<b>HRAC Group 5</b> <font size='2'> (Legacy C1 C2) </font> resistant Chenopodium album from France

International Survey of Herbicide-Resistant Weeds

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Thursday, October 31, 2024

HRAC GROUP 5 (LEGACY C1 C2) RESISTANT COMMON LAMBSQUARTERS
(Chenopodium album)

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

France

INTRODUCTION		COMMON LAMBSQUARTERS
Common Lambsquarters (Chenopodium album) is a dicot weed in the Chenopodiaceae family. In France this weed first evolved resistance to Group 5 (Legacy C1 C2) herbicides in 1978 and infests Corn (maize). 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 atrazine, metamitron, and metribuzin 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 Mar 16, 2018 )
Common Name	Common Lambsquarters
Species	Chenopodium album
Group	PSII inhibitors - Serine 264 Binders HRAC Group 5 (Legacy C1 C2)
Herbicides	atrazine, metamitron, and metribuzin
Location	France
Year	1978
Situation(s)	Corn (maize)
Contributors - (Alphabetically)	Jacques Gasquez
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NOTES ABOUT THIS BIOTYPE

GENERAL

Christophe Délye

Mechant E (2011). Metamitron resistant Chenopodium album: characterisation, detection and distribution in Belgian sugar beet. PhD thesis, Ghent University, Ghent, Belgium. 245 pages.

The original case of Group C1 resistance in CHEAL was to the triazine herbicide atrazine in 1978 (mutation at Ser264 on psbA, triazine-specific resistance). This thesis reports resistance to CHEAL resistance to metamitron, metribuzin, herbicides in the triazinones family.

Year and location seed was collected: 2005, North of France.

The type of tests that were done: dose response + target-site sequencing

The crop(s) that it was found in: Sugar beet.

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ACADEMIC ASPECTS

Confirmation Tests

Greenhouse trials comparing a known susceptible Common Lambsquarters biotype with this Common Lambsquarters 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 Common Lambsquarters 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

Studies on the mechanism of resistance of Group 5 (Legacy C1 C2) resistant Common Lambsquarters from France 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 5 (Legacy C1 C2) resistant Common Lambsquarters from France please update the database.

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CONTRIBUTING WEED SCIENTISTS

JACQUES GASQUEZ

Inra Laboratoire De Malherbologie 702 Hickory Ct Dijon, 21034, Cedex France Email Jacques Gasquez

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

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Herbicide Resistant Common Lambsquarters Globally
(Chenopodium album)

Country

FirstYear

Situation

Active Ingredients

Site of Action

Belgium

1980

Corn (maize), Potatoes, Roadsides, and Sugar beets

atrazine, metamitron, and metribuzin

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

Bulgaria

1989

Cropland

metribuzin

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

Canada (Ontario)

1973

Corn (maize), and Cropland

atrazine

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

Canada (Quebec)

1980

Corn (maize)

atrazine

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

Canada (Ontario)

2001

Soybean

thifensulfuron-methyl

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

Canada (Quebec)

2008

Soybean

thifensulfuron-methyl

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

Canada (Saskatchewan)

2009

Spring Barley, and Wheat

thifensulfuron-methyl, and tribenuron-methyl

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

Canada (Prince Edward Island)

2018

Potatoes

metribuzin

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

Canada (New Brunswick)

2018

Potatoes

metribuzin

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

Czech Republic

1986

Corn (maize), and Sugar beets

atrazine, cyanazine, lenacil, metamitron, prometon, simazine, terbuthylazine, and terbutryne

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

Finland

2015

Spring wheat

tribenuron-methyl

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

France

1978

Corn (maize)

atrazine, metamitron, and metribuzin

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

Germany

1980

Corn (maize), and Potatoes

simazine

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

Greece

2000

Potatoes

metribuzin

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

Italy

1982

Corn (maize)

atrazine

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

Netherlands

1980

Corn (maize)

atrazine

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

New Zealand

1979

Corn (maize)

atrazine

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

New Zealand

2005

Corn (maize)

aminopyralid, clopyralid, and dicamba

Auxin Mimics ( HRAC Group 4 (Legacy O)

