<b>HRAC Group 5</b> <font size='2'> (Legacy C1 C2) </font> resistant Amaranthus powellii from United States, Washington

International Survey of Herbicide-Resistant Weeds

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Thursday, November 14, 2024

HRAC GROUP 5 (LEGACY C1 C2) RESISTANT POWELL AMARANTH
(Amaranthus powellii)

PSII inhibitors - Serine 264 Binders HRAC Group 5 (Legacy C1 C2)

United States, Washington

INTRODUCTION		POWELL AMARANTH
Powell Amaranth (Amaranthus powellii) is a dicot weed in the Amaranthaceae family. In Washington this weed first evolved resistance to Group 5 (Legacy C1 C2) herbicides in 1992 and infests Mint. Group 5 (Legacy C1 C2) herbicides are known as PSII inhibitors - Serine 264 Binders (Inhbition of Photosynthesis at PSll - Serine 264 Binders ). Research has shown that these particular biotypes are resistant to terbacil and they may be cross-resistant to other Group 5 (Legacy C1 C2) herbicides. The 'Group' letters/numbers that you see throughout this web site refer to the classification of herbicides by their site of action. To see a full list of herbicides and HRAC herbicide classifications click here.

QUIK STATS (last updated Jan 01, 2014 )
Common Name	Powell Amaranth
Species	Amaranthus powellii
Group	PSII inhibitors - Serine 264 Binders HRAC Group 5 (Legacy C1 C2)
Herbicides	terbacil
Location	United States, Washington
Year	1992
Situation(s)	Mint
Contributors - (Alphabetically)	Kassim Al-Khatib, and Rick Boydston (Retired)
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NOTES ABOUT THIS BIOTYPE

GENERAL

Kassim Al-Khatib

Boydston, R. A. and K. Al-Khatib. 1992. Terbacil and bromacil cross-resistance in Powell amaranth (Amaranthus powellii). Weed Science. 40:513-516.

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ACADEMIC ASPECTS

Confirmation Tests

Greenhouse trials comparing a known susceptible Powell Amaranth biotype with this Powell Amaranth biotype have been used to confirm resistance. For further information on the tests conducted please contact the local weed scientists that provided this information.

Genetics

Genetic studies on HRAC Group 5 resistant Powell Amaranth have not been reported to the site. There may be a note below or an article discussing the genetics of this biotype in the Fact Sheets and Other Literature

Mechanism of Resistance

The mechanism of resistance for this biotype is either unknown or has not been entered in the database. If you know anything about the mechanism of resistance for this biotype then please update the database.

Relative Fitness

There is no record of differences in fitness or competitiveness of these resistant biotypes when compared to that of normal susceptible biotypes. If you have any information pertaining to the fitness of Group 5 (Legacy C1 C2) resistant Powell Amaranth from Washington please update the database.

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CONTRIBUTING WEED SCIENTISTS

KASSIM AL-KHATIB

Director and Ce Specialist, Statewide IPM Program Statewide IPM Program Integrated Pest Management 2801 Second Street #152 Davis, 95618-7774, California United States Email Kassim Al-Khatib Web : Web Site Link

RICK BOYDSTON (RETIRED)

Research Weed Scientist USDA-ARS WSU Prosser (IAREC) Hamilton Hall 24106 N Bunn Rd. Prosser, 99350, Washington United States Email Rick Boydston (Retired) Web : Web Site Link

ACKNOWLEDGEMENTS
The Herbicide Resistance Action Committee, The Weed Science Society of America, and weed scientists in Washington have been instrumental in providing you this information. Particular thanks is given to Kassim Al-Khatib, and Rick Boydston (Retired) for providing detailed information.

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Herbicide Resistant Powell Amaranth Globally
(Amaranthus powellii)

Country

FirstYear

Situation

Active Ingredients

Site of Action

Canada (Ontario)

1977

Corn (maize)

atrazine, and metribuzin

PSII inhibitors - Serine 264 Binders ( HRAC Group 5 (Legacy C1 C2)

Canada (Ontario)

1998

Corn (maize), Cropland, and Soybean

imazethapyr, and thifensulfuron-methyl

Inhibition of Acetolactate Synthase ( HRAC Group 2 (Legacy B)

Canada (Ontario)

1998

Corn (maize), Soybean, and Wheat

atrazine, imazethapyr, and metribuzin

Multiple Resistance: 2 Sites of Action
Inhibition of Acetolactate Synthase ( HRAC Group 2 (Legacy B)
PSII inhibitors - Serine 264 Binders ( HRAC Group 5 (Legacy C1 C2)

Canada (Ontario)

1999

Carrots

atrazine, linuron, monolinuron, and prometryne

PSII inhibitors - Serine 264 Binders ( HRAC Group 5 (Legacy C1 C2)

