has become a global nuisance weed and has evolved resistance to glufosinate. The involvement of target-site resistance (TSR) in glufosinate resistance in has been elucidated, while the role of nontarget-site resistance (NTSR) remains unclear. Here, we identified a glufosinate-resistant (R) population that is highly resistant to glufosinate, with a resistance index of 13.5-fold. Molecular analysis indicated that the resistance mechanism of this R population does not involve TSR. In addition, pretreatment with two known metabolic enzyme inhibitors, the cytochrome P450 (CYP450) inhibitor malathion and the glutathione S-transferase (GST) inhibitor 4-chloro-7-nitrobenzoxadiazole (NBD-Cl), increased the sensitivity of the R population to glufosinate. The results of subsequent RNA sequencing (RNA-seq) and quantitative real-time PCR (RT-qPCR) suggested that the constitutive overexpression of a GST gene () and three CYP450 genes ( and ) may play an important role in glufosinate resistance. This study provides new insights into the resistance mechanism of .
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http://dx.doi.org/10.1021/acs.jafc.3c04325 | DOI Listing |
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