A number of redroot pigweed and Powell amaranth populations from various locations in Ontario, Canada, have distinct patterns of resistance to the acetolactate synthase–inhibiting herbicides imazethapyr and thifensulfuron. This suggested the presence of diverse ALS gene mutations among these populations. Seven polymerase chain reaction primer pairs were used to amplify the gene to obtain full sequence information and to determine the identity of resistance-conferring mutations. There was a high degree of similarity in the ALS gene of the two species with only five nucleotides and one amino acid differing. A total of four herbicide resistance-conferring mutations were identified in the two species. The Ala122Thr, Ala205Val, and Trp574Leu amino acid substitutions were found in redroot pigweed whereas Ala122Thr, Trp574Leu, and Ser653Thr were detected in Powell amaranth. The pattern of resistance known to be conferred by the mutations concurred with the resistance level observed at the whole plant level. Distinct mutations being found in geographically separated populations suggest that selection for resistance occurred simultaneously in different locations. It reinforces the fact that resistance to ALS inhibitors is easily selected and that growers need to take this into account when formulating weed management strategies.

Multiple-herbicide resistance represents an added weed management challenge to growers as it can considerably reduce their options for weed control. The widespread nature of triazine resistance in Ontario coupled with the more recent appearance of resistance to ALS inhibitors in Amaranthus species warranted documenting biotypes with multiple resistance. A collection of Powell amaranth and redroot pigweed biotypes that had previously been characterized for resistance to ALS inhibitors was therefore screened with atrazine. Dose–response analysis with atrazine and imazethapyr was also conducted. High-level resistance to imazethapyr and atrazine was determined in a Powell amaranth biotype from Perth County, Ontario. This biotype had a > 1,860-fold and 109-fold resistance to atrazine and imazethapyr, respectively. Sequence analysis was conducted for the psbA and ALS genes that code for the target sites of the triazines and imidazolinones, respectively. A mutation in the psbA gene was identified that coded for an amino acid substitution of glycine for serine at residue 264 of the D1 protein. This mutation is the most likely cause for triazine resistance in this biotype. Similarly, a nucleotide substitution was identified that codes for threonine in place of serine at position 652 of the ALS protein. This mutation in the ALS gene has only been observed previously in laboratory-selected mutants of arabidopsis and tobacco and is known to endow resistance to imidazolinones in plants. It is concluded that multiple resistance in this Powell amaranth biotype is due to the presence of altered target sites for triazine and imidazolinone herbicides.

Four field studies were conducted over a 3-yr period (2011 to 2013) to determine the tolerance of four soybean cultivars to pyroxasulfone (89 and 178 g ai ha−1), flumioxazin (71 and 142 g ai ha−1), and pyroxasulfone + flumioxazin (160 and 320 g ai ha−1) applied either preplant incorporated (PPI), PRE, or at the soybean cotyledon stage (COT). When pyroxasulfone + flumioxazin was applied at 160 and 320 g ai ha−1, at the cotyledon stage soybean yield was decreased by 9 and 14%, respectively. The only other treatment that decreased soybean yield was pyroxasulfone (178 g ai ha−1) applied PPI; yield was decreased by 6% despite minimal injury and dry biomass reductions observed during the season. Soybean tolerance to pyroxasulfone or flumioxazin applied alone was generally similar and injury was less than with pyroxasulfone + flumioxazin. Similarly, herbicides applied PPI and PRE were less injurious to soybean than the COT timing. Results suggest that soybean is tolerant to PPI and PRE applications of pyroxasulfone + flumioxazin but COT applications should be avoided.

Five experiments were conducted over a 2-yr period (2013 and 2014) to evaluate POST herbicides in winter wheat fields with a history of glyphosate-resistant (GR) horseweed. Control 4 wk after treatment (WAT) with pyrasulfotole + bromoxynil was 95%. Control 8 WAT with 2,4-D, dicamba + MCPA + mecoprop, clopyralid, and pyrasulfotole + bromoxynil ranged from 89 to 97%; these herbicides also reduced GR horseweed density and biomass by 97 to 99%. Single mode of action herbicides like 2,4-D controlled GR horseweed; however, multiple modes of action should be used to prevent populations from becoming incrementally more resistant under repeated selection pressure.

Pepper growers currently have limited access to many effective broadleaf herbicides. Field trials were conducted over a 3-year period in Ontario to study the effect of tank mixtures of sulfentrazone (100 or 200 g·ha−1 a.i.) with either s-metolachlor (1200 or 2400 g·ha−1 a.i.) or dimethenamid-p (750 or 1500 g·ha−1 a.i.) on transplanted bell pepper. Under weed-free conditions, there was no visual injury or reduction in plant height, fruit number, fruit size, or marketable yield of transplanted pepper with pretransplant applications of sulfentrazone applied in tank mixtures with s-metolachlor or dimethenamid-p. The tank mixture of sulfentrazone + s-metolachlor gave greater than 85% control of redroot pigweed (Amaranthus retroflexus) and eastern black nightshade (Solanum ptycanthum), but only 70% to 76% control of velvetleaf (Abutilon theophrasti), common ragweed (Ambrosia artemisiifolia), and common lambsquarters (Chenopodium album). The combination of sulfentrazone + dimethenamid-p provided good to excellent control of all weed species except velvetleaf. Based on this study, sulfentrazone and dimethenamid-p have potential for minor use registration in pepper.