Norway

1994

Cropland

metribuzin

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

Norway

1994

Cropland

linuron

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

Poland

1991

Corn (maize), and Sugar beets

atrazine, and metamitron

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

Portugal

2003

Corn (maize)

atrazine

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

Slovenia

1996

Corn (maize)

atrazine

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

Spain

1987

Corn (maize)

atrazine

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

Sweden

2005

Potatoes, and Sugar beets

metamitron, and metribuzin

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

Switzerland

1977

Corn (maize)

atrazine

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

Ukraine

2022

Corn (maize), Soybean, Sunflower, and Wheat

florasulam, flumetsulam, imazamox, iodosulfuron-methyl-Na, thiencarbazone-methyl, thifensulfuron-methyl, and tribenuron-methyl

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

United Kingdom

1989

Cropland

simazine

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

United States (Michigan)

1975

Corn (maize), Nurseries, and Soybean

atrazine, metribuzin, and simazine

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

United States (New York)

1977

Corn (maize), and Soybean

atrazine, cyanazine, and simazine

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

United States (Virginia)

1979

Corn (maize)

atrazine

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

United States (Wisconsin)

1979

Corn (maize)

atrazine

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

United States (North Carolina)

1980

Corn (maize)

atrazine

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

United States (Pennsylvania)

1980

Corn (maize)

atrazine

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

United States (Indiana)

1980

Corn (maize), and Cropland

atrazine

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

United States (Ohio)

1981

Corn (maize)

atrazine

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

United States (Minnesota)

1982

Corn (maize)

atrazine

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

United States (Maryland)

1982

Corn (maize), and Cropland

atrazine

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

United States (Massachusetts)

1983

Corn (maize)

atrazine

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

United States (Illinois)

1985

Corn (maize)

atrazine

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

United States (Maine)

1985

Corn (maize)

atrazine

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

United States (New Hampshire)

1986

Corn (maize)

atrazine

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

United States (Delaware)

1988

Corn (maize)

atrazine

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

United States (Iowa)

1989

Corn (maize)

atrazine

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

United States (Vermont)

1991

Corn (maize)

atrazine

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

United States (Connecticut)

1992

Corn (maize)

atrazine

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

United States (Rhode Island)

1995

Corn (maize)

atrazine

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

United States (Tennessee)

1998

Corn (maize)

atrazine

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

United States (West Virginia)

2000

Corn (maize)

atrazine

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

United States (Michigan)

2001

Soybean

imazamox, and thifensulfuron-methyl

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

United States (Ohio)

2001

Soybean

thifensulfuron-methyl

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

United States (Washington)

2010

Mint, and Potatoes

metribuzin, and terbacil

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

Specific Papers about this Case

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Darmency, H. ; Gasquez, J.. 1990. Appearance and spread of triazine resistance in common lambsquarters (Chenopodium album). Weed Technology 4 : 173 - 177.

This paper is given at a symposium of the Weed Science Society of America entitled Herbicide resistance, held on 8 Feb. 1989 at Dallas, Texas. The first step in appearance of herbicide-resistant weed populations is the appearance of resistant plants or mutants. While efforts are underway to study and predict the spread of resistant plants within weed populations, knowledge of the conditions prevailing at the time of appearance of the first resistant plants is misunderstood. In studies with atrazine-resistant C. album, the population structure and variability, the presence of unusual genotypes that had a high mutation rate, the occurrence of a low-dose resistant phenotype that was the precursor of a high-dose resistant phenotype, and the potential for multiplication and spread were shown to be of major importance in the behaviour of herbicide resistance..

Tremolieres, A. ; Darmency, H. ; Gasquez, J. ; Dron, M. ; Connan, A.. 1988. Variation of transhexadecenoic acid content in two triazine resistant mutants of Chenopodium album and their susceptible progenitor. Plant Physiology 86 : 967 - 970.

