Abstract
AbstractPalmer amaranth is one of the most problematic weeds in cropping systems of North America, especially in midsouthern United States, because of its competitive ability and propensity to evolve resistance to several herbicide sites of action. Previously, we confirmed and characterized the first case of nontarget site resistance (NTSR) to fomesafen in a Palmer amaranth accession from Randolph County, AR (RCA). The primary basis of the present study was to evaluate the cross- and multiple-resistance profile of the RCA accession. The fomesafen dose-response assay in the presence of malathion revealed a lower level of RCA resistance when compared with fomesafen alone. The resistance index of the RCA accession, based on 50% biomass reduction, ranged from 63-fold (fomesafen alone) to 22-fold (malathion plus fomesafen), when compared with a 2007 susceptible, and 476-fold and 167-fold, respectively, relative to a 1986 susceptible check. The RCA accession was resistant to other protoporphyrinogen oxidase (PPO) inhibitors (i.e., flumioxazin, acifluorfen, saflufenacil) as well as the 4-hydroxyphenylpyruvate dioxygenase (HPPD) inhibitor tembotrione and acetolactate synthase (ALS) inhibitor pyrithiobac sodium. Sequencing of theALSgene revealed no point mutations, indicating that a target-site mechanism is not involved in conferring ALS-inhibitor resistance in the RCA accession. Of the three PPO-inhibiting herbicides tested in combination with the malathion, saflufenacil resulted in the greatest biomass reduction (80%;P< 0.05) and lowest survival rate (23%;P< 0.05) relative to nontreated plants. The application of cytochrome P450 or glutathioneS-transferase inhibitors with fomesafen did not lead to any adverse effects on soybean, suggesting a possible role for these compounds for management of NTSR under field conditions. These results shed light on the relative unpredictability of NTSR in conferring herbicide cross- and multiple resistance in Palmer amaranth.
Highlights
Weed resistance to herbicides may be conferred through two major mechanisms: target and nontarget site (Powles and Yu 2010)
The first target-site mechanism conferring protoporphyrinogen oxidase (PPO)-inhibitor resistance was reported in waterhemp [A. tuberculatus (Moq.) Sauer] in Illinois (Lee et al 2008; Patzoldt et al 2006), followed by Palmer amaranth in Arkansas (Salas et al 2016)
The fomesafen doses that caused 50% reduction in the aboveground dry biomass of the S1 (2007) and S2 (1986) were 3.78 and 0.50 g ai ha−1, respectively, whereas for the RCA accession, those doses were 238 g ai ha−1 and 83.8 g ai ha−1 (Table 2)
Summary
Weed resistance to herbicides may be conferred through two major mechanisms: target and nontarget site (Powles and Yu 2010). The more complex and less understood nontarget site resistance (NTSR) can be attributed to differences in herbicide uptake and translocation, metabolic detoxification, or sequestration mechanisms (Powles and Yu 2010; Yuan et al 2007). It was only in the past decade that the significance and implications of NTSR have started to unfold. The first target-site mechanism (namely, ΔG210) conferring PPO-inhibitor resistance was reported in waterhemp [A. tuberculatus (Moq.) Sauer] in Illinois (Lee et al 2008; Patzoldt et al 2006), followed by Palmer amaranth in Arkansas (Salas et al 2016). In light of the previous findings, the objectives of this study were to (1) determine the level of fomesafen resistance in the NTSR Palmer amaranth accession with/without malathion, (2) characterize cross-resistance patterns of the Palmer amaranth accession for different PPO class herbicides, and (3) determine the effects of malathion with other PPO-inhibiting herbicides (namely, flumioxazin, saflufenacil, and acifluorfen) in the Palmer amaranth accession
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