Multiple resistant Galium spurium from Canada, Alberta

International Survey of Herbicide-Resistant Weeds

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Friday, November 22, 2024

MULTIPLE RESISTANT FALSE CLEAVERS
(Galium spurium)

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

Canada, Alberta

INTRODUCTION		FALSE CLEAVERS
False Cleavers (Galium spurium) is a dicot weed in the Rubiaceae family. In Alberta this weed first evolved multiple resistance (to 2 herbicide sites of action) in 1996 and infests Canola, Cereals, and Wheat. Multiple resistance has evolved to herbicides in the Groups 2 (Legacy B), and Auxin Mimics HRAC Group 4 (Legacy O). These particular biotypes are known to have resistance to imazethapyr, metsulfuron-methyl, quinclorac, sulfometuron-methyl, thifensulfuron-methyl, triasulfuron, and tribenuron-methyl and they may be cross-resistant to other herbicides in the Groups 2 (Legacy B), and Auxin Mimics HRAC Group 4 (Legacy O). 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 18, 2014 )
Common Name	False Cleavers
Species	Galium spurium
Group	Inhibition of Acetolactate Synthase HRAC Group 2 (Legacy B) Auxin Mimics HRAC Group 4 (Legacy O)
Herbicides	imazethapyr, metsulfuron-methyl, quinclorac, sulfometuron-methyl, thifensulfuron-methyl, triasulfuron, and tribenuron-methyl
Location	Canada, Alberta
Year	1996
Situation(s)	Canola, Cereals, and Wheat
Contributors - (Alphabetically)	Linda Hall
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NOTES ABOUT THIS BIOTYPE

GENERAL

Hugh Beckie

L. M. Hall, K. M. Stromme, G. P. Horsman, and M. D. Devine. 1998. Resistance to acetolactate synthase inhibitors and quinclorac in a biotype of false cleavers (Galium spurium). Weed Sci. 46:390-396.

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MECHANISM

Hugh Beckie

ALS resistance is due to target site insensitivity, whereas the mechanism of quinclorac resistance is unknown.

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ACADEMIC ASPECTS

Confirmation Tests

Greenhouse, and Laboratory trials comparing a known susceptible False Cleavers biotype with this False Cleavers 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 2, 4 resistant False Cleavers 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 multiple resistant False Cleavers from Alberta please update the database.

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CONTRIBUTING WEED SCIENTISTS

LINDA HALL

Alberta Agriculture Plant Industry Division Agronomy Unit 4550 New Linden Hill Rd Ste 501, Edmonton, T6H 5Z2, Alberta Canada Email Linda Hall

ACKNOWLEDGEMENTS
The Herbicide Resistance Action Committee, The Weed Science Society of America, and weed scientists in Alberta have been instrumental in providing you this information. Particular thanks is given to Linda Hall for providing detailed information.

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Herbicide Resistant False Cleavers Globally
(Galium spurium)

Country

FirstYear

Situation

Active Ingredients

Site of Action

Austria

2024

Sugar beets

foramsulfuron, and thiencarbazone-methyl

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

Canada (Alberta)

1996

Canola, Cereals, and Wheat

imazethapyr, metsulfuron-methyl, quinclorac, sulfometuron-methyl, thifensulfuron-methyl, triasulfuron, and tribenuron-methyl

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

Canada (Saskatchewan)

2006

Spring Barley, and Wheat

thifensulfuron-methyl, and tribenuron-methyl

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

Canada (Manitoba)

2008

Canola

thifensulfuron-methyl, and tribenuron-methyl

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

Greece

2022

Wheat

bensulfuron-methyl, florasulam, metsulfuron-methyl, and pyroxsulam

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

Specific Papers about this Case

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Beckie, H. J. ; Warwick, S. I. ; Sauder, C. A. ; Kelln, G. M. ; Lozinski, C.. 2012. Acetolactate synthase inhibitor-resistant false cleavers (Galium spurium) in western Canada. Weed Technology 26 : 151 - 155.

