Invasive Species Compendium

Detailed coverage of invasive species threatening livelihoods and the environment worldwide

Abstract

Trp-1999-Ser mutation of acetyl-CoA carboxylase and cytochrome P450s-involved metabolism confer resistance to fenoxaprop-P-ethyl in Polypogon fugax.

Abstract

BACKGROUND: Asia minor bluegrass (Polypogon fugax Nees ex Steud.) is an invasive grass species severely infesting wheat and canola fields in China. In May 2017, a suspected resistant P. fugax population AHHY that survived fenoxaprop-P-ethyl applied at its field-recommended rate was collected from a wheat field in Huaiyuan County, Anhui Province, China. This study aimed to determine the resistance profile of AHHY to acetyl-CoA carboxylase (ACCase) inhibitors and to investigate its mechanisms of resistance to fenoxaprop. RESULTS: Single-dose testing indicated that the AHHY population had evolved resistance to fenoxaprop. The partial carboxyltransferase domain of ACCase in P. fugax was amplified and compared. Four loci encoding plastidic ACCase were isolated from both the resistant and sensitive individuals. Combining gene sequencing with the derived cleaved amplified polymorphic sequence assay, we found that 100% of the plants of AHHY carried Trp-1999-Ser mutation in their ACCase1,1-2 allele. Whole-plant dose-response bioassay indicated that AHHY was highly resistant to fenoxaprop and pinoxaden (resistance index (RI) ≥10) with low resistance to clodinafop-propargyl, sethoxydim, and clethodim (2≤ RI <5). Pre-treatment with piperonyl butoxide largely reduced (55%) the weed's resistance to fenoxaprop. Both basal and fenoxaprop-induced glutathione S-transferases activities toward 1-chloro-2, 4-dinitrobenzene were significantly higher in resistant plants than in susceptible plants. CONCLUSION: This study revealed that P. fugax had multiple alleles encoding plastidic ACCase, and reported for the first time the occurrence of Trp-1999-Ser mutation and non-target-site resistance in this species. Fenoxaprop resistance in AHHY plants was conferred by target-site mutation and P450s-involved enhanced metabolism.