4.7 Article

Metabolic Resistance to Acetyl-CoA Carboxylase-Inhibiting Herbicide Cyhalofop-Butyl in a Chinese Echinochloa crus-galli Population

Journal

AGRONOMY-BASEL
Volume 12, Issue 11, Pages -

Publisher

MDPI
DOI: 10.3390/agronomy12112724

Keywords

resistance mechanisms; metabolism; cyhalofop-butyl; Echinochloa crus-galli; resistance pattern; multiple-resistance

Funding

  1. National Natural Science Foundation
  2. [31901904]
  3. [32072435]

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A population of Echinochloa crus-galli obtained from direct-seeding rice fields in Jiangxi Province, China, exhibited high resistance levels to the herbicide cyhalofop-butyl and evolved cross-resistance to multiple herbicides. Analysis of ACCase gene sequencing and metabolic inhibition experiments suggested that the resistance may be due to enhanced metabolic activity.
A population of Echinochloa crus-galli (L.) P. Beauv obtained from direct-seeding rice fields in Jiangxi Province, China, exhibited high resistance levels (13.5-fold) to the acetyl-CoA carboxylase (ACCase)-inhibiting herbicide cyhalofop-butyl. Compared with the susceptible (S) population, this resistant (R) population evolved a cross-resistance to aryloxyphenoxypropionates (APPs) herbicides metamifop (2.9-fold) and fenoxapro-p-ethyl (4.1-fold), cyclohexanediones (CHDs) herbicide clethodim (4.7-fold), phenyl pyrazoline (DEN) herbicide pinoxaden (6.4-fold), and evolved multiple-resistance to acetolactate synthase (ALS)-inhibiting herbicide penoxsulam (3.6-fold), and auxin mimic herbicides quinclorac (>34.7-fold) and florpyrauxifen-benzyl (2.4-fold). ACCase gene sequencing did not reveal the existence of any known mutation point conferring with herbicide resistance. In addition, three metabolic inhibitors-one glutathione-S-transferase (GST) inhibitor (NBD-Cl), and two cytochrome P450 inhibitors (malathion and PBO)-did not reverse the cyhalofop-butyl resistance. Furthermore, enhanced metabolic rates of more than 60% 24 h after treatment with the active compound cyhalofop acid was observed in R plants compared to S plants. Hence, enhanced metabolism activity endows a non-target-site resistance to cyhalofop-butyl in the R population of E. crus-galli. Future research will be required to determine what metabolizing enzyme genes are responsible for cyhalofop-butyl resistance in E. crus-galli.

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