Multiple-Herbicide Resistance in a 2,4-D–Resistant Waterhemp (Amaranthus tuberculatus) Population from Nebraska

Abstract

A 2,4-D-resistant tall waterhemp population (FS) from Nebraska was evaluated for resistance to other TIR1 auxin receptor herbicides and to herbicides having alternative mechanisms of action using greenhouse bioassays and genetic markers. Atrazine, imazethapyr, lactofen, mesotrione, glufosinate, and glyphosate were applied in a single-dose bioassay, and tissue was collected from marked plants for genetic analysis. The FS population was not injured by atrazine or by imazethapyr. Approximately 50% of the plants survived lactofen and were actively growing 28 d after treatment. The population was susceptible to mesotrione, glufosinate, and glyphosate. Ametryn, chlorimuron-ethyl, 2,4-D, aminocyclopyraclor, aminopyralid, and picloram were applied in dose-response studies. The FS population was sensitive to ametryn, and the Ser-264-Gly substitution in the D1 protein was not detected, suggesting the lack of response to atrazine is not due to a target-site mutation. The FS population exhibited less than 50% injury to chlorimuron-ethyl at application rates 20 times the labeled use rate. The Ser-653-Asn acetolactate synthase (ALS) substitution, which confers resistance to imidazolinone herbicides, was present in the FS population. However, this does not explain the lack of response to the sulfonylurea herbicide, chlorimuron-ethyl. Sequencing of a portion of the PPX2L gene did not show the ΔG210 mutation that confers resistance to protoporphyrinogen oxidase-inhibiting herbicides, suggesting that other factors were responsible for waterhemp survival after lactofen application. The FS population was confirmed to be at least 30-fold resistant to 2,4-D relative to the susceptible populations. In addition, it was at least 3-fold less sensitive to aminopyralid and picloram, two other TIR1 auxin receptor herbicides, than the 2,4-D-susceptible populations were. These data indicated that the FS population contains both target and non-target site mechanisms conferring resistance to herbicides spanning at least three mechanisms of action: TIR1 auxin receptors, ALS inhibitors, and photosystem II inhibitors. Nomenclature:

Competitiveness of Herbicide-Resistant Waterhemp (Amaranthus tuberculatus) with Soybean

“…However, a non–target site resistance mechanism with reduced glyphosate uptake and translocation could also be present in this population (Sammons and Gaines 2014). The 2A-R population was identified as resistant to ALS-inhibiting herbicides through a target-site mechanism and resistant to 2,4-D and atrazine through non–target site (metabolic) mechanisms (cytochrome P450–mediated and potentially GST activity, respectively) (Crespo et al 2017; Figueiredo et al 2018; Vennapusa et al 2018). Conversely, the 2A-R population was confirmed susceptible to glyphosate and PPO-inhibiting herbicides (Crespo et al 2017).…”

“…Seeds from the 2A-R population were collected from southeastern Nebraska in 2010 from a production field of little bluestem ( Schizachyrium scoparium Michx. Nash) (Bernards et al 2012; Crespo et al 2017). The GP-R population and 2AGP-S population were collected in 2014 from soybean fields in Cass County and Fillmore County, NE, respectively (Vieira et al 2018).…”

Confirmation of 2,4‐D resistance and identification of multiple resistance in a Kansas Palmer amaranth (Amaranthus palmeri) population

“…However, low‐ to high‐level resistance (3–30‐fold) to 2,4‐D has been reported in a closely related pigweed species, i.e. common waterhemp ( Amaranthus tuberculatus ) populations from Nebraska, Missouri, and Illinois . Interestingly, the confirmed population of 2,4‐D‐resistant A. tuberculatus from Missouri was also multiple resistant to atrazine (7‐fold), chlorimuron (resistance level not determined), fomesafen (7‐fold), glyphosate (22‐fold), and mesotrione (14‐fold) herbicides …”

Herbicide resistance in Amaranthus tuberculatus†

“…Two additional 2,4-D-resistant A. tuberculatus populations, from Illinois and Nebraska, subsequently were identified from more typical row-crop production systems, and all three of these populations contained resistance spanning several other herbicide sites of action. 22,82,83 The gene(s) responsible for 2,4-D resistance in these populations is unknown, but rapid metabolism of the herbicide, likely by a P450, has been demonstrated in two of them. 45,84 A recent transcriptomic study identified two strong candidate genes, encoding a P450 and an ABC transporter.…”