Cross-resistance mechanisms to ACCase-inhibiting herbicides in short-spike canarygrass (Phalaris brachystachys)

Plant Physiol Biochem. 2020 Jun;151:681-688. doi: 10.1016/j.plaphy.2020.03.037. Epub 2020 Apr 20.

Abstract

Herbicides that inhibit acetyl-coenzyme A carboxylase (ACCase) are commonly used to control weedy grasses such as short-spike canarygrass (Phalaris brachystachys). Two resistant biotypes of P. brachystachys (R1 and R2) were found in different winter wheat fields in Iran. This study was done to confirm the suspected resistance observed in the field and to elucidate the resistance mechanisms involved. The results indicated that the both resistant biotypes showed cross-resistance to diclofop-methyl (DM), pinoxaden (PN) and cycloxydim (CD) herbicides. Based on the herbicide dose that inhibited 50% of the ACCase activity (I50), the ACCase activity of the resistant biotypes was less sensitive than the S biotype to DM, CD, and PN. No differences in translocation were detected between biotypes; most of the herbicide remained in the treated leaves. The 14C-DM metabolites were identified using thin-layer chromatography. Pre-treatment with the cytochrome P450 inhibitor ABT inhibited 14C-DM metabolism in the R1 biotype, indicating that metabolism is involved in the DM resistance in the R1 biotype. DNA sequencing studies found an Ile-1781-Thr change in both resistant biotypes, conferring cross-resistance to ACCase inhibitors. In general, in the R1 biotype which showed a higher level of resistance than that of the R2 biotype, cross-resistance was observed because of mutation and DM metabolism, while in the R2 biotype, the mutation confers resistance to ACCase-inhibiting herbicides. This is the first reported evidence of the mechanisms responsible for the resistance to ACCase herbicides in P. brachystachys. These results could be useful for improved management of resistant biotypes carrying similar mutations.

Keywords: Cytochrome P450; Enzyme assay; Metabolism; Mutation.

MeSH terms

  • Acetyl-CoA Carboxylase / antagonists & inhibitors
  • Herbicide Resistance* / genetics
  • Herbicides* / pharmacology
  • Iran
  • Mutation
  • Phalaris* / drug effects
  • Phalaris* / genetics

Substances

  • Herbicides
  • Acetyl-CoA Carboxylase