Several point mutations and metabolism confer cross-resistance to ALS-inhibiting herbicides in Tunisian wild mustard

A growing number of weed biotypes showing resistance to acetolactate synthase (ALS)-inhibitors have been reported in several species, notably including Sinapis arvensis L. Two putative resistant (R) populations of S. arvensis from Tunisia were subjected to greenhouse and laboratory investigations to validate resistance to ALS-inhibitors and to determinate the mechanisms involved. The results indicated that both populations were resistant to four distinct ALS-inhibiting herbicides, tribenuron-methyl (TM), florasulam, flucarbazone and imazamox (IMZ), thereby confirming cross-resistance between them. The dose of (TM) required to achieve a 50% reduction in plant growth (ED50) and 50% mortality (LC50) in R populations of S. arvensis was found to be at least 60 times greater than the recommended field dose (18.7 g ai ha -1 ) applied in cereal crops in Tunisia, indicating a significantly elevated resistance factor. Synergist experiments using malathion as a cytochrome P450 (Cyt-P450) inhibitor demonstrated a reduction in resistance to imazamox (IMZ) in both resistant (R) biotypes, indicating that Cyt-P450 plays a partial role in the resistance mechanism. In addition, ALS gene analysis identified three key point mutations, Pro197Ala, Asp376Glu and Trp574Leu, in both R populations. The docking analysis demonstrated that Asp376Glu mutation in S. arvensis could confer cross-resistance to IMZ and TM herbicides. CAPS and dCAPS methods were developed for detecting the Trp574Leu and Asp376Glu mutations, respectively, in S arvensis and it was shown that work efficiently. Fortunately, the study also confirmed that 2,4-D still effectively controlled S. arvensis populations. This study provides valuable insights into the mechanisms underlying herbicide resistance in S.arvensis populations from Tunisia, demonstrating that both target-site resistance (TSR) and non-target-site resistance (NTSR) contribute to the species' broad-spectrum resistance against four dissimilar ALS-inhibitors .