Detoxification mechanism of herbicide in Polypogon fugax and its influence on rhizosphere enzyme activities.

The excessive use of chemical herbicides has resulted in evolution of herbicide-resistant weeds. Cytochrome P450 monooxygenases (P450s) are vital detoxification enzymes for herbicide-resistant weeds. Herein, we confirmed a resistant (R) Polypogon fugax population showing resistance to quizalofop-p-ethyl, acetolactate synthase (ALS)-inhibiting herbicide pyroxsulam, and several other ACCase (acetyl-CoA carboxylase)-inhibiting herbicides. Molecular analysis revealed no target-site gene mutations in the R population. Foliar spraying with malathion clearly reversed the quizalofop-p-ethyl phytotoxicity. Higher level of quizalofop-p-ethyl degradation was confirmed in the R population using HPLC analysis. Subsequently, RNA-Seq transcriptome analysis indicated that the overexpression of CYP89A2 gene appeared to be responsible for reducing quizalofop-p-ethyl phytotoxicity. The molecular docking results supported a metabolic effect of CYP89A2 protein on most herbicides tested. Furthermore, we found that low doses of herbicides stimulated the rhizosphere enzyme activities in P. fugax and the increase of rhizosphere dehydrogenase of R population may be related to its resistance mechanism. In summary, our research has shown that metabolic herbicide resistance mediated by CYP89A2, contributes to quizalofop-p-ethyl resistance in P. fugax.

Glycosyltransferase genes are associated with resistance to cyhalofop-butyl in a Chinese Echinochloa crus-galli population.

BACKGROUND: Echinochloa crus-galli is the most troublesome and widespread weed of most rice-growing regions of the world. Cyhalofop-butyl, a herbicide within the acetyl-CoA carboxylase (ACCase) chemical group, has been extensively used to control barnyardgrass in rice. The repeated exposure to cyhalofop-butyl has led to resistance evolution in E. crus-galli populations. RESULTS: In this study, we identified a population of E. crus-galli (R-HN) in a rice field in Hunan, China, that developed resistance to cyhalofop-butyl at 4.49-fold the recommended field dose. No known target mutation was detected in the ACCase gene of the R-HN population by ACCase sequencing compared to sensitive populations. Both cytochrome P450 (CYP450) and glutathione S-transferase (GST) inhibitors could not significantly reverse the resistance to cyhalofop-butyl. The nontarget-site resistance (NTSR) mechanism was investigated by transcriptome sequencing. Validation of the screened candidate genes by quantitative real-time (qRT)-PCR revealed that six glycosyltransferases (GTs) and four ATP-binding cassette (ABC) transporter genes were consistently upregulated in the R-HN population. Five GTs and one ABC transporter genes were constitutively upregulated after cyhalofop-butyl treatment in the R-HN population. Molecular docking results showed that the significant binding energy of GT79, GT75L6 and GT74E among all candidate genes. CONCLUSION: Thus, the GT genes appear to be directly implicated in NTSR to cyhalofop-butyl in the R-HN populations through metabolic enhancement, but their functional characterization needs to be studied. © 2024 Society of Chemical Industry.