<b>HRAC Group 1</b> <font size='2'> (Legacy A) </font> resistant Eleusine indica from Brazil

International Survey of Herbicide-Resistant Weeds

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Thursday, November 14, 2024

HRAC GROUP 1 (LEGACY A) RESISTANT GOOSEGRASS
(Eleusine indica)

Inhibition of Acetyl CoA Carboxylase HRAC Group 1 (Legacy A)

Brazil

INTRODUCTION		GOOSEGRASS
Goosegrass (Eleusine indica) is a monocot weed in the Poaceae family. In Brazil this weed first evolved resistance to Group 1 (Legacy A) herbicides in 2003 and infests Soybean. Group 1 (Legacy A) herbicides are known as Inhibition of Acetyl CoA Carboxylase (Inhibition of Acetyl CoA Carboxylase ). Research has shown that these particular biotypes are resistant to cyhalofop-butyl, fenoxaprop-ethyl, and sethoxydim and they may be cross-resistant to other Group 1 (Legacy A) 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 Oct 21, 2007 )
Common Name	Goosegrass
Species	Eleusine indica
Group	Inhibition of Acetyl CoA Carboxylase HRAC Group 1 (Legacy A)
Herbicides	cyhalofop-butyl, fenoxaprop-ethyl, and sethoxydim
Location	Brazil
Year	2003
Situation(s)	Soybean
Contributors - (Alphabetically)	Rafael De Prado, and Ribas Vidal
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NOTES ABOUT THIS BIOTYPE

MECHANISM

Ribas Vidal

Goosegrass (Eleusine Indica): First Report Of Target Site Resistance To Accase Inhibitors In A Brazilian Biotype. J. P. Ruiz-Santaella*,1 R. Vidal,2 J. Wagner,3 R. De Prado1; 1Agricultural Chemistry and Edaphology, University of Cordoba, Córdoba, Spain, 2Plant Sciences, Federal University of Rio Grande do Sul, Porto Alegre, Brazil, 3Weed Science, University of Hohenheim, Stuttgart, Germany

Goosegrass (Eleusine indica) is a diploid grass weed which has developed resistance to ACCase inhibitors during the last ten years due to the intensive and frequent use of sethoxydim to control grass weeds in soybean crops in Brazil. Dose-response assays confirmed the resistant behavior of this biotype obtaining high RF that ranged from 143 (fenoxaprop), 126 (haloxyfop), 84 (sethoxydim) to 58 (fluazifop). ACCase in vitro assays indicated a target site resistance as the cause of reduced susceptibility to ACCase inhibitors. PCR-generated fragments of the ACCase CT domain of the resistant and sensitive reference biotype were sequenced and compared. A point mutation was detected within the triplet of asparagine at the amino acid position 2078 (referred to EMBL accession no. AJ310767) and resulted in the triplet of glycine. These results constitute the first report on the target site mutation for a Brazilian herbicide resistant weed. The mechanism of herbicide resistance in the goosegrass biotype found in Brazil, add a new species in the increasing list of target-site resistant grass weeds. E-mail: qe2rumoj@uco.es

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ACADEMIC ASPECTS

Confirmation Tests

Field, Greenhouse, and Laboratory trials comparing a known susceptible Goosegrass biotype with this Goosegrass 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 1 resistant Goosegrass indicate that the inheritance is determined by a nuclear trait. 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

Studies on the mechanism of resistance of Group 1 (Legacy A) resistant Goosegrass from Brazil indicate that resistance is due to an altered target site. There may be a note below or an article discussing the mechanism of resistance in the Fact Sheets and Other Literature

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 1 (Legacy A) resistant Goosegrass from Brazil please update the database.

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CONTRIBUTING WEED SCIENTISTS

RAFAEL DE PRADO

Universidad De Cordoba Qvimica Agricola Y Edafologa E T S Ingenieros Agronomos PO Box 119 Cordoba, E-14080, Andalusia Spain Email Rafael De Prado

RIBAS VIDAL

Professor Universidade Federal Do Rio Grande Do Sul Plant Sciences Rod. Carlos João Strass Acesso Orlando, Cx Postal 231, Porto Alegre, CEP 91001-970, RS Brazil Email Ribas Vidal

ACKNOWLEDGEMENTS
The Herbicide Resistance Action Committee, The Weed Science Society of America, and weed scientists in Brazil have been instrumental in providing you this information. Particular thanks is given to Rafael De Prado, and Ribas Vidal for providing detailed information.

