<b>HRAC Group 5</b> <font size='2'> (Legacy C1 C2) </font> resistant Senecio vulgaris from United States, California

International Survey of Herbicide-Resistant Weeds

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Tuesday, April 16, 2024

HRAC GROUP 5 (LEGACY C1 C2) RESISTANT COMMON GROUNDSEL
(Senecio vulgaris)

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

United States, California

INTRODUCTION		COMMON GROUNDSEL
Common Groundsel (Senecio vulgaris) is a dicot weed in the Asteraceae family. In California this weed first evolved resistance to Group 5 (Legacy C1 C2) herbicides in 1981 and infests Asparagus. 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 Dec 15, 2000 )
Common Name	Common Groundsel
Species	Senecio vulgaris
Group	PSII inhibitors - Serine 264 Binders HRAC Group 5 (Legacy C1 C2)
Herbicides	atrazine
Location	United States, California
Year	1981
Situation(s)	Asparagus
Contributors - (Alphabetically)	Jodie Holt
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NOTES ABOUT THIS BIOTYPE

AREAS FOUND

Jodie Holt

Salinas, California

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GENERAL

Jodie Holt

Farm Advisor provided samples; resistance was documented; no surveys were conducted.

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ACADEMIC ASPECTS

Confirmation Tests

Greenhouse trials comparing a known susceptible Common Groundsel biotype with this Common Groundsel 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 Groundsel indicate that the inheritance is determined by a one gene, dominant, cytoplasmic trait. 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 Groundsel from California 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 Groundsel from California please update the database.

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CONTRIBUTING WEED SCIENTISTS

JODIE HOLT

Professor and Associate Dean University of California Botany and Plant Sciences 900 University Drive Riverside, 92521, California United States Email Jodie Holt Web : Web Site Link

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

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Herbicide Resistant Common Groundsel Globally
(Senecio vulgaris)

Country

FirstYear

Situation

Active Ingredients

Site of Action

Belgium

1982

Corn (maize), Fruit, Nurseries, Railways, and Roadsides

simazine

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

Canada (Ontario)

1977

Corn (maize)

atrazine

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

Czech Republic

1988

Orchards, and Railways

atrazine, cyanazine, lenacil, prometryne, simazine, terbuthylazine, and terbutryne

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

France

1982

Cropland

simazine

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

France

2009

Grapes, and Wheat

flazasulfuron, florasulam, imazamox, iodosulfuron-methyl-Na, mesosulfuron-methyl, metsulfuron-methyl, prosulfuron, thiencarbazone-methyl, and tribenuron-methyl

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

Germany

1980

Orchards

atrazine

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

Netherlands

1982

Orchards

simazine

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

Norway

1996

Nurseries

simazine

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

Switzerland

1982

Grapes

simazine

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

Switzerland

1987

Vegetables

linuron

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

United Kingdom

1977

Orchards

metribuzin, and simazine

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

United States (Washington)

1970

Nurseries

simazine

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

United States (California)

1981

Asparagus

atrazine

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

United States (Michigan)

1990

Blueberries, and Corn (maize)

atrazine

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

United States (New York)

1991

Corn (maize)

atrazine, and simazine

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

United States (Oregon)

1995

Mint

bromoxynil

PSII inhibitors - Histidine 215 Binders ( HRAC Group 6 (Legacy C3)

Literature about Similar Cases

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Delye, C., R. Causse, and S. Michel. 2016. Genetic basis, evolutionary origin and spread of resistance to herbicides inhibiting acetolactate synthase in common groundsel (Senecio vulgaris).. Pest Management Science 72 : 89 - 102.

Background

Following control failure by herbicides inhibiting acetolactate-synthase (ALS) in French wheat fields and vineyards, we aimed at confirming resistance evolution and investigate the evolutionary origin and spread of resistance in the tetraploid species Senecio vulgaris (common groundsel), a widespread, highly mobile weed.

Results

Sequencing of two ALS homeologs in S. vulgaris enabled the first identification and characterisation of ALS-based resistance in this species. Cross-resistance patterns associated with Leu-197 and Ser-197 ALS1 were established using eight herbicides. Sequencing and genotyping showed that ALS-based resistance evolved by multiple, independent appearances of mutant ALS1 and ALS2 alleles followed by spread. Spread of a mutant ALS1 allele issued from one particular appearance event was observed over 60 km. Independent resistance appearance events and easy seed dispersion are the most likely reasons for populations of S. vulgaris containing different mutant ALS alleles. Accumulation of different alleles probably due to sexual reproduction was observed in the same plant.

Conclusion

Mutant ALS alleles and possibly other mechanisms cause resistance to ALS inhibitors in S. vulgaris. Management strategies should aim at limiting S. vulgaris establishment and seed set. Considering the mobility of this species, control coordination at a regional level is clearly necessary if resistance spread is to be contained.

Vila-Aiub, M M; Neve, P; Roux, F. 2011. A unified approach to the estimation and interpretation of resistance costs in plants. Heredity 107 : 386 - 394.