Two atrazine resistant mutants of C. album and their susceptible progenitor were analyzed for lipid composition. In the phosphatidyldiacylglycerol the δ3-trans-hexadecenoic acid (C16:1 trans) percentage was higher in the 2 resistant phenotypes. However, this difference appeared later in the development of the leaves and was not clearly observed in young leaves and seedlings. Thus, the increase of the C16:1 trans during the leaf development of the resistant phenotypes is probably a secondary effect of the psbA mutation that arises in compensation for some photosynthesis deficiency. The significance of the lipid differences shown between the 2 resistant mutants is discussed in terms of whether they are responsible for the 2 different levels of herbicide resistance observed in the field..

Bettini, P., S. Mcnally, M. Sevignac, H. Darmency, J. Gasquez, And M. Dron.. 1987. Atrazine resistance in Chenopodium album. Low and high levels of resistance to the herbicide are related to the same chloroplast psbA gene mutation. Plant Physiology 84 : 1442 - 1446.

Gasquez, J. ; Al-Mouemar, A. ; Darmency, H.. 1985. Triazine herbicide resistance in Chenopodium album L.: occurrence and characteristics of an intermediate biotype. Pesticide Science 16 : 392 - 396.

Intermediate (I) biotypes for triazine herbicide resistance in C. album (as defined by a peculiar fluorescence curve), had the same ID₅₀ values as resistant (R) plants for chloroplast response to atrazine, but proved to be more susceptible at lower doses. Furthermore, the lethal dose in seedling treatments was lower than that of the R plants, but 6 times higher than for susceptible (S) plants. These I characteristics of I biotypes were maternally inherited in crosses. I biotypes were isolated from various progenies of susceptible precursor (Sp) plants in 2 garden populations. This could be the first step in the occurrence of triazine herbicide resistance. However, Sp plants have not been observed in field populations. The significance of the presence of a single isozyme pattern for all Sp plants is discussed. The results suggest an evolutionary pathway from S to R plants via I biotypes..

Gasquez, J. ; Al-Mouemar, A. ; Darmency, H.. 1984. Which genes for chloroplast resistance to triazines in Chenopodium album L.?. : 281 - 286.

C. album is the most widespread weed with triazine resistant strains in France. 5 biotypes have been identified: susceptible (S), intermediate (I) and resistant (R) plants with different levels of field resistance and peculiar foliar fluorescence; a specific susceptible genotype (Sp) which produces low rates of I plants; and resistant plants (Ri) which are the offspring of treated I plants. This suggest that resistance in this sp. may occur through Sp plants producing I plants by mutation, which, if not killed by treatment, may produce R plants by selection. Inbred S, I and R plants give stable progeny. Reciprocal crosses S/cross/I, I/cross/S and S/cross/R, R/cross/S showed maternal cytoplasmic heredity, except for the S/cross/R crosses which produced a few resistant F₁. These F₁ gave I and R plants in their progeny. Reciprocal I/cross/R and R/cross/I crosses produced F₁ with female characteristics and F₂ segregated in I and R plants but with an excess of female types. These results may indicate either a complex phenomenon combining a cytoplasmic heredity and a nuclear heredity or different mutations in respect of I and R and specific mechanisms of transmission of cytoplasmic characteristics via the pollen..

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Literature about Similar Cases

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Schwartau, V. V., Mykhalska, L. M. . 2022. Herbicide-resistant weed biotypes in Ukraine. Reports of the National Academy of Sciences of Ukraine : 85 - 94.

In Ukraine, resistant to the action of herbicides — acetolactate synthase inhibitors of the imidazolinone class — imazapyr and imazamox biotypes of monocot Echinochloa crus-galli var. crus-galli, and dicot Amaranthus retroflexus, and Chenopodium album have been identified. Cross-resistance to herbicides: monocot to sulfonylurea (nicosulfuron), and triazole pyrimidines (penoxsulam); dicots to sulfonylurea foramsulfuron, iodosulfuron-methyl-sodium, thifensulfuron-methyl, tribenuron-methyl; to sulfonylaminocarbonyl triazolinone derivative — thiencarbazone-methyl; to t riazole pyrimidine derivatives — florasulam, and flumetsulam were established. The multiple resistance of Echinochloa crus-galli, Amaranthus retroflexus, and Chenopodium album to herbicides of the classes of glycine derivatives — glyphosate, monocot to graminicide pinoxaden, and dicot species to phenoxy carboxylic derivatives — 2,4-D, benzoic acid — dicamba; triketones — topramezone; diphenyl ethers — aclonifen have not been established. It was shown for the first time that herbicide compositions under the influence of the ammonium pool can increase the level of controlling resistant weed biotypes effectiveness. The identification of highly harmful ALS-resistant Echinochloa crus-galli, Amaranthus retroflexus, and Chenopodium album in the south and central part of the “grain belt” of Ukraine shows the limited effectiveness of weed control exclusively with herbicides with one mechanism of action and requires a significant revision of the principles of crop rotation formation and methods of weed control in the state to maintain high levels of profitability and productivity of agrophytocenoses. Solving these issues is urgent in order to preserve Ukraine’s potential as one of the guarantors of world food security..

