BACKGROUND 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. RESULTS 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 (LD 50 ), 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 F 2 individuals were similar to the resistant biotypes. The segregation of F 2 phenotypes fitted a 3: 1 (R: S) inheritance model. CONCLUSION 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.
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Dang et al. (2017) studied this question.
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