Palmer amaranth accessions resistant to protoporphyrinogen oxidase (PPO), 5-enolpyruvyl-shikimate-3-phosphate synthase, and acetolactate synthase (ALS)-inhibitor herbicides are widespread in the Midsouth, making control difficult. Field experiments were conducted in Marion and Crawfordsville, AR, in 2016 and 2017 to assess PRE and POST herbicides labeled for use in corn, cotton, or soybean for control of multiresistant Palmer amaranth. Accessions at both locations were resistant to glyphosate and ALS inhibitors and segregating for both the R128 and ΔG210 PPO resistance mechanisms. Of the 15 herbicide treatments tested, only atrazine (1,120 g ai ha−1), pyroxasulfone (149 g ha−1), and flumioxazin (144 g ha−1) provided 85% or greater Palmer amaranth control 14 days after treatment (DAT). Visible control ratings at 35 DAT declined sharply, with no treatment providing more than 84% control, suggesting POST applications should be made no later than 28 DAT. Glufosinate (594 and 818 g ha−1), dicamba (560 g ae ha−1), 2,4-D plus glyphosate (784 g ae ha−1 plus 834 g ae ha−1), and paraquat (700 g ha−1) applied POST to 7- to 10-cm plants reduced Palmer amaranth density 83% or more 14 DAT. Both glyphosate (1,266 g ha−1) and pyrithiobac sodium (73 g ha−1) provided less than 7% Palmer amaranth control. Although flumioxazin alone at a labeled rate controlled Palmer amaranth 82% in the PRE experiment, PPO inhibitors by themselves applied POST provided no more than 37% control at 14 DAT. Effective foliar herbicides applied POST, including residual herbicides, should be made when Palmer amaranth are less than 10-cm tall for optimal control of these multiresistant Palmer amaranth accessions.

Palmer 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 the ALS gene 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 glutathione S-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.

Greenhouse studies were conducted to determine purple and yellow nutsedge response to selective placement of a 5-cm layer of pyrithiobac sodium-treated soil above, below, or above and below nutsedge tubers. Pyrithiobac sodium at 36 or 72 g ae ha−1 applied postemergence as foliar, soil, or foliar and soil treatments also was evaluated. Pyrithiobac sodium applied above, below, or above and below nutsedge tubers reduced yellow and purple nutsedge shoot number, shoot regrowth, and root-tuber dry weight at least 90%. Foliar-only treatment of pyrithiobac sodium was less effective at reducing emerged purple and yellow nutsedge numbers than application to soil only or to foliage and soil. Best reduction in yellow and purple nutsedge growth with pyrithiobac sodium was obtained with soil-incorporated treatments.

An experiment was conducted at four locations in North Carolina during 1994 and 1995 to evaluate weed control, cotton yield, fiber quality, and net returns in no-tillage bromoxynil-tolerant cotton. The experiment focused on using bromoxynil or pyrithiobac sodium applied early POST over-the-top as alternatives to fluometuron plus MSMA applied early POST directed. Fluometuron plus MSMA was more effective than bromoxynil or pyrithiobac sodium on tall morningglory, large crabgrass, goosegrass, and broadleaf signalgrass. Bromoxynil and fluometuron plus MSMA were similarly effective on common lambsquarters, common ragweed, and eclipta and more effective than pyrithiobac sodium. Pyrithiobac sodium and fluometuron plus MSMA were similarly effective on smooth pigweed and Palmer amaranth and more effective than bromoxynil. Prickly sida control by bromoxynil and pyrithiobac sodium was equal to or greater than control by fluometuron plus MSMA. All early POST herbicides controlled pitted morningglory similarly. Regardless of the early POST herbicides used, fluometuron applied PRE and cyanazine plus MSMA applied late POST directed increased control of most weeds and increased cotton yield and net returns. Bromoxynil and pyrithiobac sodium effectively substituted for fluometuron plus MSMA only in systems that included fluometuron applied PRE and cyanazine plus MSMA applied late POST directed. Effects of herbicide systems on cotton fiber quality were minor.

Field experiments were conducted in Georgia to evaluate weed control and crop tolerance with glufosinate applied to ‘PHY 485 WRF®’ cotton. This glyphosate-resistant cotton also contains a gene, used as a selectable marker, for glufosinate resistance. Three experiments were maintained weed-free and focused on crop tolerance; a fourth experiment focused on control of pitted morningglory and glyphosate-resistant Palmer amaranth. In two experiments, PHY 485 WRF cotton was visibly injured 15 and 20% or less by glufosinate ammonium salt at 430 and 860 g ae/ha, respectively, applied POST two or three times. In a third experiment, glufosinate at 550 g/ha injured cotton up to 36%. Pyrithiobac or glyphosate mixed with glufosinate did not increase injury compared to glufosinate applied alone; S-metolachlor mixed with glufosinate increased injury by six to seven percentage points. Cotton injury was not detectable 14 to 21 d after glufosinate application, and cotton yields were not reduced by glufosinate or glufosinate mixtures. A program of pendimethalin PRE, glyphosate applied POST twice, and diuron plus MSMA POST-directed controlled glyphosate-resistant Palmer amaranth only 17% late in the season. S-metolachlor included with the initial glyphosate application did not increase control, and pyrithiobac increased late-season control by only 13 percentage points. Palmer amaranth was controlled 90% or more when glufosinate replaced glyphosate in the aforementioned system. Pitted morningglory was controlled 99% by all glufosinate programs and mixtures of glyphosate plus pyrithiobac. Seed cotton yields with glufosinate-based systems were at least 3.3 times greater than yields with glyphosate-based systems because of differences in control of glyphosate-resistant Palmer amaranth.