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.
Keywords: PDS; Sisymbrium orientale L.; diflufenican; phytoene desaturase; single dominant gene; target-site mutation.
© 2018 Society of Chemical Industry.