Occurrence of different resistance mechanisms to ALS inhibitors in European Sorghum halepense

populations resistant to ALS inhibitors have become a threat in European maize fi elds. Four Hungarian and two Italian S. halepense populations resistant to the ALS inhibitor nicosulfuron were investigated to elucidate the level of resistance and mechanisms underlying the resistance. A greenhouse dose-response experiment testing four diff erent ALS-inhibiting herbicides (foramsulfuron, nicosulfuron, imazamox and bispyribac-Na) was performed and a purifi ed seed stock from resistant plants was used to determine the presence of target-site and non-target-site resistance mechanism(s) through: (1) molecular analysis to detect the mutant ALS alleles; (2) in vitro ALS enzyme bioassay; (3) treatment with metabolic inhibitor (i.e. malathion 2 kg ha-1) to investigate the possible presence of enhanced metabolism. The two Italian populations (07-13 and 12-54a) were highly cross-resistant to all the ALS inhibitors tested and the mutant ALS allele Leu574 was identifi ed in all the plants. Diff erent responses were instead observed when the plants of both populations were treated with herbicide plus malathion: plants of population 12-54a showed a signifi cant decrease in plant survival and fresh weight with respect to plants of population 07-13. This suggests that an enhanced metabolism may also be involved in the resistance. The Hungarian populations (08- 16, 11-34, 11-40 and 12-49a) proved to be controlled by imazamox, while they were resistant (with diff erent levels) to sulfonylureas and bispyribac-Na. All Hungarian populations, but not all plants of population 12-49a, presented the mutant allele Glu376. ALS enzyme bioassay and treatment with malathion confi rmed that in plants of these populations the resistance is very likely due to both target-site and enhanced metabolism of P450 enzymes. The results clearly suggest that resistance to ALS inhibitors in S. halepense can be due to mutant ALS alleles and metabolic resistance.