Cleavers species (false cleavers and catchweed bedstraw) are among the top 10 most abundant weeds across the prairie region of western Canada, and are increasing in relative abundance at the fastest rate since the 1970s. In 2008, two false cleavers populations from Tisdale and Choiceland, Saskatchewan, were suspected of acetolactate synthase (ALS)-inhibitor resistance. Dose-response experiments were conducted with the use of imazethapyr and florasulam, both ALS inhibitors, as well as fluroxypyr, a synthetic auxin. Additionally, a 1,954-base-pair region of the ALS gene including sites known to confer ALS resistance were sequenced. Both populations were highly resistant to imazethapyr (resistance factors greater than 100), one population (Tisdale) was highly resistant to florasulam (Choiceland population susceptible, although a second, larger screening of 200 individuals indicated low frequency [2%] florasulam resistance), and both populations were susceptible to fluroxypyr. All sequenced Tisdale individuals screened with imazethapyr posessed the Trp₅₇₄Leu mutation. In contrast, three point mutations were found for Choiceland individuals sequenced: Ser₆₅₃Asn, Trp₅₇₄Leu, and Asp₃₇₆Glu. These ALS target-site mutations have not been documented previously in this species..

Eerd, L. L. van ; Stephenson, G. R. ; Kwiatkowski, J. ; Grossmann, K. ; Hall, J. C.. 2005. Physiological and biochemical characterization of quinclorac resistance in a false cleavers (Galium spurium L.) biotype. Journal of Agricultural and Food Chemistry 53 : 1144 - 1151.

The physiological and biochemical basis for quinclorac resistance in a false cleavers (Galium spurium L.) biotype was investigated. There was no difference between herbicide resistant (R) and susceptible (S) false cleavers biotypes in response to 2,4-D, clopyralid, glyphosate, glufosinate-ammonium, or bentazon. On the basis of GR₅₀ (growth reduction of 50%) or LD₅₀ (lethal dose to 50% of tested plants) values, the R biotype was highly resistant to the acetolactate synthase (ALS) inhibitor, thifensulfuron-methyl (GR₅₀ resistance ratio R/S=57), and quinolinecarboxylic acids (quinclorac R/S=46), resistant to MCPA (R/S=12), and moderately resistant to the auxinic herbicides picloram (R/S=3), dicamba (R/S=3), fluroxypyr (R/S=3), and triclopyr (R/S=2). The mechanism of quinclorac resistance was not due to differences in [¹⁴C]quinclorac absorption, translocation, root exudation, or metabolism. Seventy-two hours after root application of quinclorac, ethylene increased ca. 3-fold in S but not R plants when compared to controls, while ABA increased ca. 14-fold in S as opposed to ca. 3-fold in R plants suggesting an alteration in the auxin signal transduction pathway, or altered target site causes resistance in false cleavers. The R false cleavers biotype may be an excellent model system to further examine the auxin signal transduction pathway and the mechanism of quinclorac and auxinic herbicide action..

Eerd, L. L. van ; McLean, M. D. ; Stephenson, G. R. ; Hall, J. C.. 2004. Resistance to quinclorac and ALS-inhibitor herbicides in Galium spurium is conferred by two distinct genes. Weed Research (Oxford) 44 : 355 - 365.

Classical Mendelian experiments were conducted to determine the genetics and inheritance of quinclorac and acetolactate synthase (ALS)-inhibitor resistance in a biotype of Galium spurium. Plants were screened with the formulated product of either quinclorac or the ALS-inhibitor, thifensulfuron, at the field dose of 125 or 6 g active ingredient (a.i.) ha^-1 respectively. Segregation in the F₂ generation indicated that quinclorac resistance was a single, recessive nuclear trait, based on a 1:3 segregation ratio [resistant:susceptible (R:S)]. Resistance to ALS inhibitors was due to a single, dominant nuclear trait, segregating in the F₂ generation in a 3:1 ratio (R:S). The genetic models were confirmed by herbicide screens of F₁ and backcrosses between the F₁ and the S parent. F₂ plants that survived quinclorac treatment set seed and the resulting F₃ progeny were screened with either herbicide. Quinclorac-treated F₃ plants segregated in a 1:0 ratio (R:S), hence F₂ progenitors were homozygous for quinclorac resistance. In contrast, F₃ progeny segregated into three ratios: 1:0, 3:1 and 0:1 (R:S) in response to ALS-inhibitor treatment. This segregation pattern indicates that their F₂ parents were either homozygous or heterozygous for ALS-inhibitor resistance. Therefore, there were clearly two distinct resistance mechanisms encoded by two genes that were not tightly linked as demonstrated by segregation patterns of the F₃..

Hall, L. M. ; Stromme, K. M. ; Horsman, G. P.. 1998. Resistance to acetolactate synthase inhibitors and quinclorac in a biotype of false cleavers (Galium spurium). Weed Science 46 : 390 - 396.