Canada (Manitoba)

2008

Beans, and Wheat

thifensulfuron-methyl, and tribenuron-methyl

Inhibition of Acetolactate Synthase ( HRAC Group 2 (Legacy B)

Canada (Quebec)

2012

Carrots

linuron

PSII inhibitors - Serine 264 Binders ( HRAC Group 5 (Legacy C1 C2)

Canada (Quebec)

2012

Soybean

imazethapyr

Inhibition of Acetolactate Synthase ( HRAC Group 2 (Legacy B)

Canada (Ontario)

2019

Soybean

aminocyclopyrachlor, dichlorprop, imazethapyr, MCPA, and mecoprop

Multiple Resistance: 2 Sites of Action
Inhibition of Acetolactate Synthase ( HRAC Group 2 (Legacy B)
Auxin Mimics ( HRAC Group 4 (Legacy O)

Czech Republic

1989

Orchards

atrazine, cyanazine, prometryne, simazine, and terbutryne

PSII inhibitors - Serine 264 Binders ( HRAC Group 5 (Legacy C1 C2)

France

1982

Corn (maize)

atrazine

PSII inhibitors - Serine 264 Binders ( HRAC Group 5 (Legacy C1 C2)

Switzerland

1986

Corn (maize)

atrazine

PSII inhibitors - Serine 264 Binders ( HRAC Group 5 (Legacy C1 C2)

United States (Washington)

1992

Mint

terbacil

PSII inhibitors - Serine 264 Binders ( HRAC Group 5 (Legacy C1 C2)

United States (Ohio)

1996

Soybean

imazaquin

Inhibition of Acetolactate Synthase ( HRAC Group 2 (Legacy B)

United States (Michigan)

2001

Asparagus, and Nurseries

atrazine, and diuron

PSII inhibitors - Serine 264 Binders ( HRAC Group 5 (Legacy C1 C2)

Literature about Similar Cases

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Gaines, T. A. ; Ward, S. M. ; Bukun, B. ; Preston, C. ; Leach, J. E. ; Westra, P.. 2012. Interspecific hybridization transfers a previously unknown glyphosate resistance mechanism in Amaranthus species. Evolutionary Applications 5 : 29 - 38.

A previously unknown glyphosate resistance mechanism, amplification of the 5-enolpyruvyl shikimate-3-phosphate synthase gene, was recently reported in Amaranthus palmeri. This evolved mechanism could introgress to other weedy Amaranthus species through interspecific hybridization, representing an avenue for acquisition of a novel adaptive trait. The objective of this study was to evaluate the potential for this glyphosate resistance trait to transfer via pollen from A. palmeri to five other weedy Amaranthus species (Amaranthus hybridus, Amaranthus powellii, Amaranthus retroflexus, Amaranthus spinosus, and Amaranthus tuberculatus). Field and greenhouse crosses were conducted using glyphosate-resistant male A. palmeri as pollen donors and the other Amaranthus species as pollen recipients. Hybridization between A. palmeri and A. spinosus occurred with frequencies in the field studies ranging from <0.01% to 0.4%, and 1.4% in greenhouse crosses. A majority of the A. spinosus × A. palmeri hybrids grown to flowering were monoecious and produced viable seed. Hybridization occurred in the field study between A. palmeri and A. tuberculatus (<0.2%), and between A. palmeri and A. hybridus (<0.01%). This is the first documentation of hybridization between A. palmeri and both A. spinosus and A. hybridus..

Ashigh, J. ; Corbett, C. A. L. ; Smith, P. J. ; Laplante, J. ; Tardif, F. J.. 2009. Characterization and diagnostic tests of resistance to acetohydroxyacid synthase inhibitors due to an Asp₃₇₆Glu substitution in Amaranthus powellii. Pesticide Biochemistry and Physiology 95 : 38 - 46.

A population of Amaranthus powellii that had survived imazethapyr did not have any of the documented AHAS mutations causing resistance in this species in Ontario. The goal of this research was to confirm resistance in this population, determine its molecular basis and develop diagnostic tests. Whole plant dose-response experiments showed the resistant population had greater than 25-fold resistance to the selective agent imazethapyr at the whole plant level. Whole plant resistance to other herbicides ranged between 9-fold to flumetsulam and 85-fold to flucarbazone. This was confirmed at the enzyme level with resistance ranging between 25-fold to imazethapyr and 485-fold to thifensulfuron. AHAS from the resistant population had 16% higher specific activity than that of the susceptible population and it was also less sensitive to feedback inhibition by valine, leucine and isoleucine. Genomic DNA was extracted to PCR amplify and sequence the AHAS gene and to determine the applicability of diagnostic tests. Sequencing of the AHAS gene revealed a single point mutation of thymine₁₁₂₅ to guanine coding for an Asp₃₇₆Glu substitution. Two different diagnostic tests, restriction fragment length polymorphism and PCR amplification of specific allele, were able to correctly identify the resistant population from the susceptible control and from other resistant populations. Although this mutation appears to confer higher resistance to pyrithiobac and flucarbazone, two herbicides not registered in Eastern Canada, it endows plants with enough protection to allow survival to imazethapyr, the main selective agent in Ontario..

