Thiobencarb resistance mechanism is distinct from CYP81A-based cross-resistance in late watergrass (Echinochloa phyllopogon)

Abstract

AbstractThe genetic and molecular basis of resistance evolution in weeds to multiple herbicides remains unclear despite being a great threat to agriculture. A population of late watergrass [Echinochloa phyllopogon(Stapf.) Koso-Pol.] was reported to exhibit resistance to ≥15 herbicides from six sites of action, including thiobencarb (TB). While previous studies disclosed that the resistance to a majority of herbicides such as acetolactate synthase (ALS) and acetyl-CoA carboxylase inhibitors is caused by the overexpression of herbicide-metabolizing cytochrome P450s (CYP81A12andCYP81A21), the resistance mechanisms to some herbicides remain unknown. Here, we analyzed the resistance segregation in the progenies between resistant and sensitive populations and performed a transgenic plant sensitivity assay to resolve whether TB resistance is endowed by the sameCYP81A12/21-based cross-resistance mechanism or other unknown multiple-resistance mechanisms. In the F6progenies, resistance to the ALS inhibitor bensulfuron-methyl cosegregated with the resistances to many other herbicides under theCYP81A12/21-based cross-resistance mechanism; however, TB resistance segregated independently. Furthermore,CYP81A12/21failed to confer TB resistance in transgenicArabidopsis thalianaL. Heynh, thus confirming that TB resistance in resistantE. phyllopogonis not endowed by the two P450s that are responsible for the metabolism-based cross-resistance. This study provides evidence that resistance inE. phyllopogonto herbicides with multiple sites of action is endowed by both P450-based and other uncharacterized non–target site based mechanisms. Our findings add another layer in the understanding of resistance evolution to multiple herbicides inE. phyllopogon. Identification of the key genes endowing TB resistance will be the future direction of this research.