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Avena fatua (wild oat) populations with resistance (R) to one or more herbicides have been described in numerous cropping systems worldwide. We previously reported that the R3 and R4 wild oat populations from Montana, USA, were resistant to four herbicides representing three different modes of action: tralkoxydim [acetyl-CoA carboxylase (ACCase] inhibitor), imazamethabenz and flucarbazone [acetolactate synthase (ALS) inhibitors] and difenzoquat (growth inhibitor). We now quantify resistance levels of these populations to triallate [very long chain fatty acid (VLCFA) biosynthesis inhibitor], pinoxaden (ACCase inhibitor) and paraquat (photosystem I inhibitor). Glasshouse doseresponse experiments showed that, compared with the means of two susceptible (S) populations, the R3 and R4 populations were 17.5-and 18.1-fold more resistant to triallate, 3.6-and 3.7-fold more resistant to pinoxaden, respectively, and 3.2-fold (R3) more resistant to paraquat. Pre-treatment of R plants with the cytochrome P450 inhibitor malathion partially reversed the resistance phenotype for flucarbazone (both populations), imazamethabenz (R4), difenzoquat (R4) and pinoxaden (R3), but not for tralkoxydim, fenoxaprop-P-ethyl or triallate. Target site point mutations known to confer resistance to ALS or ACCase inhibitors were not detected via DNA sequencing and allele-specific PCR assays in R plants, suggesting the involvement of non-target site resistance mechanism(s) for these herbicides. Together, our results complete the initial characterisation of wild oat populations that are resistant to seven (R3) or six (R4) herbicides from five or four mode of action families respectively.

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