A false cleavers (G. spurium) population that survived treatment with triasulfuron/bromoxynil in 1996 was identified in central Alberta, Canada, in a field that had been treated with acetolactate synthase (ALS) inhibitors in 3 of the previous 6 years. In greenhouse studies, this biotype was highly resistant to the ALS inhibitors triasulfuron, thifensulfuron + tribenuron, and sulfometuron and moderately resistant to imazethapyr; GR50s were >16, >5, >1.0, and 9.9, respectively. Cross-resistance was also identified to the auxin-type herbicide quinclorac (GR50 >6.7) but not to fluroxypyr (GR50 = 1) or MCPA + mecoprop + dicamba. Quinclorac had not been used previously in this field. Analysis of ALS extracted from the resistant biotype and a susceptible biotype from a nearby location indicated that resistance to ALS inhibitors was due to an altered target site with reduced sensitivity to a broad range of ALS inhibitors. The ALS I50s for triasulfuron, metsulfuron, chlorsulfuron, thifensulfuron, and imazethapyr were 36, 34, 92, 96, and 14 times higher, respectively, for the resistant compared to the susceptible biotype. The mechanism of resistance to quinclorac is unknown. This is the first report of high-level herbicide resistance in this weed species..

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Literature about Similar Cases

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Haukkapää, A. L. ; Junnila, S. ; Eriksson, C. ; Tulisalo, U. ; Seppänen, M.. 2005. Efficacy of imazamox in imidazolinone-resistant spring oilseed rape in Finland. Agricultural and Food Science 14 : 377 - 388.

Imidazolinonies (IMIs) are a group of herbicides inhibiting acetolactate synthase (ALS) activity. They control the growth of many broadleaved weeds and annual grass species. Herbicide resistance against imidazolinonies has been transferred in some crop species, for example in oilseed rape. IMI-resistant oilseed rape cultivars have been developed by a mutation in ALS. They have been on the market for a few years, especially in North America. To determine if imazamox, an imidazolinone herbicide, and IMI-resistant oilseed rape cultivars are suitable for cultivation in Finland, 4 herbicide trials in 3 locations in Finland was conducted. Imazamox had no negative effect on yield or oil quality characters of IMI-resistant oilseed rape. Some transient chlorosis was observed immediately after the treatment, but it was not apparent after a few days. The effects of imazamox against the most troublesome weeds in oilseed field in Finland, Chenopodium album and Galium spurium, were very good. Imazamox had good or moderate effects on Stellaria media, whereas its effects on Viola arvensis, Lapsana communis and Fallopia convolvulus [Polygonum convolvulus] were insufficient. If the total weed number was high or the emergence of oilseed rape was slow, the application of imazamox increased the yield of oilseed rape compared to untreated control. Imazamox is a good alternative in controlling weeds for Finnish oilseed fields. Therefore, it would be beneficial to transfer the IMI-resistance into Finnish oilseed and turnip rape lines..

Eerd, L. L. van ; Stephenson, G. R. ; Hall, J. C.. 2001. Response of a quinclorac-resistant false cleaver (Galium spurium) biotype to several auxinic herbicides. : 595 - 600.

Due to lack of control following treatment with an acetolactate synthase (ALS) herbicide, G. spurium seeds were collected from a field in Alberta, Canada. ALS resistance was due to target-site insensitivity resulting from a point mutation in the ALS gene. This ALS resistant biotype was also resistant to quinclorac. We are interested in characterizing quinclorac resistance in this G. spurium biotype, particularly the pattern of response to other auxinic herbicides. Plants were treated at the 3- to 4-whorl stage of development with 1/4, 1, and 4 times the field dose of the following auxinic herbicides (1× dose in g a.i./ha): quinclorac (125.0), triclopyr (229.7), dicamba (290.4), fluroxypyr (144.1), picloram (273.8), clopyralid (306.2), and 2,4-D (568.5). Plants were harvested 14 days after treatment. Symptoms varied with the different herbicides and ranged from leaf hyponasty/epinasty to whole plant wilting and death. LD₅₀ values for quinclorac-resistant and susceptible biotypes were >1500 and 47 g a.i./ha, respectively. Based on calculated LD₅₀ values, the resistant biotype was moderately resistance to triclopyr but not to the other auxinic herbicides tested. Cross-resistance of this G. spurium biotype to quinclorac and triclopyr suggests that the mechanism of resistance may be similar and related to similar chemical structure. However, differences in phytotoxic response of both biotypes suggest that each auxinic herbicide tested cause slightly different physiological responses in G. spurium..

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