Target-site (TSR) and non-target-site (NTSR) mechanisms confer resistance to ALS-inhibiting herbicides in Conyza bonariensis and Conyza sumatrensis

Conyza bonariensis (syn. Erigeron bonariensis) and Conyza sumatrensis (syn. Erigeron sumatrensis) are important herbicide-resistant weeds in agricultural systems worldwide. This study aimed to elucidate the mechanisms underlying resistance to acetolactate synthase (ALS)-inhibiting herbicides in biotypes from Uruguay. Dose–response assays with chlorimuron and diclosulam were conducted in the presence and absence of cytochrome P450 inhibitors (malathion or piperonyl butoxide), alongside partial sequencing of the ALS gene. Resistant biotypes of both species exhibited target-site mutations at codon Pro197, resulting in a Pro197Arg substitution in C. bonariensis and a Pro197Thr in C. sumatrensis, confirming target-site resistance (TSR). Additionally, the application of cytochrome P450 inhibitors significantly reduced resistance levels, as evidenced by marked decreases in resistance factors and herbicide dose requirements, indicating the involvement of enhanced metabolic detoxification (non-target-site resistance, NTSR). The coexistence of TSR and NTSR mechanisms demonstrates a complex resistance pattern that may contribute to cross-resistance among ALS-inhibiting herbicides. These findings highlight the role of metabolic resistance in amplifying resistance levels and emphasize the need for integrated weed management strategies, including herbicide mode-of-action rotation and diversified control practices, to mitigate the evolution and spread of herbicide-resistant Conyza spp.