Quizalofop-p-ethyl resistance in Polypogon fugax involves glutathione S-transferases

Background

Asiaminor bluegrass (Polypogon fugax) is one of the main weeds invading Chinese canola fields. The P. fugax resistant population SC-R, which survived quizalofop-p-ethyl at the field-recommended rate (67.5 g ha−1), was collected from a canola field in Qingsheng County in China. The present study aimed to (1) characterize the SC-R resistance pattern to acetyl-CoA carboxylase (ACCase)-inhibiting herbicides, and (2) investigate the mechanism of quizalofop-p-ethyl resistance in this population.

Results

Dose–response studies showed that resistance to quizalofop-p-ethyl and haloxyfop occurred in the SC-R population. Four transcripts/genes encoding the plastidic ACCase carboxyl-transferase domain were isolated from the P. fugax plants. No mutations in the four ACCase genes were detected in the SC-R population compared to the SC-S population. Pre-treatment with the known glutathione S-transferase (GST) inhibitor 4-chloro-7-nitrobenzoxadiazole (NBD Cl), reversed resistance to quizalofop-p-ethyl and partially reversed resistance to haloxyfop-R-methyl in the resistant population (SC-R). However, the cytochrome P450 inhibitor malathion did not reverse the resistance. There was no difference in basal GST activity (using CDNB as a substrate), but there was higher inducible GST activity in SC-R relative to SC-S. Two GST genes, GST2c and GSTL3, were constitutively overexpressed in the resistant SC-R population.

Conclusion

This study confirmed that resistance to quizalofop-p-ethyl in the resistant P. fugax population is likely nontargetsite based involving GST, and this resistance mechanism also partially confers haloxyfop-R-methyl resistance.