Abstract

Two oriental mustard populations (P2 and P13) collected from Port Broughton, South Australia were identified as resistant to 2,4-D. The level of resistance, mechanism and the mode of inheritance for 2,4-D resistance in these populations were investigated. Populations P2 and P13 were confirmed to be resistant to 2,4-D at the field rate (600 g a.e. ha-1 ). P2 and P13 were 81- and 67-fold more resistant than the susceptible populations (S1 and S2) at the dose required for 50% mortality (LD50 ), respectively. No predicted amino acid modification was detected in sequences of potential target-site genes (ABP, TIR1 and AFB5). Resistant populations had reduced 2,4-D translocation compared with the susceptible populations, with 77% of [14 C]2,4-D retained in the treated leaf versus 32% at 72 h after treatment. Resistance to 2,4-D is encoded on the nuclear genome and is dominant, as the response to 2,4-D of all F2 individuals were similar to the resistant biotypes. The segregation of F2 phenotypes fitted a 3: 1 (R: S) inheritance model. Resistance to 2,4-D in oriental mustard is likely due to reduced translocation of 2,4-D out of the treated leaf. Inheritance of 2,4-D resistance is conferred by a single gene with a high level of dominance. © 2017 Society of Chemical Industry.

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