A goosegrass biotype with suspected resistance to acetyl-CoA carboxylase(ACCase) inhibitors was identified in Georgia. The objectives of thisresearch were to evaluate the resistance level of this biotype to ACCaseinhibitors, efficacy of various herbicide mechanisms of action for control,and the physiological and molecular basis of resistance. In greenhouseexperiments, the rate of diclofop-methyl that reduced dry shoot biomass 50% (SR50) from the nontreated for the resistant (R) andsusceptible (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 wascross resistant to clethodim, fenoxaprop, and fluazifop. The R and Sbiotypes were equally susceptible to foramsulfuron, glyphosate, monosodiummethylarsenate (MSMA), and topramezone. In laboratory experiments, the twobiotypes had similar foliar absorption of 14C-diclofop-methyl.Both biotypes metabolized 14C-diclofop-methyl to diclofop acidand a polar conjugate, but the R biotype averaged ∼2 times greatermetabolism than the S biotype. Gene sequencing revealed an Asp-2078-Glysubstitution in the ACCase of the R biotype that has previously conferredresistance to ACCase inhibitors. A second mutation was identified in the Rbiotype that yielded a Thr-1805-Ser substitution that has been previouslyreported, but is not associated with ACCase resistance in other species.Thus, the Asp-2078-Gly substitution is the basis for resistance to ACCaseinhibitors for the R biotype. This is the first report of ACCase-inhibitorresistance in goosegrass from the United States and from a turfgrasssystem.