Ashigh, J., C. L. Corbett, P. J. Smith, J. Laplante, And F. J. Tardif.. 2009. Characterization and diagnostic tests of resistance to acetohydroxyacid synthase inhibitors due to an Asp376Glu substitution in Amaranthus powellii. Pesticide Biochemistry and Physiology 95 : 38 - 46.

A population of Amaranthus powellii that had survived imazethapyr did not have any of the documented AHAS mutations causing resistance in this species in Ontario. The goal of this research was to confirm resistance in this population, determine its molecular basis and develop diagnostic tests. Whole plant dose–response experiments showed the resistant population had greater than 25-fold resistance to the selective agent imazethapyr at the whole plant level. Whole plant resistance to other herbicides ranged between 9-fold to flumetsulam and 85-fold to flucarbazone. This was confirmed at the enzyme level with resistance ranging between 25-fold to imazethapyr and 485-fold to thifensulfuron. AHAS from the resistant population had 16% higher specific activity than that of the susceptible population and it was also less sensitive to feedback inhibition by valine, leucine and isoleucine. Genomic DNA was extracted to PCR amplify and sequence the AHAS gene and to determine the applicability of diagnostic tests. Sequencing of the AHAS gene revealed a single point mutation of thymine1125 to guanine coding for an Asp376Glu substitution. Two different diagnostic tests, restriction fragment length polymorphism and PCR amplification of specific allele, were able to correctly identify the resistant population from the susceptible control and from other resistant populations. Although this mutation appears to confer higher resistance to pyrithiobac and flucarbazone, two herbicides not registered in Eastern Canada, it endows plants with enough protection to allow survival to imazethapyr, the main selective agent in Ontario..

Corbett, C. A. L. ; Tardif, F. J.. 2008. Detection of resistance to acetohydroxyacid synthase inhibitors in Amaranthus sp. using DNA polymorphisms. Pesticide Biochemistry and Physiology 92 : 48 - 55.

Resistance to acetohydroxyacid synthase inhibitors is very widespread worldwide and is generally due to various point mutations in the gene coding for the target enzyme. Rapid resistance confirmation is key for the proper management of resistance. We aimed at determining whether two DNA-based tests, PCR-RFLP and PCR amplification of specific alleles (PASA), could reliably identify common AHAS mutations in Amaranthus sp., and whether individual tests could be multiplexed. DNA was extracted from eight populations of Amaranthus powellii and Amaranthus retroflexus possessing four different resistance alleles. Gains or losses of endonuclease recognition sites due to the presence of resistance alleles allowed reliable detection of all alleles. PASA used an allele-specific primer with a 3′-terminal mismatch to wildtype DNA to selectively amplify a resistance allele. All four resistance alleles were efficiently identified with PASA. Both tests were multiplexed to allow more efficient identification of resistance and up to four distinct mutations could be revealed by a single test. Those tests were relatively easy to use, inexpensive and allowed quick identification of resistance..

Tardif, F. J. ; Rajcan, I. ; Costea, M.. 2006. A mutation in the herbicide target site acetohydroxyacid synthase produces morphological and structural alterations and reduces fitness in Amaranthus powellii. New Phytologist 169 : 251 - 264.

We investigated the effect of a herbicide resistance-conferring mutation on fitness in Amaranthus powellii. Morphological and histological observations were made. Growth and leaf appearance were recorded for six resistant and six susceptible populations. The competitiveness of a susceptible population was compared with that of a resistant population using a replacement series experiment. Leaves of the resistant plants were distorted and much smaller than those of susceptible plants. Additionally, they exhibited an abnormal morphological and structural pattern consisting of a mosaic of heterogeneous areas in the same leaf blade. The roots and stems had similar structures in susceptible and resistant plants, but the former were up to four times more developed. The resistant plants were slower to develop and produced 67% less biomass and 58% lower leaf area than susceptible plants. Under competitive conditions, one susceptible population outperformed one resistant population by 7-15 times. The Trp₅₇₄Leu acetohydroxyacid synthase (AHAS) mutation appears to have considerable pleiotropic effects on the early growth and development of the plants which, in competitive conditions, greatly reduce fitness..

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