3 years ago

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

Anita Küpper, Lothar Lorentz, Patrick J. Tranel, Falco Peter, Todd A. Gaines, Peter Zöllner, Roland Beffa
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 due to enhanced metabolism. The objective of this study was to identify and quantify the metabolites formed in susceptible (NES) and NER biotypes. RESULTS NER and NES formed the same metabolites. Tembotrione metabolism in NER differed from 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 on 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.

Publisher URL: http://onlinelibrary.wiley.com/resolve/doi

DOI: 10.1002/ps.4786

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