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

INTERNATIONAL HERBICIDE-RESISTANT WEED DATABASE

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

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

Belgium

INTRODUCTION		COMMON LAMBSQUARTERS
Common Lambsquarters (Chenopodium album) is a dicot weed in the Chenopodiaceae family. In Belgium this weed first evolved resistance to Group 5 (Legacy C1 C2) herbicides in 1980 and infests Corn (maize), Potatoes, Roadsides, and Sugar beets. 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 Feb 07, 2014 )
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	Belgium
Year	1980
Situation(s)	Corn (maize), Potatoes, Roadsides, and Sugar beets
Contributors - (Alphabetically)	Robert Bulcke, and Benny De Cauwer
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NOTES ABOUT THIS BIOTYPE

AREAS FOUND

Robert Bulcke

In all 9 provinces of Belgium.

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AREAS FOUND

Benny De Cauwer

In all provinces of Belgium except Luxembourg province, it is spread over the entire sugar beet area.

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CROSS RESISTANCE

Benny De Cauwer

This biotype is moderately resistant to metamitron preplant incorporated (PPI) (resistance index RI = 75) and low level resistant to metamitron applied postemergence (POST) (RI = 7); it is highly resistant to metribuzin (POST) (RI > 100) and moderately resistant to metribuzin (PPI) (RI = 62-70). [(PhD theses: Els Mechant (2011) and Jonas Aper (2012)]. It resembles the atrazine resistant C. album biotype (selected in maize during the 1980’s). However, most of the metamitron-resistant populations were selected by metamitron (sugar beet) or metribuzin (potato grown in rotation with sugar beet).

This biotype is highly cross-resistant to: atrazine and terbuthylazine (RI >1000), and moderately cross-resistant to chloridazon (RI = 10-16). It is also low level cross-resistant to lenacil (RI = 5) and linuron (RI = 2). It is susceptible to negative cross-resistant to bentazon (RI=0.6), ioxynil, aclonifen, clomazone, mesotrione, pendimethalin, acetochlor, dimethenamid-P, flufenacet, pethoxamide, S-metolachlor, ethofumesate and triallate (PhD thesis Els Mechant).

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DOSE RESPONSE

Benny De Cauwer

Field, Greenhouse, and Laboratory trials comparing a known susceptible Lambsquarters biotype with this 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.

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GENERAL

Benny De Cauwer

Fitness
Triazine- and triazinone-resistant weeds often exhibit a lower relative fitness when compared to susceptible biotypes. The most common mutation conferring triazine resistance (Ser 264 to Gly mutation of the psbA gene) also causes a reduction in CO2 fixation, quantum yield, and seed and biomass production. There is no record in this database referring specifically to fitness studies on Group C1/5 resistant Lambsquarters from Belgium.

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GENERAL

Robert Bulcke

Chenopodium album and Solanum nigrum are the most ommon and important R-biotypes, especially in silage corn.

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GENETICS

Benny De Cauwer

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MECHANISM

Benny De Cauwer

DNA analysis performed on Belgian resistant C. album populations demonstrated that metamitron resistance is caused by a serine264 to glycine mutation on the chloroplast psbA gene (i.e. target-site resistance), although the existence of an additional (non-target-site) resistance mechanism that contributes to metamitron-resistance cannot be excluded.

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ACADEMIC ASPECTS

Confirmation Tests

Field, Greenhouse, and Laboratory 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 Belgium 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

Researchers have indicated that Group 5/C1 C2 resistant Common Lambsquarters is ecologically less fit than normal susceptible Common Lambsquarters. There may be a note below or an article discussing the fitness of this biotype in the Fact Sheets and Other Literature

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CONTRIBUTING WEED SCIENTISTS

ROBERT BULCKE

University Gent Lab. Of Herbology - U. G. Plant Div 635 Capitol St NE, Weed Control Program Gent, B-9000 Belgium Email Robert Bulcke

BENNY DE CAUWER

Doctor assistant, Research associate University of Ghent, faculty of Bioscience-engineering Dept. Plant Production Weed Science Unit Coupure Links 653 9000 Gent, 9000 Belgium Email Benny De Cauwer

ACKNOWLEDGEMENTS
The Herbicide Resistance Action Committee, The Weed Science Society of America, and weed scientists in Belgium have been instrumental in providing you this information. Particular thanks is given to Robert Bulcke, and Benny De Cauwer 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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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.

Aper J, De Riek J, Mechant E, Bulcke R, Reheul D.. 2011. Local spread of metamitron resistantChenopodium albumL. patches. 76 : 491 - 499.

