Molecular basis of resistance to sulfonylureas in Papaver rhoeas

Molecular basis of ALS- and/or ACCase-inhibitor resistance in shortawn foxtail (Alopecurus aequalis Sobol.)

“…However, following several years of successful control, more and more researchers are detecting resistance to mesosulfuron-methyl in some grass species [15,20,21].…”

Occurrence, genetic control and evolution of non-target-site based resistance to herbicides inhibiting acetolactate synthase (ALS) in the dicot weed Papaver rhoeas

“…In all cases studied, TSR has been identified. The mutation(s) responsible for the resistance were essentially found at codon Pro197 in the ALS gene [29][30][31][32][33] and, in extremely low frequency, at codon Trp574 [33]. However, recent results have shown that P. rhoeas plants with identical genotypes at ALS could exhibit differences in sensitivity to ALS inhibitors [33].…”

Evaluation of resistance to acetolactate synthase inhibiting herbicide in wild mustard (Sinapis arvensis L.)

“…ALS enzyme is the target-site of different chemical families such as sulfonylureas, imidazolinones, triazolopyrimidines, pyrimidinylthiobenzoates and sulfonylaminocarbonyl-triazolinones (Cruz-Hipolito et al, 2013). In case of target site based herbicide resistance, herbicide cannot bind to the enzyme catalytic site (Pang et al, 2002;Duran-Prado et al, 2004;Duggleby et al, 2008;Powles & Yu, 2010;Jian et al, 2011). Common amino acid substitutions in the ALS gene that confirmed target site resistance and provide protection against herbicide damage are Ala-122, Pro-197, Ala-205, Asp-376, Arg-377, Trp-574, Ser-653 and Gly-654 (Yu & Powles, 2014;Cross et al, 2015).…”

“…So, molecular approaches include sequencing (Corbett & Tardif, 2006), enable deciphering the genetic basis of resistant (Duran-Prado et al, 2004;Duggleby et al, 2008;Breccia et al, 2013;Ochogavia et al, 2014;Tranel et al, 2014). Therefore, in this study, it was investigated that whether target-site mutation confers resistance to ALS inhibitor herbicide with two active ingredient (mesosulfuron + iodosulfuron) in wild mustard (S. arvensis) or not, and, if so, the resistance levels for each homozygous/heterozygous mutation were also determined.…”