Mechanism of resistance to mesotrione in an Amaranthus tuberculatus population from Nebraska, USA

Abstract

Amaranthus tuberculatus is a troublesome weed in corn and soybean production systems in Midwestern USA, due in part to its ability to evolve multiple resistance to key herbicides including 4-hydroxyphenylpyruvate dioxygenase (HPPD). Here we have investigated the mechanism of resistance to mesotrione, an important chemical for managing broadleaf weeds in corn, in a multiple herbicide resistant population (NEB) from Nebraska. NEB showed a 2.4-fold and 45-fold resistance increase to mesotrione compared to a standard sensitive population (SEN) in pre-emergence and post-emergence dose-response pot tests, respectively. Sequencing of the whole HPPD gene from 12 each of sensitive and resistant plants did not detect any target-site mutations that could be associated with post-emergence resistance to mesotrione in NEB. Resistance was not due to HPPD gene duplication or over-expression before or after herbicide treatment, as revealed by qPCR. Additionally, no difference in mesotrione uptake was detected between NEB and SEN. In contrast, higher levels of mesotrione metabolism via 4-hydroxylation of the dione ring were observed in NEB compared to the sensitive population. Overall, the NEB population was characterised by lower levels of parent mesotrione exported to other parts of the plant, either as a consequence of metabolism in the treated leaves and/or impaired translocation of the herbicide. This study demonstrates another case of non-target-site based resistance to an important class of herbicides in an A. tuberculatus population. The knowledge generated here will help design strategies for managing multiple herbicide resistance in this problematic weed species.

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

“…No differences in tembotrione uptake were observed between NER and NES, as has been shown before in HPPD inhibitor‐resistant A. tuberculatus and A. palmeri . HPPD inhibitors are translocated in both phloem and xylem .…”

“…Hydroxylation (M3) took place at a higher rate in NER plants compared with NES plants, as has been shown in mesotrione‐resistant A. tuberculatus from Illinois and Nebraska . Tembotrione hydroxylation takes place faster than hydroxylation of mesotrione, which could be correlated to tembotrione being absorbed more than twice as fast as mesotrione .…”

“…Both target‐site and non‐target‐site‐based mechanisms of resistance were identified, including enhanced metabolism, and a 4‐ to 12‐fold increase in HPPD transcript levels linked to an increase in HPPD protein in the resistant plants . Enhanced metabolism but no change in HPPD expression was also shown in the HPPD inhibitor‐resistant A. tuberculatus population from Illinois when compared with a susceptible line . Non‐target‐site resistance (NTSR) via enhanced metabolism in weeds has been suggested to be conferred by cytochrome P450s, glutathione S‐transferases (GSTs), glycosyl transferases (GTs), aryl acylamidases, and ATP‐binding cassette (ABC) transporters ABC transporters …”

Reversing resistance to tembotrione in an Amaranthus tuberculatus (var. rudis) population from Nebraska, USA with cytochrome P450 inhibitors

“…Mesotrione resistance in HPPD‐R is due to detoxification of parent compound into 4‐hydroxymesotrione, and it is not associated with TSR mechanisms . HPPD resistance in A. palmeri from Kansas was shown to involve enhanced metabolism of mesotrione and tembotrione, along with the potential contribution of increased HPPD expression .…”

“…This population was highly resistant to mesotrione (18×), followed by (fb) tembotrione (6×), and topramezone (2×). The mechanism of resistance to mesotrione in this HPPD‐R population is enhanced herbicide metabolism . Therefore, experiments were conducted in the field, greenhouse, and laboratory to determine if the mechanism of resistance was metabolism based via cytochrome 450 enzymes and to investigate the role of P450 inhibitor synergists in reversing resistance in HPPD‐R.…”