Abstract
Herbicide-resistant corn poppy (Papaver rhoeas L.) is one of the most important broadleaved weeds and the number of resistant cases is still growing. The aims of this study were to confirm the resistance of P. rhoeas from Tunisia to ALS inhibitors and auxin mimics and investigate the mechanisms of Target-Site Resistance (TSR) and Non-Target Site Resistance (NTSR) involved. Dose–response trials to determine cross-resistance patterns for ALS inhibitors and auxin mimics were conducted in a greenhouse. In this study, multiple resistance to tribenuron-methyl and dicamba but not to 2,4-D was found in P. rhoeas populations. Cross-resistance to imazamox was confirmed as well. Sequence analysis of the ALS gene detected target-site mutations in codon 197 of the ALS gene, namely, Pro197His, Pro197Thr, Pro197Leu, and Pro197Asn. In this study, the metabolism experiments with malathion (a cytochrome P450 inhibitor) showed that malathion reduced resistance to imazamox, indicating that P450 is involved in the resistance. TSR and NTSR mechanisms to ALS inhibitors likely coexist. The findings of this study revealed a significant synergistic interaction between malathion and dicamba in particular populations, suggesting that the resistance to auxin mimics can be conferred by enhanced metabolism.
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