Abstract
Background
Among the weeds in Iran, resistant Lolium rigidum Gaud is considered a troublesome weed in winter cereals due to its tendency to evolve cross (CR) and multiple resistance (MR) to herbicides.
Objective
This research examined the patterns and mechanisms of L. rigidum resistance to clodinafop-propargyl (CP) and mesosulfuron methyl+iodosulfuron methyl (MI).
Methods
Experiments were conducted on four putative-resistant L. rigidum biotypes and one susceptible biotype. The dose-response assay was performed on the biotypes with CP and MI. CR and MR were investigated with haloxyfop-R-methyl (HRM), sethoxydim (SD), pinoxaden (PN). and isoproturon+ diflufenican (ID) herbicides. An indirect study of the metabolism of herbicides was carried out using the cytochrome P450 monooxygenase (CYP450) inhibitors 1-aminobenzotriazole (ABT), piperonyl butoxide (PBO) and malathion. Finally, sequencing of ALS and ACCase genes was performed to investigate target-site resistance.
Results
All putative-resistant L. rigidum biotypes were resistant to CP, MI, and HRM, but susceptible to SD, PN, and ID. The indirect study showed that the P450 enzyme had no role in the evolution of resistance in L. rigidum biotypes. Resistance in this species was due to Ile-1781-Leu and Pro-197-Ser substitutions on ACCase and ALS encoding genes led to resistance, respectively.
Conclusions
Resistance in the studied L. rigidum biotypes to ALS and ACCase inhibiting was due of target site resistance. If these resistant biotypes are not controlled, they will become a problem for farmers in the region.
Cytochrome P450; multiple resistance; TSR and NTSR; wheat