Yu Q.,Australian Herbicide Resistance Initiative M086 |
Han H.,Australian Herbicide Resistance Initiative M086 |
Cawthray G.R.,Australian Herbicide Resistance Initiative M086 |
Wang S.F.,University of Western Australia |
And 2 more authors.
Plant, Cell and Environment | Year: 2013
Lolium rigidum is an obligately cross-pollinated, genetically diverse species and an economically important herbicide resistance-prone weed. Our previous work has demonstrated that recurrent selection of initially susceptible L.rigidum populations with low herbicide rates results in rapid herbicide resistance evolution. Here we report on the mechanisms endowing low-dose-selected diclofop-methyl resistance in L.rigidum. Results showed that resistance was not due to target-site ACCase mutations or overproduction, or differential herbicide leaf uptake and translocation. The in vivo de-esterification of diclofop-methyl into phytotoxic diclofop acid was rapid and similar in resistant versus susceptible populations. However, further metabolism of diclofop acid into non-toxic metabolites was always faster in resistant plants than susceptible plants, resulting in up to 2.6-fold lower level of diclofop acid in resistant plants. This corresponded well with up to twofold higher level of diclofop acid metabolites in resistant plants. The major polar metabolites of diclofop acid chromatographically resembled those of wheat, a naturally tolerant species. Clearly, recurrent selection at reduced herbicide rates selected for non-target-site-based enhanced rates of herbicide metabolism, likely involving cytochrome P450 monooxygenases. © 2012 Blackwell Publishing Ltd. Source