ABSTRACT
Two mutations Leu498 and Glu425 in the PDS gene were identified as the main cause conferring resistance to diflufenican and picolinafen in two oriental mustard populations P3 and P40. As mutations are suspected to affect fitness, this study was designed to test this hypothesis using the F2 of two crosses P3.2 (P3ââ¯×â¯Sâ) and P40.5 (P40ââ¯×â¯Sâ) of oriental mustard. The F2 plants, which segregated for target-site point mutations of PDS gene (Leu498 and Glu425) grown in monoculture and under competition with wheat in pot-trials and evaluated for growth and fecundity. All F2 individuals were genotyped by using Cleaved Amplified Polymorphic Sequence (CAPS) technique. Regression analysis showed no fitness cost in the resistant plants because no significant difference was identified in seed and biomass production within RR, RS and SS individuals. The absence of measurable negative effects on fitness associated mutations suggests that the frequency of the PDS resistance alleles will not decline in the absence of selection pressure of PDS-inhibitors.
Subject(s)
Herbicides/pharmacology , Mustard Plant/drug effects , Mustard Plant/metabolism , Niacinamide/analogs & derivatives , Oxidoreductases/genetics , Herbicide Resistance , Mustard Plant/genetics , Mutation/genetics , Niacinamide/pharmacology , Oxidoreductases/metabolism , Plant Proteins/genetics , Plant Proteins/metabolismABSTRACT
BACKGROUND: An oriental mustard population (P3) collected near Quambatook, Victoria was identified as being resistant to diflufenican by screening with the field rate (200 g a.i. ha-1 ) of the herbicide. The mechanism(s) of diflufenican resistance and its inheritance in this population were therefore investigated. RESULTS: Dose-response experiments confirmed that population P3 was 140-fold more resistant to diflufenican than susceptible populations, as determined by the comparison of 50% lethal (LD50 ) values. The phytoene desaturase (PDS) gene from five individuals each of the S1 [susceptible (S)] and P3 [resistant (R)] populations was sequenced, and a substitution of valine for leucine at position 526 (Leu-526-Val) was detected in all five individuals of P3, but not in the S1 population. Inheritance studies showed that diflufenican resistance is encoded in the nuclear genome and is dominant, as the response to diflufenican at 200 g a.i. ha-1 of F1 families was equivalent to that of the resistant biotype. The segregation of F2 phenotypes fitted a 3:1 inheritance model. Segregation of 42 F2 individuals by genotype sequencing fitted a 1:2:1 (ss:Rs:RR) ratio. CONCLUSION: Resistance to diflufenican in oriental mustard is conferred by the Leu-526-Val mutation in the PDS gene. Inheritance of resistance is managed by a single gene with high levels of dominance. © 2018 Society of Chemical Industry.
