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The mechanism of diflufenican resistance and its inheritance in oriental mustard ( Sisymbrium orientale L.) from Australia
Author(s) -
Dang Hue Thi,
Malone Jenna Moira,
Boutsalis Peter,
Gill Gurjeet,
Preston Christopher
Publication year - 2018
Publication title -
pest management science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.296
H-Index - 125
eISSN - 1526-4998
pISSN - 1526-498X
DOI - 10.1002/ps.4858
Subject(s) - biology , genetics , population , gene , inheritance (genetic algorithm) , genotype , dominance (genetics) , botany , medicine , environmental health
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 (LD 50 ) 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 F 1 families was equivalent to that of the resistant biotype. The segregation of F 2 phenotypes fitted a 3:1 inheritance model. Segregation of 42 F 2 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