Mechanism of atrazine resistance in atrazine- and HPPD inhibitor-resistant Palmer amaranth (Amaranthus palmeri S. Wats.) from Nebraska

Abstract

Palmer amaranth (Amaranthus palmeri S. Wats.) is one of the most problematic weed species in agronomic crops in the United States. A Palmer amaranth biotype multiple-resistant to atrazine and 4-hydroxyphenylpyruvate dioxygenase (HPPD) inhibitors was reported in a seed corn production field in Nebraska. Rapid detoxification mediated by cytochrome P450 monooxygenases and increased HPPD gene expression were reported as the mechanisms of mesotrione resistance in atrazine- and HPPD inhibitor-resistant Palmer amaranth biotype from Nebraska; however, the mechanism of atrazine resistance is unknown. The objectives of this study were to investigate target site or non-target site based mechanisms conferring atrazine resistance in Palmer amaranth from Nebraska. 14C-atrazine absorption and translocation studies revealed that reduced atrazine absorption or translocation were not involved as one of the mechanisms of atrazine resistance. Instead, greater 14C-atrazine absorption and recovery in treated leaves were observed in resistant compared with susceptible Palmer amaranth. No known mutations including Ser264Gly substitution in the psbA gene causing target site based atrazine resistance were observed. However, the parent 14C-atrazine was metabolized rapidly <4 h after treatment in resistant plants, conferring enhanced atrazine metabolism as the mechanism of resistance.