Target‐site resistance to acetolactate synthase (ALS)‐inhibiting herbicides in <scp><i>Amaranthus palmeri</i></scp> from Argentina

Larran, Alvaro Santiago; Palmieri, Valeria E.; Perotti, Valeria; Lieber, Lucas; Tuesca, Daniel; Permingeat, Hugo R.

doi:10.1002/ps.4662

Cited by 29 publications

(37 citation statements)

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“…In Argentina, two ALS inhibitor‐resistant Palmer amaranth localities had the mutations Trp574Leu, Ser653Asn and Ala122Ser. One locality had the Trp574Leu mutation only, whereas the other had both Ser653Asn and Ala122Ser mutations …”

Section: Resultsmentioning

confidence: 99%

“…One locality had the Trp574Leu mutation only, whereas the other had both Ser653Asn and Ala122Ser mutations. 28 The Pro197Ala and Ala122Thr mutations in ALS had not been reported previously in Palmer amaranth. To verify whether these mutations occur in the same allele (double mutation) or in different alleles, the amplified gene product will need to be cloned before sequencing.…”

Section: Als Sequence Analysismentioning

confidence: 92%

“…In tall waterhemp and smooth pigweed, ALS mutations at positions Trp574 or Ser653, and Ala122, Ala205, Asp376, Trp574 or Ser653, respectively confer resistance to ALS inhibitors. Resistance to ALS inhibitors in Palmer amaranth in the USA is due to amino acid substitutions at Ala122, Pro197, Trp574 or Ser653 . Palmer amaranth localities across the USA are also mostly resistant to glyphosate, due to multiplication of the target gene, 5‐enolpyruvylshikimate‐3‐phosphate synthase ( EPSPS ) .…”

Section: Introductionmentioning

confidence: 99%

“…Resistance to ALS inhibitors in Palmer amaranth in the USA is due to amino acid substitutions at Ala122, Pro197, Trp574 or Ser653. 15,28,29 Palmer amaranth localities across the USA are also mostly resistant to glyphosate, due to multiplication of the target gene, 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS). 30 Whether target gene amplification contributes to some cases of ALS inhibitor resistance in Palmer amaranth is not known.…”

Section: Introductionmentioning

confidence: 99%

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Target‐site mutation accumulation among ALS inhibitor‐resistant Palmer amaranth

Singh

Salas-Perez

et al. 2018

Pest Management Science

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BACKGROUND Palmer amaranth (Amaranthus palmeri S. Wats) is one of the most common and troublesome weeds in the USA. Palmer amaranth resistance to acetolactate synthase (ALS) inhibitors is widespread in the USA, as in Arkansas. The cross‐resistance patterns and mechanism of resistance are not known. Experiments were conducted to determine cross‐resistance to ALS inhibitors and identify target‐site mutations in 20 Palmer amaranth localities from 13 counties in Arkansas. RESULTS All Palmer amaranth localities tested had plants cross‐resistant to imazethapyr, flumetsulam, primisulfuron, pyrithiobac and trifloxysulfuron. The dose of trifloxysulfuron that caused 50% control was 21–56‐fold greater for resistant accessions than for susceptible ones. All but three resistant plants analyzed had one or two relative copies of ALS; one plant had seven relative copies. All resistant plants tested (18 localities) carried the Trp574Leu mutation, which is known to confer broad resistance to ALS inhibitors, supporting the cross‐resistance pattern observed. Besides the Trp574Leu mutation, 30% of localities had individuals with one additional resistance‐conferring mutation including Ala122Thr, Pro197Ala or Ser653Asn. CONCLUSION The Trp574Leu mutation in ALS is the primary mechanism of resistance to ALS inhibitors in Palmer amaranth from Arkansas, USA. In some localities, multiple mutations have accumulated in one plant. All localities tested contained plants with resistance to five families of ALS inhibitors. Localities with extremely high resistance to ALS inhibitors, and those outside the subset we studied, may harbor non‐target site resistance mechanisms. ALS inhibitors are generally no longer effective on Palmer amaranth in these localities from the US mid‐south. © 2018 Society of Chemical Industry

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Section: Resultsmentioning

confidence: 99%

Section: Als Sequence Analysismentioning

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Target‐site mutation accumulation among ALS inhibitor‐resistant Palmer amaranth

