First report of Quizalofop-p-ethyl resistance in Eriochloa villosa involving non-target-site mechanisms.

Background

The emergence and spread of herbicide-resistant weeds pose a major challenge to sustainable weed management strategies. As a troublesome grass weed in soybean and maize agroecosystems, Eriochloa villosa (Thunb.) Kunth has attracted increasing attention, but the mechanism of its resistance to herbicides that inhibit acetyl-CoA carboxylase (ACCase) has not been elucidated. To elucidate the mechanisms underlying quizalofop-p-ethyl resistance, a resistant E. villosa population from Liaoning Province, China, was studied using physiological, biochemical, molecular and transcriptomic approaches.

Results

Whole-plant dose-response analysis revealed a moderate resistance in the resistant (R) population (resistance index = 5.23), with 50% reduction in growth values of 55.11 and 10.53 g a.i. ha-1 for the R and susceptible (S) populations, respectively. Sequence analysis of the ACCase gene revealed the absence of previously reported resistance-conferring substitutions, and ACCase expression showed no significant difference between the R and S populations. Furthermore, no significant differences in ACCase sensitivity were observed in all tested quizalofop-p-ethyl concentrations, collectively excluding the involvement of target-site resistance. Transcriptomic analysis revealed several candidate genes, including cytochrome P450 (CYP450) genes CYP724B1, CYP90A1, CYP89A2 and CYP81Q32, as well as the ATP-binding cassette (ABC) transporters gene ABCF5, that exhibited elevated transcript levels in the R population and validated by quantitative reverse-transcription (qRT)-PCR analysis. Kyoto Encyclopedia of Genes and Genomes analysis indicated extensive involvement of plant hormone signaling pathways, particularly the abscisic acid and jasmonic acid pathways. Additionally, the R population exhibited significantly higher CYP450 abundance than the S population.

Conclusion

This study represents the first characterization of ACCase inhibitor resistance in E. villosa and reveals that quizalofop-p-ethyl resistance is mainly attributed to enhanced nontarget-site mechanisms, likely involving CYP450-mediated detoxification and ABC transporter activity. © 2026 Society of Chemical Industry.