Abstract

Summary Sonchus oleraceus biotypes resistant to simazine were identified by chlorophyll fluorescence analysis of intact leaves. The mechanisms of resistance were determined on the basis of cpDNA and glutathione S‐transferase (GST) activity analyses. The results of the cpDNA analysis showed that most of the resistant biotypes had a Ser 264 Gly mutation in the psbA gene, which is responsible for an amino acid substitution in the D‐1 protein sequence. The cpDNA fragments were amplified by polymerase chain reaction and digested with restriction enzyme MaeI. Two restriction bands of 338 and 75 bp were recorded in biotypes with the target mutation, while three bands (218, 120 and 75 bp) were present in biotypes without this mutation. A second mechanism of resistance in this species was through the detoxification of simazine by conjugation with glutathione. In resistant biotypes without the above‐mentioned mutation, the average level of GST (simazine) activity in leaves was 4.5‐fold greater than in the resistant biotypes with the target mutation and 8.3‐fold greater than in the susceptible biotypes. Resistance as a result of the target mutation was more common than that achieved through detoxification by glutathione conjugation of simazine.

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