Plants exhibit a number of adaptive defence traits that endow resistance to past and current abiotic and biotic stresses. It is generally accepted that these adaptations will incur a cost when plants are not challenged by the stress to which they have become adapted--the so-called 'cost of adaptation'. The need to minimise or account for allelic variation at other fitness-related loci (genetic background control) is frequently overlooked when assessing resistance costs associated with plant defence traits. We provide a synthesis of the various experimental protocols that accomplish this essential requirement. We also differentiate those methods that enable the identification of the trait-specific or mechanistic basis of costs (direct methods) from those that provide an estimate of the impact of costs by examining the evolutionary trajectories of resistance allele frequencies at the population level (indirect methods). The advantages and disadvantages for each proposed experimental design are discussed. We conclude that plant resistance systems provide an ideal model to address fundamental questions about the cost of adaptation to stress. We also propose some ways to expand the scope of future studies for further fundamental and applied insight into the significance of adaptation costs.

Moss, S. R. ; Marshall, R. ; Hull, R. ; Alarcon-Reverte, R.. 2011. Current status of herbicide-resistant weeds in the United Kingdom. Aspects of Applied Biology : 1 - 10.

This paper updates information on the status of resistant weeds of arable crops in the UK, last compiled in 2005. It is estimated that resistant Alopecurus myosuroides (blackgrass) occurs on at least 80% of the 20,000 farms that spray regularly for control of this weed. Resistance to mesosulfuron+iodosulfuron, first used in the UK in autumn 2003, has been detected on >400 farms in 26 counties of England. Lolium multiflorum (Italian rye-grass) resistant to at least one herbicide mode of action has been found on >450 farms in 33 counties and resistant Avena spp. (wild-oats) on >250 farms in 28 counties of England. ALS-resistant Stellaria media (common chickweed) was found on >40 farms in 13 counties in England, Scotland and Northern Ireland. This represents the first documented case of a herbicide-resistant weed in Northern Ireland. ALS-resistant Papaver rhoeas (common poppy) was found on >25 farms in nine counties of England. ALS-resistance in Tripleurospermum inodorum (scentless mayweed) was documented for the first time in England, with resistant populations being found on three farms in Yorkshire. Partial resistance to the triazinone herbicides, metribuzin and metamitron, was also documented for the first time in England in Senecio vulgaris (groundsel), which also showed complete resistance to triazine herbicides..

Salzmann, D. ; Handley, R. J. ; Müller-Schärer, H.. 2008. Functional significance of triazine-herbicide resistance in defence of Senecio vulgaris against a rust fungus. Basic and Applied Ecology 9 : 577 - 587.

We investigated the functional significance of plant performance (dry mass, photosynthesis) in plant defence (resistance and tolerance) against pathogen infection, and potential negative cross-resistance between herbicide resistance and plant defence against disease. We compared isonuclear triazine-herbicide-resistant (TR) and -susceptible (TS) biotypes of Senecio vulgaris, in the presence and absence of infection by the rust Puccinia lagenophorae. In a growth chamber study with two reduced irradiance levels, rust infection had a severe effect on plant performance with infected plants having 55% less dry mass and 54% reduced whole-plant photosynthesis than non-infected plants. The TR biotype was more susceptible (reduced resistance) to the pathogen, but the biotypes did not differ in their ability to compensate for rust infection (tolerance). TR plants were less productive than TS plants when grown non-shaded (ca. 10% full sunlight) but not when shaded (ca. 5% full sunlight). This is especially important for situations, where S. vulgaris grows under the crop canopy (e.g. in maize). Here, very low light levels might contribute to a numerical increase of TR relative to TS plants even when only occasionally treated with triazine. Whole-plant photosynthesis was reduced by 21% in TR plants as compared to the TS biotype, and by 59% in plants grown in the shaded as compared to the non-shaded treatment. When whole-plant photosynthesis values were corrected for the estimated leaf area of plants, we found no significant variation between biotypes, shade treatments or rust treatments. In experimental mixed TR:TS field populations, the proportion of TR plants decreased more rapidly in rust-infected populations than uninfected. This finding, together with the lower resistance in the TR than the TS biotype to the rust fungus observed in the growth chamber experiment, may indicate negative cross-resistance, which is a potential tool in the management of herbicide-resistant weeds..

Salava, J. ; Chodová, D.. 2007. The present state of herbicide resistance of weed populations in the Czech Republic. Journal of Plant Protection Research 47 : 437 - 444.

In 1985-2002 thirteen weeds resistant to atrazine were selected by a repeated application of triazine herbicides on arable land, in orchards, non-agricultural land and at railways in the Czech Republic. Recently Digitaria sanguinalis biotypes resistant to atrazine have been found at three railway junctions. Long-lasting application of the active ingredient imazapyr at railways caused selection of resistant Kochia scoparia biotypes. High resistance to chlorsulfuron has been discovered in five Apera spica-venti biotypes originating in winter cereals fields. The molecular basis of resistance to atrazine has been identified in the following weeds: Kochia scoparia, Solanum nigrum, Senecio vulgaris, Conyza canadensis, Digitaria sanguinalis, Amaranthus retroflexus and Chenopodium album. The resistance was conferred by a glycine for serine substitution at residue 264 of the D1 protein in all of those weeds. The resistance to imazapyr in Czech Kochia scoparia biotypes was conferred by a mutation at codon 574 of the ALS gene. Analysis of the results of DNA sequencing indicated, that the mutation induced a leucine for tryptophane substitution. There was excellent correspondence between the phenotypic resistance to herbicides of individual plants and the presence of mutations..

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