A biotype of green foxtail found in Spain exhibited cross-resistance among acetyl-CoA carboxylase (ACCase)–inhibiting herbicides. Field doses that totally inhibited shoot fresh weight in the susceptible (S) biotype were determined for six aryloxyphenoxypropionates (clodinafop, diclofop, fenoxaprop-P, fluazifop-P, haloxyfop-P, and propaquizafop) and six cyclohexanediones (clefoxydim, clethodim, cycloxydim, sethoxydim, tepraloxydim, and tralkoxydim). The resistant (R) biotype showed cross-resistance to all herbicides except fenoxaprop-P, propaquizafop, clefoxydim, and tepraloxydim. There were no differences in the absorption, translocation, and metabolism of [¹⁴C]diclofop between the S and R biotypes. On the basis of herbicide dose that inhibited ACCase activity by 50% (I₅₀ values), ACCase of the R biotype was 5.8-, 13.9-, 20.0-, 102.4-, 416.7-, and 625.0-fold less sensitive to clethodim, haloxyfop, diclofop, fluazifop, cycloxydim, and sethoxydim, respectively, than that of the S biotype. Two multifunctional ACCase isoforms (ACCase I and ACCase II) were purified partially and separated. ACCase II was highly resistant to diclofop acid in both biotypes, with I₅₀ values ranging between 92 and 95 μM. However, the I₅₀ values observed for ACCase I revealed that the R biotype was 30.8-fold less sensitive to diclofop than the S biotype. These results suggest the mechanism of resistance in green foxtail to diclofop relates to an altered ACCase I isoform.

Nomenclature: Clefoxydim; clethodim; clodinafop; cycloxydim; diclofop; fenoxaprop; fluazifop-P; haloxyfop-P; propaquizafop; sethoxydim; tepraloxydim; tralkoxydim; green foxtail, Setaria viridis (L.) Beauv. SETVI.