Target-site Mutation and Fitness Cost of Acetolactate Synthase Inhibitor-resistant Annual Bluegrass

Abstract

<jats:p>Annual bluegrass (<jats:italic>Poa annua</jats:italic> L.) is an annual weed that is particularly troublesome in managed turfgrass. It has been controlled conventionally with herbicides, including acetolactate synthase (ALS) inhibitors. However, resistance to ALS inhibitors has been documented throughout the southeastern United States since 2012. A rate<jats:bold>–</jats:bold><jats:bold>response trial was conducted to confirm and determine the resistance level of suspected resistant <jats:italic>P. annua</jats:italic> biotypes from Mississippi (Reunion), followed by DNA sequencing to determine whether the mechanism of resistance is a target-site mutatio n. In addition, a fitness assay was conducted together with a susceptible biotype to determine whether resistance to ALS inhibitors is associated with decreased fitness. Reunion was at least 45 times more resistant to foramsulfuron than the standard susceptible biotype based on I<jats:sub>50</jats:sub> estimates [<jats:italic>I</jats:italic><jats:sub>50</jats:sub> is the rate of herbicide giving a 50% response (50% visual necrosis)], requiring a predicted 331 g a.i./ha foramsulfuron for 50% control. DNA sequencing results identified a Trp574-to-Leu mutation in the ALS gene of the Reunion biotype, which has been shown by other studies to confer resistance to ALS inhibitors. Measurement of fitness parameters among the Reunion and susceptible biotypes demonstrated reduced seed yield, tillering, and flowering time in the resistant Reunion biotype, suggesting that ALS inhibitor resistance is possibly correlated to decreased fitness in <jats:italic>P. annua</jats:italic>. Alternative methods to control <jats:italic>P. annua</jats:italic> need to be considered as a result of the evolution of herbicide-resistant biotypes. An integrated management strategy to control <jats:italic>P. annua</jats:italic> weeds will help prevent further evolution of resistance. Because this study evaluated only the target-site mechanism of resistance, it is also necessary to determine whether the resistant biotype has reduced uptake, translocation, or enhanced metabolism as additional mechanisms of resistance. Consequently, a fitness study encompassing a more comprehensive list of plant parameters will provide conclusions of the fitness costs associated with ALS inhibitor resistance in <jats:italic>P. annua.</jats:italic> Chemical names: Foramsulfuron {1-(4,6-dimethoxypyrimidin-2-yl)-3-[2-(dimethylcarbamoyl)-5-formamidophenylsulfonyl] urea}.</jats:bold></jats:p>

Crop Diversification for Improved Weed Management: A Review

“…In addition to this, some weeds have developed resistance to multiple modes of action while others have (developed decreased sensitivity to herbicides [21][22][23]. Both target-site and non-target-site mutations in the herbicide-resistant weeds have been reported [24,25]. These observations indicate over-reliance on herbicides as a non-sustainable measure for weed control.…”

Seed production potential of Echinochloa colona exposed to sublethal doses of four commonly-used rice herbicides and high-temperature stress

“…(or other weed species) and some of these mutations may carry fitness cost (Panozzo et al, 2021). One example is the 60% reduction in grain yield of ALS-resistant annual bluegrass harboring L574W mutation (Tseng et al, 2019). At this point, G5 plants are not yet resistant to the full dose of imazethapyr.…”

“…Conversely, fitness cost has also been reported for glyphosate-resistant goosegrass (Eleusina indica (L.) Gaertn.) and imazethapyr-resistant annual bluegrass (Poa annua L.) which exhibited 5% and 60% reduction in seed production, respectively (Han et al, 2017;Tseng et al, 2019) but such cases are rarely observed in the field. Quinclorac-resistant junglerice from Arkansas, USA, does not exhibit fitness cost (Penka, 2018) and no fitness penalties have been reported for glufosinate-or FPBresistant weeds thus far.…”

Target-site and non–target site mechanisms of pronamide resistance in annual bluegrass (Poa annua) populations from Mississippi golf courses

“…TSR is due to a deletion of an amino acid or substitutions of different amino acids in the herbicide target protein, which may prevent the occurrence of herbicide interactions (Dayan et al 2018; Kukorelli et al 2013; Petit et al 2010). Target-site mutations contribute to P. annua resistance to ACCase, ALS, microtubule-assembly, PSII, and EPSPS inhibitors (Barua et al 2020; Cross et al 2015; Délye and Michel 2005; McElroy et al 2013; Svyantek et al 2016; Tseng et al 2019). Target-site mutations reported for mitotic-inhibiting herbicides confer resistance to the dinitroaniline herbicides.…”