Common lambsquarters (Chenopodium album L.) is a broadleaf weed that can severely damage soybean fields. Two C. album populations (1744 and 1731) suspected resistant to imazethapyr were investigated for resistance levels to imazethapyr, thifensulfuron-methyl, and fomesafen and their resistance mechanisms were investigated. Whole-plant dose-response assays revealed that, compared to the susceptible (S) population, the 1744 population was 16.5-fold resistant to imazethapyr, slightly resistant to thifensulfuron-methyl (resistance index [R/S], <3). The 1731 population was 18.8-fold resistant to imazethapyr, 2.9-fold resistant to thifensulfuron-methyl, and 5.1-fold resistant to fomesafen. In vitro acetolactate synthase (ALS) assays showed 17.1-fold and 19.3-fold resistance levels of 1744 and 1731 populations to imazethapyr respectively. ALS gene sequence analysis identified Ala122Thr amino acid substitution in the 1744 population and Ser653Thr amino acid substitution in the 1731 population. No mutations of the protoporphyrinogen oxidase (PPO) gene were detected. However, pre-treatment with malathion reversed fomesafen resistance, suggesting nontarget-site resistance mechanisms likely play a role in the 1731 population.
Keywords: Fomesafen; Imazethapyr; Multi-resistance; Mutation; Nontarget-site resistance.
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