<b>HRAC Group 5</b> <font size='2'> (Legacy C1 C2) </font> resistant Chenopodium album var. striatum (=C. strictum var. glaucophyllum) from United States, Michigan

INTERNATIONAL HERBICIDE-RESISTANT WEED DATABASE

HRAC GROUP 5 (LEGACY C1 C2) RESISTANT LATEFLOWERING GOOSEFOOT
(Chenopodium album var. striatum (=C. strictum var. glaucophyllum))

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

United States, Michigan

INTRODUCTION		LATEFLOWERING GOOSEFOOT
Lateflowering Goosefoot (Chenopodium album var. striatum (=C. strictum var. glaucophyllum)) is a dicot weed in the Chenopodiaceae family. In Michigan this weed first evolved resistance to Group 5 (Legacy C1 C2) herbicides in 2004 and infests Corn (maize), and Soybean. 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 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 05, 2007 )
Common Name	Lateflowering Goosefoot
Species	Chenopodium album var. striatum (=C. strictum var. glaucophyllum)
Group	PSII inhibitors - Serine 264 Binders HRAC Group 5 (Legacy C1 C2)
Herbicides	atrazine
Location	United States, Michigan
Year	2004
Situation(s)	Corn (maize), and Soybean
Contributors - (Alphabetically)	Steven Gower
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ACADEMIC ASPECTS

Confirmation Tests

Greenhouse trials comparing a known susceptible Lateflowering Goosefoot biotype with this Lateflowering Goosefoot 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 Lateflowering Goosefoot 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 5 (Legacy C1 C2) resistant Lateflowering Goosefoot from Michigan please update the database.

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CONTRIBUTING WEED SCIENTISTS

STEVEN GOWER

Former Weed Science Diagnostician (Now with Monsanto) Michigan State University Diagnostic Services 578 Wilson Rd. East Lansing, 48824, Michigan United States Email Steven Gower

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

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Herbicide Resistant Lateflowering Goosefoot Globally
(Chenopodium album var. striatum (=C. strictum var. glaucophyllum))

Country

FirstYear

Situation

Active Ingredients

Site of Action

Canada (Ontario)

1976

Corn (maize), and Cropland

atrazine

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

Czech Republic

1989

Corn (maize), and Sugar beets

atrazine, lenacil, prometryne, simazine, and terbutryne

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

United States (Michigan)

2004

Corn (maize), and Soybean

atrazine

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

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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