Thiel, H. ; Varrelmann, M.. 2014. Identification of a new PSII target site psbA mutation leading to D1 amino acid Leu₂₁₈Val exchange in the Chenopodium album D1 protein and comparison to cross-resistance profiles of known modifications at positions 251 and 264. Pest Management Science 70 : 278 - 285.

BACKGROUND: Resistance of Chenopodium album to triazinones and triazines can be caused by two amino acid exchanges, serine-264-glycine (Ser₂₆₄Gly) and alanine-251-valine (Ala₂₅₁Val), in the chloroplast D1 protein. This paper describes the identification of a biotype with a leucine-218-valine (Leu₂₁₈Val) switch found in German sugar beet fields with unsatisfactory weed control. A greenhouse experiment has been performed to compare the resistance profile of the newly identified biotype with biotypes that carry the Ser₂₆₄Gly and Ala₂₅₁Val mutations. RESULTS: Application rate-response curves obtained from the greenhouse experiment showed that the Leu₂₁₈Val exchange induced significant resistance against the triazinones but not against terbuthylazine. The level of resistance against the triazinones was higher in the Ser₂₆₄Gly and Ala₂₅₁Val biotypes compared with the Leu₂₁₈Val biotype. All biotypes tested were more resistant to metribuzin than to metamitron. Following terbuthylazine treatment, Ser₂₆₄Gly displayed a high level of resistance, Ala₂₅₁Val showed moderate resistance. A PCR-RFLP assay for Ser₂₆₄Gly has been extended to include detection of Ala₂₅₁Val and Leu₂₁₈Val mutations. CONCLUSION: The D1 Leu₂₁₈Val substitution in C. album confers significant resistance to triazinones. This suggests that Leu₂₁₈Val is involved in the binding of triazinones. First establishment of the resistance profiles of the three psbA mutations suggests that these mutations have been independently selected..

Aper, J. ; Mechant, E. ; Riek, J. de ; Laere, K. van ; Bulcke, R. ; Reheul, D.. 2012. Analysis of local spread of metamitron-resistant Chenopodium album patches in Belgium. Weed Research (Oxford) 52 : 421 - 429.

Tracing spread of weeds with molecular markers can give valuable information on the importance of migration mechanisms. This study investigated the local spread of metamitron-resistant Chenopodium album patches in the west of the province West Flanders (Belgium) using amplified fragment length polymorphism (AFLP) markers. During the summer of 2009, leaf samples of C. album plants were harvested in 27 patches, distributed over 10 sugar beet fields and one maize field. The fields were grouped in four local clusters, each corresponding to a farmer who cultivated these fields. A cleaved amplified polymorphic sequence procedure identified the Ser₂₆₄ to Gly mutation in the D1 protein, endowing resistance to metamitron, a key herbicide applied in sugar beet. The majority of the sampled plants within a patch (97% on average) carried this mutation. Genetic variation among the four farmers' locations (12%) and among the C. album patches within the farmers' locations (14%) was significant according to amova (P<0.001). In addition, Mantel tests confirmed a positive correlation between genetic distance (linearised φ_PT between pairs of patches) and the logarithm of geographic distance for the complete data set (Mantel coefficient significant at P=0.001), suggesting isolation by distance. Nevertheless, genetic similarity between patches from different fields indicated that seed transport by agricultural machinery and manure is likely to have an important impact on the spread of metamitron-resistant biotypes. Farmers should become aware of the resistance problem as soon as possible, in order to prevent further spread in their fields..

