Johnsongrass (Sorghum halepense (L.) Moench) resistance to cycloxydim, fluazifop and propaquizafop and its impact on growth rate

Abstract

One putative-resistant (R) johnsongrass (Sorghum halepense L. Moench) population, originating from a cotton monoculture field in northern Greece, was evaluated for the possible evolution of cross-resistance to acetyl-CoA carboxylase (ACCase)- and multiple resistance to acetolactate synthase (ALS)-inhibiting herbicides, and to elucidate the levels and underlying mechanisms of resistance. Whole-plant rate-response assays showed that the R population was highly cross-resistant to the post-emergence applied ACCase-inhibiting herbicides fluazifop-P-butyl, propaquizafop (aryloxyphenoxypropionates) and cycloxydim (cyclohexanedione), but susceptible to the ACCase-inhibitor clethodim (cyclohexanedione) and the ALS-inhibitor nicosulfuron. The analysis of the ACCase gene sequence revealed a point mutation (ATA to WTA/TTA) at 1781 residue in the CT domain of ACCase, resulting in an amino acid substitution from isoleucine (Ile) to leucine (Leu). However, all sequenced plants of the S johnsongrass population were found with the wild-type allele encoding Ile-1781. The R johnsongrass population, grown without competition, produced more fresh weight, rhizome biomass and number of panicles than the S population. These findings indicate clearly that the R johnsongrass population has evolved target-site cross-resistance to three ACCase-inhibitors that increased most of its growth traits as compared with the S population, suggesting a fitness advantage associated with the ACCase Leu-1781 mutation