Singh

Salas-Perez

et al. 2018

Pest Management Science

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“…Some mechanisms of resistance to herbicides have been studied in A. hybridus. In the biotypes cited in Argentina, ALS inhibitor herbicides resistance is due to site-specific mutation [8]. Glyphosate resistance mechanism is still unknown, but in a biotype of A. palmeri in USA, gene amplification was proven to be the cause [9,10].…”

Section: Introductionmentioning

confidence: 99%

First Report of Amaranthus hybridus with Multiple Resistance to 2,4-D, Dicamba, and Glyphosate

et al. 2018

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In many countries, Amaranthus hybridus is a widespread weed in agricultural systems. The high prolificacy and invasive capacity as well as the resistance of some biotypes to herbicides are among the complications of handling this weed. This paper reports on the first A. hybridus biotypes with resistance to auxinic herbicides and multiple resistance to auxinic herbicides and the EPSPs inhibitor, glyphosate. Several dose response assays were carried out to determine and compare sensitivity of six population of A. hybridus to glyphosate, 2,4-D, and dicamba. In addition, shikimic acid accumulation and piperonil butoxide effects on 2,4-D and dicamba metabolism were tested in the same populations. The results showed four populations were resistant to dicamba and three of these were also resistant to 2,4-D, while only one population was resistant to glyphosate. The glyphosate-resistant population also showed multiple resistance to auxinic herbicides. Pretreatment with piperonil butoxide (PBO) followed by 2,4-D or dicamba resulted in the death of all individual weeds independent of herbicide or population.

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A novel triple amino acid substitution in the EPSPS found in a high‐level glyphosate‐resistant Amaranthus hybridus population from Argentina

Perotti

Larran

Palmieri

et al. 2019

Pest Management Science

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BACKGROUND: The evolution of herbicide-resistant weeds is one of the most important concerns of global agriculture. Amaranthus hybridus L. is a competitive weed for summer crops in South America. In this article, we intend to unravel the molecular mechanisms by which an A. hybridus population from Argentina has become resistant to extraordinarily high levels of glyphosate. RESULTS:The glyphosate-resistant population (A) exhibited particularly high parameters of resistance (GR 50 = 20 900 g ai ha −1 , Rf = 314), with all plants completing a normal life cycle even after 32X dose application. No shikimic acid accumulation was detected in the resistant plants at any of the glyphosate concentrations tested. Molecular and genetic analyses revealed a novel triple substitution (TAP-IVS: T102I, A103V, and P106S) in the 5-enol-pyruvylshikimate-3-phosphate synthase (EPSPS) enzyme of population A and an incipient increase on the epsps relative copy number but without effects on the epsps transcription levels. The novel mechanism was prevalent, with 48% and 52% of the individuals being homozygous and heterozygous for the triple substitution, respectively. In silico conformational studies revealed that TAP-IVS triple substitution would generate an EPSPS with a functional active site but with an increased restriction to glyphosate binding. CONCLUSION: The prevalence of the TAP-IVS triple substitution as the sole mechanism detected in the highly glyphosate resistant population suggests the evolution of a new glyphosate resistance mechanism arising in A. hybridus. This is the first report of a naturally occurring EPSPS triple substitution and the first glyphosate target-site resistance mechanism described in A. hybridus. /journal/ps estimation of plant fitness costs associated with herbicide-resistance genes. Weed Sci 63:203-216 (2015). 42 Schönbrunn E, Eschenburg S, Shuttleworth WA, Schloss JV, Amrhein N, Evans JN, et al., Interaction of the herbicide glyphosate with its target enzyme 5-enolpyruvylshikimate 3-phosphate synthase in atomic detail. Proc Natl Acad Sci 98:1376-1380 (2001). 43 Pollegioni L, Schonbrunn E and Siehl D, Molecular basis of glyphosate resistance-different approaches through protein engineering.

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Target‐site resistance to acetolactate synthase (ALS)‐inhibiting herbicides in Amaranthus palmeri from Argentina

Abstract: This is the first report of als resistance alleles in A. palmeri in Argentina. The data support the involvement of a target-site mechanism of resistance to ALS-inhibiting herbicides. © 2017 Society of Chemical Industry.

Cited by 29 publications

References 37 publications

Target‐site mutation accumulation among ALS inhibitor‐resistant Palmer amaranth

Target‐site mutation accumulation among ALS inhibitor‐resistant Palmer amaranth

First Report of Amaranthus hybridus with Multiple Resistance to 2,4-D, Dicamba, and Glyphosate

A novel triple amino acid substitution in the EPSPS found in a high‐level glyphosate‐resistant Amaranthus hybridus population from Argentina

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