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Herbicide Resistant Goosegrass Globally
(Eleusine indica)

Country

FirstYear

Situation

Active Ingredients

Site of Action

Argentina

2012

Corn (maize), Fallow, and Soybean

glyphosate

Inhibition of Enolpyruvyl Shikimate Phosphate Synthase ( HRAC Group 9 (Legacy G)

Australia (Queensland)

2015

Sugarcane for sugar

paraquat

PS I Electron Diversion ( HRAC Group 22 (Legacy D)

Bolivia

2005

Rice, Soybean, and Wheat

clethodim, cyhalofop-butyl, fluazifop-butyl, and haloxyfop-methyl

Inhibition of Acetyl CoA Carboxylase ( HRAC Group 1 (Legacy A)

Bolivia

2007

Soybean

glyphosate

Inhibition of Enolpyruvyl Shikimate Phosphate Synthase ( HRAC Group 9 (Legacy G)

Brazil

2003

Soybean

cyhalofop-butyl, fenoxaprop-ethyl, and sethoxydim

Inhibition of Acetyl CoA Carboxylase ( HRAC Group 1 (Legacy A)

Brazil

2016

Corn (maize), Soybean, and Wheat

glyphosate

Inhibition of Enolpyruvyl Shikimate Phosphate Synthase ( HRAC Group 9 (Legacy G)

Brazil

2017

Beans, Corn (maize), Cotton, and Soybean

fenoxaprop-ethyl, glyphosate, and haloxyfop-methyl

Multiple Resistance: 2 Sites of Action
Inhibition of Acetyl CoA Carboxylase ( HRAC Group 1 (Legacy A)
Inhibition of Enolpyruvyl Shikimate Phosphate Synthase ( HRAC Group 9 (Legacy G)

China

2010

Unspecified

paraquat

PS I Electron Diversion ( HRAC Group 22 (Legacy D)

China

2010

Orchards

glyphosate

Inhibition of Enolpyruvyl Shikimate Phosphate Synthase ( HRAC Group 9 (Legacy G)

Colombia

2006

Coffee, and Corn (maize)

glyphosate

Inhibition of Enolpyruvyl Shikimate Phosphate Synthase ( HRAC Group 9 (Legacy G)

Colombia

2016

Corn (maize)

glyphosate, and paraquat

Multiple Resistance: 2 Sites of Action
PS I Electron Diversion ( HRAC Group 22 (Legacy D)
Inhibition of Enolpyruvyl Shikimate Phosphate Synthase ( HRAC Group 9 (Legacy G)

Costa Rica

1989

Industrial sites

imazapyr

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

Costa Rica

2010

Pejibaye palm

glyphosate

Inhibition of Enolpyruvyl Shikimate Phosphate Synthase ( HRAC Group 9 (Legacy G)

Indonesia

2012

Oil Palm Nursery

glyphosate, and paraquat

Multiple Resistance: 2 Sites of Action
PS I Electron Diversion ( HRAC Group 22 (Legacy D)
Inhibition of Enolpyruvyl Shikimate Phosphate Synthase ( HRAC Group 9 (Legacy G)

Indonesia

2012

Corn (maize)

paraquat

PS I Electron Diversion ( HRAC Group 22 (Legacy D)

Italy

2019

Nurseries

glyphosate

Inhibition of Enolpyruvyl Shikimate Phosphate Synthase ( HRAC Group 9 (Legacy G)

Japan

2013

Rice Paddy Levee

glyphosate

Inhibition of Enolpyruvyl Shikimate Phosphate Synthase ( HRAC Group 9 (Legacy G)

Malaysia

1990

Cropland, and Vegetables

fluazifop-butyl, and propaquizafop

Inhibition of Acetyl CoA Carboxylase ( HRAC Group 1 (Legacy A)

Malaysia

1990

Vegetables

paraquat

PS I Electron Diversion ( HRAC Group 22 (Legacy D)

Malaysia

1997

Orchards

fluazifop-butyl, and glyphosate

Multiple Resistance: 2 Sites of Action
Inhibition of Acetyl CoA Carboxylase ( HRAC Group 1 (Legacy A)
Inhibition of Enolpyruvyl Shikimate Phosphate Synthase ( HRAC Group 9 (Legacy G)

Malaysia

2009

Vegetables

glufosinate-ammonium, and paraquat

Multiple Resistance: 2 Sites of Action
PS I Electron Diversion ( HRAC Group 22 (Legacy D)
Inhibition of Glutamine Synthetase ( HRAC Group 10 (Legacy H)

Malaysia

2009

Oil Palm Nursery

butroxydim, fluazifop-butyl, glufosinate-ammonium, glyphosate, haloxyfop-methyl, and paraquat

