Evolution of target and non-target based multiple herbicide resistance in a single Palmer amaranth (Amaranthus palmeri) population from Kansas

Abstract

The evolution of resistance to multiple herbicides in Palmer amaranth is a major challenge for its management. In this study, a Palmer amaranth population from Hutchinson, Kansas (HMR), was characterized for resistance to inhibitors of photosystem II (PSII) (e.g., atrazine), acetolactate synthase (ALS) (e.g., chlorsulfuron), and EPSP synthase (EPSPS) (e.g., glyphosate), and this resistance was investigated. About 100 HMR plants were treated with field-recommended doses (1×) of atrazine, chlorsulfuron, and glyphosate, separately along with Hutchinson multiple-herbicide (atrazine, chlorsulfuron, and glyphosate)–susceptible (HMS) Palmer amaranth as control. The mechanism of resistance to these herbicides was investigated by sequencing or amplifying the psbA, ALS, and EPSPS genes, the molecular targets of atrazine, chlorsulfuron, and glyphosate, respectively. Fifty-two percent of plants survived a 1× (2,240 g ai ha−1) atrazine application with no known psbA gene mutation, indicating the predominance of a non–target site resistance mechanism to this herbicide. Forty-two percent of plants survived a 1× (18 g ai ha−1) dose of chlorsulfuron with proline197serine, proline197threonine, proline197alanine, and proline197asparagine, or tryptophan574leucine mutations in the ALS gene. About 40% of the plants survived a 1× (840 g ae ha−1) dose of glyphosate with no known mutations in the EPSPS gene. Quantitative PCR results revealed increased EPSPS copy number (50 to 140) as the mechanism of glyphosate resistance in the survivors. The most important finding of this study was the evolution of resistance to at least two sites of action (SOAs) (~50% of plants) and to all three herbicides due to target site as well as non–target site mechanisms. The high incidence of individual plants with resistance to multiple SOAs poses a challenge for effective management of this weed.

Predominance of Metabolic Resistance in a Six-Way-Resistant Palmer Amaranth (Amaranthus palmeri) Population

“…Nucleotide sequence alignment of the ALS gene of the KCTR, KSS, and MSS plants showed lack of the four previously reported mutations ( Nakka et al, 2017c ; Küpper et al, 2017 ; Singh et al, 2019 ; Chaudhari et al, 2020 ) known to confer resistance ALS-inhibitor herbicides in Palmer amaranth ( Figure 2 ). Even though some nucleotide polymorphisms were detected, none of them were consistent among the resistant plants or resulted in amino acid substitution ( Figure 2 ).…”

“…In this research, we report for the first time the evolution of six-way resistance in a single Palmer amaranth population, i.e., KCTR with predominance of metabolic resistance mechanisms. Previously Palmer amaranth populations with resistance to three and five SOAs have been reported ( Nakka et al, 2017a , b , c ; Kumar et al, 2019 ; Chaudhari et al, 2020 ). Similar to our findings, the six-way resistant common waterhemp population was also documented in Missouri ( Shergill et al, 2018 ).…”

“…Although mutations in herbicide target genes conferring resistance are rare evolutionary events, mutations in the ALS gene at eight positions (four positions in Palmer amaranth) were found to confer resistance to several classes of ALS inhibitors in weeds ( Tranel and Wright, 2002 ; Yu and Powles, 2014 ; Heap, 2020 ). Several amino acid substitutions at the ALS gene have been documented in Palmer amaranth populations from Kansas ( Nakka et al, 2017c ; Chaudhari et al, 2020 ). Interestingly, upon sequencing the whole ALS gene, the KCTR plants showed no presence of any of these substitutions ( Figure 2 ).…”

“…Palmer amaranth has currently evolved resistance to eight herbicide sites of action (SOAs) in the United States, including 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS-), acetolactate synthase- (ALS-), photosystem II- (PS II-), 4-hydroxyphenylpyruvate dioxygenase- (HPPD-), protoporphyrinogen oxidase- (PPO-), long-chain fatty acid- (LCFA-), microtubule-inhibitor herbicides, and synthetic auxins ( Heap, 2020 ). Previously, resistance to up to five SOAs, i.e., ALS-, EPSPS-, PS II-, HPPD-inhibitor herbicides, and synthetic auxins, was reported in different populations of Palmer amaranth from Kansas ( Nakka et al, 2017a , b , c ; Kumar et al, 2019 ; Chaudhari et al, 2020 ).…”

“…Importantly, the field where the KSR population was collected had a history of use of ALS- and PS II-, but not HPPD-inhibitor herbicides, validating the implications of metabolic resistance in bestowing cross-resistance to herbicides that were not previously used ( Nakka et al, 2017b ; Nandula et al, 2019 ). More recently, a three-way resistant Palmer amaranth population (HMR) was documented in Kansas with resistance to ALS-, PS II-, and EPSPS-inhibitor herbicides ( Chaudhari et al, 2020 ). Several mutations in the ALS gene, such as P197S, P197T, P197A, and P197A, or T574L were documented in HMR.…”