Enhanced metabolic detoxification is associated with fluroxypyr resistance inBassia 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 an agronomically problematic Great Plains tumbleweed, kochia (Bassia scoparia). A 2014 field survey for herbicide resistance in kochia populations across Colorado identified a putative fluroxypyr resistant population that was assessed for response to five different herbicides representing four different herbicide modes of action. These included fluroxypyr and dicamba (auxin-mimics), atrazine (photosystem II inhibitor), glyphosate (EPSPS inhibitor), and chlorsulfuron (acetolactate synthase inhibitor). The greenhouse screen identified that this kochia population was resistant to fluroxypyr and chlorsulfuron, but sensitive to glyphosate, atrazine, and dicamba. This population was designated Flur-R. Subsequent dose response studies determined that 75% of the Flur-R population survived 628 g ae ha-1of fluroxypyr (4X the label application rate in wheat fallow, which is 157 g ae ha-1at 1X). Flur-R was 40 times more resistant to fluroxypyr than a susceptible population (J01-S) collected from the same field survey (LD50720 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 9425 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. Formation and flux of these metabolites was 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.Significance StatementHerbicide resistance is an ever-present issue in weeds of cropping and rangeland systems. By understanding genetic mechanisms of resistance in individual cases of herbicide resistance, we can extrapolate important information such as how quickly resistance to a specific herbicide can spread. Every characterized herbicide resistance mechanism contributes to a working database used to address herbicide resistance in an agricultural or open-space setting. Knowing the exact mechanism of resistance helps researchers and industry members understand why herbicide applications are failing, and if resistant plants can still be controlled with other herbicide modes of action. In kochia line Flur-R, there is strong evidence to support a non-target site resistance mechanism, specifically herbicide degradation via increased enzymatic activity. Increased fluroxypyr degradation represents a novel resistance mechanism to fluroxypyr in the weedBassia scoparia.