A Statewide Survey of PPO-Inhibitor Resistance and the Prevalent Target-Site Mechanisms in Palmer amaranth (Amaranthus palmeri) Accessions from Arkansas

Abstract

Palmer amaranth is one of the most problematic weeds in the midsouthern United States, and the evolution of resistance to protoporphyrinogen oxidase (PPO) inhibitors in biotypes already resistant to glyphosate and acetolactate synthase (ALS) inhibitors is a major cause of concern to soybean and cotton growers in these states. A late-season weed-escape survey was conducted in the major row crop–producing counties (29 counties) to determine the severity of PPO-inhibitor resistance in Arkansas. A total of 227 Palmer amaranth accessions were sprayed with fomesafen at 395 g ha−1to identify putative resistant plants. A TaqMan qPCR assay was used to confirm the presence of the ΔG210 codon deletion or the R128G/M (homologous to R98 mutation in common ragweed) target-site resistance mechanisms in thePPX2gene. Out of the 227 accessions screened, 44 were completely controlled with fomesafen, and 16 had only one or two severely injured plants (≥98% mortality) when compared with the 1986 susceptible check (100% mortality). The remaining 167 accessions were genotypically screened, and 82 (49%) accessions were found to harbor the ΔG210 deletion in thePPX2gene. The R128G was observed in 47 (28%) out of the 167 accessions screened. The mutation R128M, on the other hand was rare, found in only three accessions. About 13% of the accessions were segregating for both the ΔG210 and R128G mutations. Sixteen percent of the tested accessions had mortality ratings <90% and did not test positive for the ΔG210 or the R128G/M resistance mechanisms, indicating that a novel target or non–target site resistance mechanism is likely. Overall, PPO inhibitor–resistant Palmer amaranth is widespread in Arkansas, and the ΔG210 resistance mechanism is especially dominant in the northeast corridor, while the R128G mutation is more prevalent in counties near Memphis, TN.

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

“…Furthermore, A. palmeri population with multiple resistance to mesotrione (10–18‐fold), chlorsulfuron (> 275‐fold), and atrazine (160–198‐fold) has also been reported in Kansas . Low‐ to high‐level resistance (6–18‐fold) to fomesafen has recently been characterized among A. palmeri populations in Arkansas . Evolution of 2,4‐D resistance in A. palmeri is a new phenomenon and has not been documented previously.…”

“…In that same population, rapid detoxification via glutathione S ‐transferase (GST) conjugation was also found to confer high‐level (160–198‐fold) resistance to atrazine . A codon deletion (ΔG210) or single point mutations in the PPX2 gene mainly confers resistance to fomesafen in PPO‐resistant A. palmeri populations; however, the possibility of non‐target‐site based mechanisms (cytochrome P450‐mediated and GST‐based) has recently been suggested in the PPO‐resistant A. palmeri population in Arkansas . Similarly, the enhanced metabolism of 2,4‐D via cytochrome P450 monooxygenase has been found to confer 2,4‐D resistance in A. tuberculatus populations from Nebraska and Missouri .…”

“…More recently, several A. palmeri populations with multiple resistance to glyphosate and mesotrione have been characterized in Arkansas . In addition, widespread resistance to PPO inhibitors has also been reported among A. palmeri populations in Arkansas . Similarly, A. palmeri with multiple resistance to glyphosate and pyrithiobac has been reported in Georgia .…”

Investigating target‐site resistance mechanism to the PPO‐inhibiting herbicide fomesafen in waterhemp and interspecific hybridization of Amaranthus species using next generation sequencing

“…Waterhemp resistance to PPO‐inhibiting herbicides (PPO‐R) was first reported in a Kansas, USA soybean field in 2001 with a mechanism of resistance subsequently identified as a ΔG210 codon deletion of the PPX2 gene, which results in less competitive inhibition of the herbicide due to an alteration in the binding pocket . An additional mutation site at R128 of PPX2 has also been reported in the PPO‐R weeds Palmer amaranth ( Amaranthus palmeri S. Watson) and common ragweed ( Ambrosia artemisiifolia L.) (referred to R98 in their study) . According to the crystal structure analysis of PPO, R128 is a direct substrate‐binding site and thus, alterations at this amino acid position result in functional protein changes.…”

“…12,13 An additional mutation site at R128 of PPX2 has also been reported in the PPO-R weeds Palmer amaranth (Amaranthus palmeri S. Watson) and common ragweed (Ambrosia artemisiifolia L.) (referred to R98 in their study). [14][15][16][17] According to the crystal structure analysis of PPO, R128 is a direct substrate-binding site 18 and thus, alterations at this amino acid position result in functional protein changes. The R128A substitution in a human PPO protein resulted in an enlarged substrate-binding pocket, 19 whereas this same substitution in tobacco PPO protein resulted in nearly 60-fold greater enzyme activity.…”