Multiple Resistance: 4 Sites of Action
Inhibition of Acetyl CoA Carboxylase ( HRAC Group 1 (Legacy A)
PS I Electron Diversion ( HRAC Group 22 (Legacy D)
Inhibition of Enolpyruvyl Shikimate Phosphate Synthase ( HRAC Group 9 (Legacy G)
Inhibition of Glutamine Synthetase ( HRAC Group 10 (Legacy H)

Mexico

2016

Oranges

glyphosate

Inhibition of Enolpyruvyl Shikimate Phosphate Synthase ( HRAC Group 9 (Legacy G)

United States (North Carolina)

1973

Cotton

trifluralin

Inhibition of Microtubule Assembly ( HRAC Group 3 (Legacy K1)

United States (South Carolina)

1974

Cotton, and Soybean

trifluralin

Inhibition of Microtubule Assembly ( HRAC Group 3 (Legacy K1)

United States (Alabama)

1987

Cotton

trifluralin

Inhibition of Microtubule Assembly ( HRAC Group 3 (Legacy K1)

United States (Tennessee)

1988

Cotton, Golf courses, and Turf

pendimethalin, prodiamine, and trifluralin

Inhibition of Microtubule Assembly ( HRAC Group 3 (Legacy K1)

United States (Arkansas)

1989

Cotton, and Cropland

trifluralin

Inhibition of Microtubule Assembly ( HRAC Group 3 (Legacy K1)

United States (Georgia)

1992

Cotton, Golf courses, and Turf

trifluralin

Inhibition of Microtubule Assembly ( HRAC Group 3 (Legacy K1)

United States (Mississippi)

1994

Cotton

pendimethalin, and trifluralin

Inhibition of Microtubule Assembly ( HRAC Group 3 (Legacy K1)

United States (Florida)

1996

Tomatoes

paraquat

PS I Electron Diversion ( HRAC Group 22 (Legacy D)

United States (Hawaii)

2003

Turf

metribuzin

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

United States (Mississippi)

2010

Cotton

glyphosate

Inhibition of Enolpyruvyl Shikimate Phosphate Synthase ( HRAC Group 9 (Legacy G)

United States (Tennessee)

2011

Soybean

glyphosate

Inhibition of Enolpyruvyl Shikimate Phosphate Synthase ( HRAC Group 9 (Legacy G)

United States (North Carolina)

2015

Golf courses

oxadiazon

Inhibition of Protoporphyrinogen Oxidase ( HRAC Group 14 (Legacy E)

United States (Virginia)

2015

Golf courses

oxadiazon

Inhibition of Protoporphyrinogen Oxidase ( HRAC Group 14 (Legacy E)

United States (Alabama)

2019

Tomatoes

paraquat

PS I Electron Diversion ( HRAC Group 22 (Legacy D)

Literature about Similar Cases

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Takano, H., R. Mendes, L. Scoz, R. Ovejero, J. Constantin, T. Gaines, P. Westra, F. Dayan, and R. Oliveira. 2019. Proline 106 EPSPS mutation imparting glyphosate resistance in goosegrass (Eleusine indica) emerges in South America. Weed Science 67 : 48 - 56.

Glyphosate-resistant (GR) goosegrass [Eleusine indica (L.) Gaertn.] was recently identified in Brazil, but its resistance mechanism was unknown. This study elucidated the resistance mechanism in this species and developed a molecular marker for rapid detection of this target-site resistance trait. The resistance factor for the resistant biotype was 4.4-fold compared with the glyphosate-susceptible (GS) in greenhouse dose–response experiments. This was accompanied by a similar (4-fold) difference in the levels of in vitro and in planta shikimate accumulation in these biotypes. However, there was no difference in uptake, translocation, or metabolism of glyphosate between the GS and GR biotypes. Moreover, both biotypes showed similar values for 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS) copy number and transcription. Sequencing of a 330-bp fragment of the EPSPS gene identified a single-nucleotide polymorphism that led to a Pro-106-Ser amino acid substitution in the enzyme from the GR biotype. This mutation imparted a 3.8-fold increase in the amount of glyphosate required to inhibit 50% of EPSPS activity, confirming the role of this amino acid substitution in resistance to glyphosate. A quantitative PCR–based genotyping assay was developed for the rapid detection of resistant plants containing this Pro-106-Ser mutation..

Gherekhloo, J., Fernández-Moreno, P.T., Alcántara-de la Cruz, R., Sánchez-González, E., Cruz-Hipolito, H.E., Domínguez-Valenzuela, J.A. and De Prado, R.. 2017. Pro-106-Ser mutation and EPSPS overexpression acting together simultaneously in glyphosate-resistant goosegrass (Eleusine indica). Scientific Reports 7 : 6702 - .