Molecular markers can provide valuable information on the spread of resistant weed biotypes. In particular, tracing local spread of resistant weed patches will give details on the importance of seed migration with machinery, manure, wind or birds. This study investigated the local spread of metamitron resistantChenopodium albumL. patches in the southwest region of the province West-Flanders (Belgium). During the summer of 2009, leaf and seed samples were harvested in 27 patches, distributed over 10 sugar beet fields and 1 maize field. The fields were grouped in four local clusters. Each cluster corresponded with the farmer who cultivated these fields. A cleaved amplified polymorphic sequence (CAPS) 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. Amplified fragment length polymorphism (AFLP) analysis was performed with 4 primer pairs and yielded 270 molecular markers, polymorphic for the whole dataset (303 samples). Analysis of molecular variance revealed that a significant part of the genetic variability was attributed to variation among the four farmer locations (12 %) and variation amongChenopodium albumpatches within the farmer locations (14%). In addition, Mantel tests revealed a positive correlation between genetic distances (linearised phipt between pairs of patches) and geographic distances (Mantel-coefficient significant at p = 0.002), suggesting isolation-by-distance. In one field, a decreased genetic diversity and strong genetic relationships between all the patches in this field supported the hypothesis of a recent introduction of resistant biotypes. Furthermore, genetic similarity between patches from different fields from the same farmer and from different farmers indicated that seed transport between neighbouring fields is likely to have an important impact on the spread of metamitron resistant biotypes.

Thiel, H. ; Kluth, C. ; Varrelmann, M.. 2010. A new molecular method for the rapid detection of a metamitron-resistant target site in Chenopodium album. Pest Management Science 66 : 1011 - 1017.

BACKGROUND: Resistance to photosystem II inhibitors - triazines (atrazine) and triazinones (metamitron, metribuzin) - in Chenopodium album L. is caused by the serine 264 to glycine mutation in the D1 protein. This mutation has been detected in C. album collections from Belgium with unsatisfactory metamitron efficacy in the field and was confirmed in greenhouse resistance bioassays. Incomplete herbicide efficacy in practice can also be caused by reduced uptake due to environmental conditions. Hence, for reliable differentiation and resistance identification, a rapid method for mutation detection in the target gene psbA is required. RESULTS: Dose-response curves obtained in herbicide greenhouse assays with metamitron-resistant and -susceptible reference biotypes showed that a dose of 2 L ha^-1 metamitron was suitable for discrimination. A psbA PCR-RFLP was developed, based on the presence of a FspBI restriction enzyme recognition site, covering D1 codon 264 in susceptible genotypes. A paper-based DNA extraction allowed direct processing of leaf samples already in the field. In order to detect the mutation even in mixed seed samples, a nested PCR-RFLP was also developed. CONCLUSION: The method allows exhaustive surveys screening C. album leaf or seed samples for the occurrence of the D1 Ser264Gly mutation to confirm or disprove metamitron resistance in the case of unsatisfactory control..

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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..

Agrikola, Y. ; Petersen, J.. 2012. Importance and approaches for the control of different photosystem-II-inhibitor resistant Chenopodium album biotypes in sugar beet and potatoes. Julius-Kühn-Archiv 1 : 111 - 118.

Resistance in weeds to PS-II herbicides is well known. From the end of the 1970s resistance to triazines in maize represented a particular problem. Today, because of the variety of alternative active ingredients for use on maize, this problem is considered to be solved. This is different for sugarbeet and potatoes because hardly any new herbicides have been developed during the last 20 years. Chenopodium album is a major weed in all summer crops. In maize, resistance to triazines (target-site resistance (TSR) at position 264 on the D1 protein) is known. In recent years, new TSRs in C. album (position 251 in Sweden and 218 in Lower Saxony, Germany) have been found. These biotypes exhibit resistance to triazinones and chloridazon but showed no cross-resistances to triazines. An outdoor pot trial with sugarbeet and potatoes showed that higher dosages of ethofumesate in sugarbeet and aclonifen in potatoes are able to control triazine- and triazinone-resistant C. album biotypes to a certain extent or even completely, respectively. A competition pot trial with maize and different C. album biotypes showed no significant differences in weed fitness concerning the parameters plant height, biomass and seed production..

Thiel, H. ; Varrelmann, M.. 2012. Cross resistance of different target site resistances in the psbA gene in Chenopodium album against herbicides of the Triazine und Triazinone groups. Julius-Kühn-Archiv : .

Ayala, J. ; Pérez, A. ; Rodríguez, M. ; Hernández, J. M.. 2011. Preliminary results on the detection of populations of Chenopodium spp. less sensitive to herbicides in sugar beet in the province of León. : 113 - 116.

Chenopodium control in sugar beet, was considered so far satisfactory. In 2010 and 2011, field trials have been carried out on populations of Chenopodium less sensitive to herbicide active ingredients (a.i.), in the province of León. Effectiveness of 100% on C. album and 94.7% on C. opulifolium were obtained. In laboratory has been determined the presence of a mutation in the target site of action of inhibitors of PSII at position 264 (amino acid change of serine to glycine). Most a.i. used in sugar beet act on PSII, so there is a need to establish control strategies in rotation with a.i. that act by different mechanisms. During autumn 2010 a survey was carried out to quantify the frequency of less sensitive populations. It has been estimated that 25% of the plots have presented difficulties for the control of Chenopodium..

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