Tembotrione detoxification in 4-hydroxyphenylpyruvate dioxygenase (HPPD) inhibitor-resistant Palmer amaranth (Amaranthus palmeri S. Wats.)

BACKGROUND: Resistance to the 4-hydroxyphenylpyruvate dioxygenase (HPPD)-inhibiting herbicide tembotrione in an Amaranthus palmeri population from Nebraska (NER) has previously been confirmed to be attributable to enhanced metabolism. The objective of this study was to identify and quantify the metabolites formed in Nebraska susceptible (NES) and resistant (NER) biotypes. RESULTS: NER and NES formed the same metabolites. Tembotrione metabolism in NER differed from that in NES in that resistant plants showed faster 4-hydroxylation followed by glycosylation. The T₅₀ value (time for 50% production of the maximum 4-hydroxylation product) was 4.9 and 11.9 h for NER and NES, respectively. This process is typically catalyzed by cytochrome P450 enzymes. Metabolism differences between NER and NES were most prominent under 28 °C conditions and herbicide application at the four-leaf stage. CONCLUSION: Further research with the aim of identifying the gene or genes responsible for conferring metabolic resistance to HPPD inhibitors should focus on cytochrome P450s. Such research is important because non-target-site-based resistance (NTSR) poses the threat of cross resistance to other chemical classes of HPPD inhibitors, other herbicide modes of action, or even unknown herbicides.