Catchweed bedstraw (Galium aparine L.) is a problematic dicot weed that occurs in major winter wheat (Triticum aestivum L.) fields in China. Tribenuron-methyl has been widely used to control broadleaf weeds since 1988 in China. However, overuse has led to the resistance evolution of G. aparine to tribenuron-methyl. In this study, 20 G. aparine populations collected from Shandong and Henan provinces were used to determine tribenuron-methyl resistance and target-site resistance mechanisms. In dose–response experiments, 12 G. aparine populations showed different resistance levels (2.92 to 842.41-fold) to tribenuron-methyl compared with the susceptible population. Five different acetolactate synthase (ALS) mutations (Pro-197-Leu, Pro-197-Ser, Pro-197-His, Asp-376-Glu, and Trp-574-Leu) were detected in different resistant populations. Individuals heterozygous for Pro-197-Ser and Trp-574-Leu mutations were also observed in a resistant population (HN6). In addition, pHB4 (Pro-197-Ser), pHB7 (Pro-197-His), pHB8 (Pro-197-Leu), pHB5 (Asp-376-Glu), and pHB3 (Trp-574-Leu) subpopulations individually homozygous for specific ALS mutations were generated to evaluate the cross-resistance to ALS-inhibiting herbicides. The pHB4, pHB7, pHB8, pHB5, and pHB3 subpopulations all were resistant to sulfonylurea, pyrazosulfuron-ethyl, triazolopyrimidine, flumetsulam, sulfonylamino-carbonyl-triazolinone, flucarbazone-sodium, pyrimidinyl thiobenzoate, pyribenzoxim, and the imidazolinone imazethapyr. These results indicated the diversity of the resistance-conferring ALS mutations in G. aparine, and all these mutations resulted in broad cross-resistance to five kinds of ALS-inhibiting herbicides.

Populations of rigid ryegrass suspected of resistance to trifluralin due to control failures exhibited varying levels of susceptibility to trifluralin, with 15 out of 17 populations deemed resistant (>20% plant survival). Detailed dose–response studies were conducted on one highly resistant field-evolved population (SLR74), one known multiply resistant population (SLR31), and one susceptible population (VLR1). On the basis of the dose required to kill 50% of treated plants (LD50), SLR74 had 15-fold greater resistance than VLR1, whereas, the multiply resistant SLR31 had 10-fold greater resistance than VLR1. Similarly, on the basis of dose required to reduce shoot biomass by 50% (GR50), SLR74 had 17-fold greater resistance than VLR1, and SLR31 had 8-fold greater resistance than VLR1. Sequencing of the α-tubulin gene from resistant plants of different populations confirmed the presence of a previously known goosegrass mutation causing an amino acid substitution at position 239 from threonine to isoleucine in resistant population SLR74. This mutation was also found in 4 out of 5 individuals in another highly resistant population TR2 and in 3 out of 5 individuals of TR4. An amino acid substitution from valine to phenylalanine at position 202 was also observed in TR4 (3 out of 5 plants) and TR2 (1 out of 5 plants). There was no target-site mutation identified in SLR31. This study documents the first known case of field-evolved target-site resistance to dinitroaniline herbicides in a population of rigid ryegrass.

Mayweed chamomile seeds were collected from six different fields across the Pacific Northwest. All populations (each collection site was considered a population) were suspected to have some level of acetolactate synthase (ALS) resistance. Greenhouse and laboratory studies were conducted to determine if these populations were resistant to three different classes of ALS inhibitors: sulfonylureas (SU), imidazolinones (IMI), and triazolopyrimidines (TP). A whole-plant dose–response and in vitro ALS activity studies confirmed cross-resistance to thifensulfuron + tribenuron/chlorsulfuron (SU), imazethapyr (IMI), and cloransulam (TP); however, resistance varied by herbicide class and population. Two ALS isoforms of the ALS gene (ALS1 and ALS2) were identified in mayweed chamomile; however, only mutations in ALS1 were responsible for resistance. No mutations were found in ALS2. Sequence analysis of the partial ALS gene identified four point mutations at position 197 (Pro197 to Leu, Gln, Thr, or Ser) in the resistant populations. This study demonstrates genotypic variation associated with cross-resistance to ALS inhibitors within and between populations.