Aper, J. ; Mechant, E. ; Rubin, B. ; Heyerick, A. ; Callebaut, G. ; Mangelinckx, S. ; Deforce, D. ; Kimpe, N. de ; Bulcke, R. ; Reheul, D.. 2012. Absorption, translocation and metabolism of metamitron in Chenopodium album. Pest Management Science 68 : 209 - 216.

BACKGROUND: In recent years, common lambsquarters (Chenopodium album L.) populations from sugar beet fields in different European countries have responded as resistant to the as-triazinone metamitron. The populations have been found to have the same D1 point mutation as known for atrazine-resistant biotypes (Ser₂₆₄ to Gly). However, pot experiments revealed that metamitron resistance is not as clear-cut as observed with triazine resistance in the past. The objectives of this study were to clarify the absorption, translocation and metabolic fate of metamitron in C. album. RESULTS: Root absorption and foliar absorption experiments showed minor differences in absorption, translocation and metabolism of metamitron between the susceptible and resistant C. album populations. A rapid metabolism in the C. album populations was observed when metamitron was absorbed by the roots. The primary products of metamitron metabolism were identified as deamino-metamitron and metamitron-N-glucoside. PABA, known to inhibit the deamination of metribuzin, did not alter the metabolism of metamitron, and nor did the cytochrome P450 inhibitor PBO. However, inhibition of metamitron metabolism in the presence of the cytochrome P450 inhibitor ABT was demonstrated. CONCLUSION: Metamitron metabolism in C. album may act as a basic tolerance mechanism, which can be important in circumstances favouring this degradation pathway..

Aper J, De Riek J, De Cauwer B, Bulcke R, Reheul D. 2012. The origin of metamitron resistant Chenopodium album populations in sugar beet. Communications in agricultural and applied biological sciences 77 : 335 - 342.

Chenopodium albumL. is a major weed in spring-planted crops in the temperate regions of the world. Since 2000, farmers have reported an unsatisfactory control of this weed in sugar beet fields in Belgium, France and The Netherlands. Frequently, the survivingC. albumplants are resistant to metamitron, a key herbicide in this crop. Metamitron resistance inC. albumis caused by a Ser264 to Gly mutation in the psbA gene on the chloroplast genome, which prevents binding of metamitron to its target site. This mutation causes also resistance to other herbicides with a similar mode of action, like metribuzin -applied in potato- and atrazine in particular. Atrazine has been applied very frequently in maize in the 1970s and the 1980s, but is now banned in Europe due to environmental reasons. The persistent use of atrazine in maize confronted Belgian and other European farmers in the early 1980s with atrazine resistantC. albumwith the same Ser264 to Gly mutation. The problems with atrazine resistantC. albumdisappeared when other herbicides were applied in maize. Unfortunately, this is not the case for metamitron resistantC. albumin sugar beet, because no replacement herbicide is readily available. The history of atrazine use in maize brought up a question concerning the origin of the current metamitron resistantC. albumpopulations. Have these populations been selected locally by regular use of metamitron in sugar beet or did the selection occur earlier by atrazine use when maize was grown in the same fields? This would have serious implications regarding the reversibility of herbicide resistance. Therefore, soil samples were collected on 16 fields with different histories: five fields with an organic management over 25 years, two fields with a history of atrazine resistantC. album, five fields with metamitron resistantC. albumin sugar beet and four fields which were under permanent grassland for 10 years, preceded by a regular rotation in which sugar beet was a key crop. The seeds ofC. albumwere extracted from the soil and germinated on a germination table. Germinated seeds were allowed to grow in a growth chamber. Metamitron resistance was determined by a chlorophyll fluorescence test and leaf material was sampled for AFLP-analysis. For all fields, estimations were made of the size of the seed bank (i.e. an indirect estimate of population size), the frequency of resistant plants and the genetic diversity of resistant and susceptible populations. The results indicate that herbicide-resistant C. album populations are persistent and maintain their adaptive capacity, challenging future management of metamitron resistantC. album.

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