydim and all the other aryloxyphenoxypropionates tested. There were no differences in the retention, penetration, and translocation of diclofop-methyl between resistant and susceptible biotypes. ACCase from the resistant biotype was slightly less sensitive to the aryloxyphenoxypropionates and cyclohexanediones assayed than was ACCase from the susceptible biotype; however, these values where 10 times lower than those described in other resistant weed biotypes with mutated ACCase. Metabolism studies revealed that both biotypes were able to conjugate diclofop-methyl metabolites via ester conjugation and aryl-O-glucosidation. However, the resistant biotype was able to conjugate twice the amount observed in the susceptible biotype 72 hr after treatment. The cytochrome P450 monooxygenase inhibitor 1-aminobenzotriazole strongly inhibited metabolite conjugation in both resistant and susceptible plants, probably by reducing the formation of aryl hydroxy derivatives. This reduction of conjugate formation due to cytochrome P450 inhibition supports the role of this enzymatic system in the mechanism of resistance to diclofop-methyl in the resistant biotype ofA. myosuroides.