Enhanced metabolic detoxification is associated with fluroxypyr resistance in Bassia scoparia

Abstract

AbstractAuxin‐mimic herbicides chemically mimic the phytohormone indole‐3‐acetic‐acid (IAA). Within the auxin‐mimic herbicide class, the herbicide fluroxypyr has been extensively used to control kochia (Bassia scoparia). A 2014 field survey for herbicide resistance in kochia populations across Colorado identified a putative fluroxypyr‐resistant (Flur‐R) population that was assessed for response to fluroxypyr and dicamba (auxin‐mimics), atrazine (photosystem II inhibitor), glyphosate (EPSPS inhibitor), and chlorsulfuron (acetolactate synthase inhibitor). This population was resistant to fluroxypyr and chlorsulfuron but sensitive to glyphosate, atrazine, and dicamba. Subsequent dose‐response studies determined that Flur‐R was 40 times more resistant to fluroxypyr than a susceptible population (J01‐S) collected from the same field survey (LD50 720 and 20 g ae ha−1, respectively). Auxin‐responsive gene expression increased following fluroxypyr treatment in Flur‐R, J01‐S, and in a dicamba‐resistant, fluroxypyr‐susceptible line 9,425 in an RNA‐sequencing experiment. In Flur‐R, several transcripts with molecular functions for conjugation and transport were constitutively higher expressed, such as glutathione S‐transferases (GSTs), UDP‐glucosyl transferase (GT), and ATP binding cassette transporters (ABC transporters). After analyzing metabolic profiles over time, both Flur‐R and J01‐S rapidly converted [14C]‐fluroxypyr ester, the herbicide formulation applied to plants, to [14C]‐fluroxypyr acid, the biologically active form of the herbicide, and three unknown metabolites. The formation and flux of these metabolites were faster in Flur‐R than J01‐S, reducing the concentration of phytotoxic fluroxypyr acid. One unique metabolite was present in Flur‐R that was not present in the J01‐S metabolic profile. Gene sequence variant analysis specifically for auxin receptor and signaling proteins revealed the absence of non‐synonymous mutations affecting auxin signaling and binding in candidate auxin target site genes, further supporting our hypothesis that non‐target site metabolic degradation is contributing to fluroxypyr resistance in Flur‐R.