A goosegrass biotype with suspected resistance to acetyl-CoA carboxylase (ACCase) inhibitors was identified in Georgia. The objectives of this research were to evaluate the resistance level of this biotype to ACCase inhibitors, efficacy of various herbicide mechanisms of action for control, and the physiological and molecular basis of resistance. In greenhouse experiments, the rate of diclofop-methyl that reduced dry shoot biomass 50% (SR₅₀) from the nontreated for the resistant (R) and susceptible (S) biotypes measured 4,100 and 221 g ai ha⁻¹, respectively. The SR₅₀ for sethoxydim measured 615 and 143 g ai ha⁻¹ for the R and S biotype, respectively. The R biotype was cross resistant to clethodim, fenoxaprop, and fluazifop. The R and S biotypes were equally susceptible to foramsulfuron, glyphosate, monosodium methylarsenate (MSMA), and topramezone. In laboratory experiments, the two biotypes had similar foliar absorption of ¹⁴C-diclofop-methyl. Both biotypes metabolized ¹⁴C-diclofop-methyl to diclofop acid and a polar conjugate, but the R biotype averaged ∼2 times greater metabolism than the S biotype. Gene sequencing revealed an Asp-2078-Gly substitution in the ACCase of the R biotype that has previously conferred resistance to ACCase inhibitors. A second mutation was identified in the R biotype that yielded a Thr-1805-Ser substitution that has been previously reported, but is not associated with ACCase resistance in other species. Thus, the Asp-2078-Gly substitution is the basis for resistance to ACCase inhibitors for the R biotype. This is the first report of ACCase-inhibitor resistance in goosegrass from the United States and from a turfgrass system.

Nomenclature: Goosegrass, Eleusine indica (L.) Gaertn.