<b>HRAC Group 3</b> <font size='2'> (Legacy K1) </font> resistant Eleusine indica from United States, Arkansas

International Survey of Herbicide-Resistant Weeds

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Thursday, October 31, 2024

HRAC GROUP 3 (LEGACY K1) RESISTANT GOOSEGRASS
(Eleusine indica)

Inhibition of Microtubule AssemblyHRAC Group 3 (Legacy K1)

United States, Arkansas

INTRODUCTION		GOOSEGRASS
Goosegrass (Eleusine indica) is a monocot weed in the Poaceae family. In Arkansas this weed first evolved resistance to Group 3 (Legacy K1) herbicides in 1989 and infests Cotton, and Cropland. Group 3 (Legacy K1) herbicides are known as Inhibition of Microtubule Assembly (Inhibition of Microtubule Assembly ). Research has shown that these particular biotypes are resistant to trifluralin and they may be cross-resistant to other Group 3 (Legacy K1) 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 Sep 15, 2000 )
Common Name	Goosegrass
Species	Eleusine indica
Group	Inhibition of Microtubule Assembly HRAC Group 3 (Legacy K1)
Herbicides	trifluralin
Location	United States, Arkansas
Year	1989
Situation(s)	Cotton, and Cropland
Contributors - (Alphabetically)	Ford Baldwin, and Ronald Talbert : Retired
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ACADEMIC ASPECTS

Confirmation Tests

Greenhouse 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 3 resistant Goosegrass 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 3 (Legacy K1) resistant Goosegrass from Arkansas please update the database.

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CONTRIBUTING WEED SCIENTISTS

FORD BALDWIN

Practical Weed Consultants, Llc. 67 East Four Dinkus Rd Austin, 72007, Arkansas United States Email Ford Baldwin

RONALD TALBERT : RETIRED

Retired From University Of Arkansas P.O Box 2159 None, 72007, Arkansas United States Email Ronald Talbert : Retired

ACKNOWLEDGEMENTS
The Herbicide Resistance Action Committee, The Weed Science Society of America, and weed scientists in Arkansas have been instrumental in providing you this information. Particular thanks is given to Ford Baldwin, and Ronald Talbert : Retired 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)

Specific Papers about this Case

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Waldin, T. R. ; Ellis, J. R. ; Hussey, P. J.. 1992. Tubulin-isotype analysis of two grass species-resistant to dinitroaniline herbicides. Planta 188 : 258 - 264.

Trifluralin-resistant biotypes of Eleusine indica (goosegrass) and Setaria viridis (green foxtail) exhibit cross-resistance to other dinitroaniline herbicides including pendimethalin, oryzalin and chlorthal-dimethyl. Since microtubules are considered the primary target site for dinitroaniline herbicides it was investigated whether the differential sensitivity of resistant and susceptible biotypes of these species results from modified tubulin polypeptides. One-dimensional and two-dimensional PAGE combined with immunoblotting using well-characterized anti-tubulin monoclonal antibodies were used to display the family of tubulin isotypes in each species. Seedlings of E. indica exhibited four β-tubulin isotypes and one α-tubulin isotype, whereas those of S. viridis exhibited two β-tubulin and two α-tubulin isotypes. Comparison of the susceptible and resistant biotypes within each species revealed no differences in electrophoretic properties of the multiple tubulin isotypes. These results provide no evidence that resistance to dinitroaniline herbicides is associated with a modified tubulin polypeptide in these biotypes of E. indica or S. viridis..

Appleby, Arnold P And Radosevich, Steven R. 1991. Cellular Characteristics of Dinitroaniline Herbicide-Resistant Goosegrass (Eleusine indica). Weed Science 39 : 6 - 12.

Primary root cells from five dinitroaniline-resistant (R) and three susceptible (S) goosegrass biotypes from North Carolina and South Carolina were observed by transmission electron microscopy to determine whether resistance was associated with changes in cell wall formation. Cell wall malformations were found in some cells from two of the R-biotypes and in one of the S-biotypes. Malformations consisted of partially deposited cell walls and the inclusion of cell wall material in the cytoplasm. Some of the affected cells also had abnormal, lobed nuclei and malformed mitochondria. There seems to be little or no correlation between dinitroaniline resistance and cell wall malformations.

