Seeds from five suspected acetyl-CoA carboxylase (ACCase) inhibitor–resistant wild oat biotypes (R1 to R5) were collected in wheat and lentil fields in the Pacific Northwest. Based on whole plant dose–response experiments, the five resistant biotypes were 2 to 24 times more resistant to the aryloxyphenoxypropionate (APP) herbicides (fenoxaprop, diclofop, and quizalofop) compared with the susceptible biotype. However, none of the resistant biotypes were resistant to the cyclohexanedione (CHD) herbicides, sethoxydim and clethodim. R2 was the only biotype resistant to tralkoxydim and pinoxaden, a phenylpyrazolin herbicide and an ACCase inhibitor. The R2 biotype was 35 and 16 times more resistant to tralkoxydim and pinoxaden, respectively, when compared with the susceptible biotype. The levels of resistance and cross-resistance patterns varied among biotypes indicating either more than one mechanism of resistance or different resistance mutations in these wild oat biotypes. The CHD herbicides, sethoxydim and clethodim, could be used to control these resistant biotypes. Except for the R2 biotype, pinoxaden could be used to control the resistant wild oat biotypes. The resistance patterns of these wild oat biotypes are an indication of the difficulty in predicting cross-resistance among the ACCase inhibitor herbicides.

Nomenclature: Clethodim, diclofop, fenoxaprop, pinoxaden, quizalofop, sethoxydim, tralkoxydim, wild oat, Avena fatua L. AVEFA, lentil, Lens culinaris Medik, wheat, Triticum aestivum L