Tribenuron-methyl-resistant Descurainia sophia L. exhibits negative cross-resistance to imazethapyr conferred by a Pro197Ser mutation in acetolactate synthase and reduced metabolism.

BACKGROUND

Descurainia sophia L. is one of the most notorious weeds infesting winter wheat in China. Mutations at Pro197 in acetolactate synthase (ALS) results in resistance of D. sophia to tribenuron-methyl and cross-resistance to many ALS inhibitors. Negative cross-resistance to imazethapyr was observed in tribenuron-methyl-resistant (TR) D. sophia with the Pro197Ser mutation in a previous study. In the present research, another TR D. sophia with the Pro197Ser mutation was obtained. To explore the mechanisms of negative cross-resistance, the ALS sensitivity, the absorption and metabolism of imazethapyr in tribenuron-methyl-susceptible (TS) and TR D. sophia were studied.

RESULTS

The TR D. sophia population with the Pro197Ser mutation (pHB23) displayed negative cross-resistance to imazethapyr and no cross-resistance to imazamox and imazapic. In contrast, TR D. sophia populations with other Pro197 mutations had no or low resistance to imazethapyr. The ALS in the pHB23 population was more susceptible to imazethapyr than that in the TS population. There was no difference in the absorption of imazethapyr, imazamox, and imazapic between TS and pHB23 plants. However, the metabolism of imazethapyr in TS D. sophia was faster than that in pHB23 plants up to 1 week after treatment. There was no significant difference in the metabolism of imazamox and imazapic between TS and pHB23 plants.

CONCLUSION

The TR D. sophia population with the Pro197Ser mutation exhibited negative cross-resistance to imazethapyr, which was likely due to reduced metabolism and increased sensitivity of ALS to imazethapyr. © 2021 Society of Chemical Industry.