Vaughn, K. C. ; Vaughan, M. A. l ; Gossett, B. J.. 1990. A biotype of goosegrass (Eleusine indica) with an intermediate level of dinitroaniline herbicide resistance. Weed Technology 4 : 157 - 162.

This is a paper given at a symposium of the Weed Science Society of America entitled Herbicide resistance, held on 8 Feb. 1989 at Dallas, Texas. Two kinds of dinitroaniline-resistant biotypes of goosegrass (E. indica) have been found in counties in South Carolina where trifluralin is used for weed control. One biotype (R) resists trifluralin about 1000- to 10 000-fold. The other biotype (I) is intermediate in resistance between the R and susceptible (S) biotypes, resisting trifluralin about 50-fold. Growth studies and root tip squashes were used to determine the level of resistance to other dinitroaniline herbicides. The R biotype is cross resistant to all dinitroaniline herbicides, and the I biotype is highly resistant to some and is resistant to others only at a low level. The cross resistance of the I biotype to other dinitroaniline herbicides does not correlate with structural or solubility characteristics of the herbicides. EM investigations indicated that cell plate formation (controlled by phragmoplast microtubule arrays) is affected at lower herbicide concn than spindle microtubule formations. The level of herbicide resistance, the pattern of cross resistance, and the ultrastructural effects induced by the herbicide indicate that the I biotype has a unique mechanism of resistance from the R biotype..

Valverde, B. E., S. R. Radosevich, And A. P. Appleby.. 1988. Growth and competitive ability of dinitroaniline-herbicide resistant and susceptible goosegrass (Eleusine indica) biotypes. Proceedings of the Western Society of Weed Science 41 : 81.

Leaf area, DW and RGR did not differ among 3 resistant and 3 susceptible biotypes of E. indica but, when grown at differing desities, the resources partitioned to seed production by a resistant biotype decreased more as plant density increased than did those in a susceptible biotype.

Vaughn, K C; Marks, M D; Weeks, D P. 1987. A Dinitroaniline-Resistant Mutant of Eleusine indica Exhibits Cross-Resistance and Supersensitivity to Antimicrotubule Herbicides and Drugs. Plant Physiology 83 : 956 - 964.

A dinitroaniline-resistant (R) biotype of Eleusine indica (L.) Gaertner. (goosegrass) is demonstrated to be cross-resistant to a structurally non-related herbicide, amiprophosmethyl, and supersensitive to two other classes of compounds which disrupt mitosis. These characteristics of the R biotype were discovered in a comparative test of the effects of 24 different antimitotic compounds on the R biotype and susceptible (S) wild-type Eleusine. The compounds tested could be classified into three groups based upon their effects on mitosis in root tips of the susceptible (S) biotype. Class I compounds induced effects like the well known mitotic disrupter colchicine: absence of cortical and spindle microtubules, mitosis arrested at prometaphase, and the formation of polymorphic nuclei after arrested mitosis. The R biotype was resistant to treatment with some class I inhibitors (all dinitroaniline herbicides and amiprophosmethyl) but not all (e.g. colchicine, podophyllotoxin, vinblastine, and pronamide). Roots of the R biotype, when treated with either dinitroaniline herbicides or amiprophosmethyl, exhibited no or only small increases in the mitotic index nor were the spindle and cortical microtubules affected. Compounds of class II (carbamate herbicides and griseofulvin) cause misorientation of microtubules which results in multinucleated cells. Compounds of class III (caffeine and structually related alkaloids) cause imcomplete cell walls to form at telophase. Each of these last two classes of compounds affected the R biotype more than the S biotype (supersensitivity). The cross-resistance and high levels of resistance of the R biotype of Eleusine to the dinitroaniline herbicides and the structurally distinct herbicide, amiprophosmethyl, indicate that a mechanism of resistance based upon metabolic modification, translocation, or compartmentation of the herbicides is probably not operative.

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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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