Glyphosate has been used for more than 15 years for weed management in citrus groves in the Gulf of Mexico, at up to 3–4 applications per year. Goosegrass (Eleusine indica (L.) Gaertn.) control has sometimes failed. In this research, the mechanisms governing three goosegrass biotypes (Ein-Or from an orange grove, and Ein-Pl1 and Ein-Pl2 from Persian lime groves) with suspected resistance to glyphosate were characterized and compared to a susceptible biotype (Ein-S). Dose-response and shikimate accumulation assays confirmed resistance of the resistant (R) biotypes. There were no differences in glyphosate absorption, but the R biotypes retained up to 62–78% of the herbicide in the treated leaf at 96 h after treatment (HAT), in comparison to the Ein-S biotype (36%). The 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS) activity in the Ein-Or and Ein-S biotypes was over 100-fold lower than the Ein-Pl1 and Ein-Pl2 ones. The latter showed a high EPSPS-basal activity, a mutation at Pro-106-Ser position in the EPSPS gene, and EPSPS overexpression. The EPSPS basal and EPSPS overexpression were positively correlated. The R goosegrass biotypes displayed poor glyphosate translocation. Furthermore, this grassweed showed, for the first time, two mechanisms at the target-site level (Pro-106-Ser mutation + EPSPS overexpression) acting together simultaneously against glyphosate..

Chen, J., H. Huang, C. Zhang, S. Wei, Z. Huang, J. Chen, and X. Wang. 2015. Mutations and amplification of EPSPS gene confer resistance to glyphosate in goosegrass (Eleusine indica). Planta 242 : 859 - 868.

Glyphosate has been used widely in the south of China. The high selection pressure from glyphosate use has led to the evolution of resistance to glyphosate in weeds. We investigated the molecular mechanisms of three recently discovered glyphosate-resistant Eleusine indicapopulations (R1, R2 and R3). The results showed that R1 and R2 had double Thr102Ile and Pro106Ser mutation and a single mutation of Pro106Leu in the 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS) gene, respectively. Escherichia coli containing the mutated EPSPS genes was tolerant to glyphosate. EPSPS activity in R1 and R2 plants was higher than in the sensitive plants. There was no amino acid substitution in EPSPS gene in R3. However, expression of EPSPS in R3 plants was higher than in glyphosate-susceptible (S) population (13.8-fold) after glyphosate treatment. EPSPS enzyme activity in both R3 and S plants was inhibited by glyphosate, while shikimate accumulation in R3 was significantly lower than for the S population. Further analysis revealed that the genome of R3 contained 28.3-fold more copies of the EPSPS gene than that of susceptible population. EPSPS expression was positively correlated with copy number of EPSPS. In conclusion, mutation of the EPSPS gene and increased EPSPS expression are part of the molecular mechanisms of resistance to glyphosate in Eleusine indica..

Yu, Q., A. Jalaludin, H. Han, M. Chen, R.D. Sammons, and S. Powles. 2015. Evolution of a Double Amino Acid Substitution in the 5-Enolpyruvylshikimate-3-Phosphate Synthase in Eleusine indica Conferring High-Level Glyphosate Resistance. Plant Physiology 167 : 1440 - 1447.

Glyphosate is the most important and widely used herbicide in world agriculture. Intensive glyphosate selection has resulted in the widespread evolution of glyphosate-resistant weed populations, threatening the sustainability of this valuable once-in-a-century agrochemical. Field-evolved glyphosate resistance due to known resistance mechanisms is generally low to modest. Here, working with a highly glyphosate-resistant Eleusine indica population, we identified a double amino acid substitution (T102I + P106S [TIPS]) in the 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS) gene in glyphosate-resistant individuals. This TIPSmutation recreates the biotechnology-engineered commercial first generation glyphosate-tolerant EPSPS in corn (Zea mays) and now in other crops. In E. indica, the naturally evolved TIPS mutants are highly (more than 180-fold) resistant to glyphosate compared with the wild type and more resistant (more than 32-fold) than the previously known P106S mutants. The E. indica TIPS EPSPS showed very high-level (2,647-fold) in vitro resistance to glyphosate relative to the wild type and is more resistant (600-fold) than the P106S variant. The evolution of the TIPSmutation in crop fields under glyphosate selection is likely a sequential event, with the P106S mutation being selected first and fixed, followed by the T102I mutation to create the highly resistant TIPS EPSPS. The sequential evolution of the TIPS mutation endowing high-level glyphosate resistance is an important mechanism by which plants adapt to intense herbicide selection and a dramatic example of evolution in action..

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