<b>HRAC Group 4</b> <font size='2'> (Legacy O) </font> resistant Centaurea solstitialis from United States, Washington

International Survey of Herbicide-Resistant Weeds

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Thursday, October 31, 2024

HRAC GROUP 4 (LEGACY O) RESISTANT YELLOW STARTHISTLE
(Centaurea solstitialis)

Auxin Mimics HRAC Group 4 (Legacy O)

United States, Washington

INTRODUCTION		YELLOW STARTHISTLE
Yellow Starthistle (Centaurea solstitialis) is a dicot weed in the Asteraceae family. In Washington this weed first evolved resistance to Group 4 (Legacy O) herbicides in 1988 and infests Roadsides. Group 4 (Legacy O) herbicides are known as Auxin Mimics (Auxin Mimics ). Research has shown that these particular biotypes are resistant to picloram and they may be cross-resistant to other Group 4 (Legacy O) 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 Sep 15, 2000 )
Common Name	Yellow Starthistle
Species	Centaurea solstitialis
Group	Auxin Mimics HRAC Group 4 (Legacy O)
Herbicides	picloram
Location	United States, Washington
Year	1988
Situation(s)	Roadsides
Contributors - (Alphabetically)	Steven Seefeldt
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NOTES ABOUT THIS BIOTYPE

GENERAL

Steve Seefeldt is now working on resistant weeds in NewZealand.

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ACADEMIC ASPECTS

Confirmation Tests

Greenhouse, and Laboratory trials comparing a known susceptible Yellow Starthistle biotype with this Yellow Starthistle 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 4 resistant Yellow Starthistle 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 4 (Legacy O) resistant Yellow Starthistle from Washington please update the database.

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CONTRIBUTING WEED SCIENTISTS

STEVEN SEEFELDT

Ruakura Agricultural Research Centre Agresearch Universidad Nacional La Plata Casilla De Correo 31, Cátedra De Cereales Hamilton New Zealand Email Steven Seefeldt

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

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Herbicide Resistant Yellow Starthistle Globally
(Centaurea solstitialis)

Country

FirstYear

Situation

Active Ingredients

Site of Action

United States (Washington)

1988

Roadsides

picloram

Auxin Mimics ( HRAC Group 4 (Legacy O)

Literature about Similar Cases

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Sabba, R. P. ; Ray, I. M. ; Lownds, N. ; Sterling, T. M.. 2003. Inheritance of resistance to clopyralid and picloram in yellow starthistle (Centaurea solstitialis L.) is controlled by a single nuclear recessive gene. Journal of Heredity 94 : 523 - 527.

The noxious weed yellow starthistle (Centaurea solstitialis L.) can be controlled effectively at the seedling stage with foliar application of the auxinic herbicides picloram or clopyralid. Although resistance to these herbicides is rare, a yellow starthistle biotype resistant to picloram and cross-resistant to clopyralid was observed in 1989 near Dayton, WA, in a pasture that had been subjected to intensive picloram selective pressure. Our objective was to determine the mode of inheritance for this resistance trait. Transmission of the resistant phenotype was monitored in reciprocal F₁ crosses between susceptible (SCI) and resistant (RDW) plants, their testcross and pseudo-F₂ progeny. Progeny from all crosses, as well as RDW and SCI seedlings of original populations, were sprayed with picloram or clopyralid to distinguish between susceptible and resistant individuals. All F₁ progeny were susceptible to both herbicides, indicating that the resistance trait was of nuclear origin and recessive in nature. Segregation of the resistant phenotype among pseudo-F₂ and testcross progeny of F₁ genotypes demonstrated monofactorial inheritance (P>.25) for resistance to both herbicides. The conclusion that resistance is conferred by a single recessive allele is consistent with the observation that no other picloram-resistant yellow starthistle populations have been identified in the area since picloram selection pressure was abated..

Shinn, S. L. ; Thill, D. C.. 2002. The response of yellow starthistle (Centaurea solstitialis), annual grasses, and smooth brome (Bromus inermis) to imazapic and picloram. Weed Technology 16 : 366 - 370.

Competition from annual grasses and yellow starthistle (C. solstitialis) can severely reduce perennial grass forage production and quality in pasture and rangeland. The purpose of this study was to determine yellow starthistle and weedy annual grass control by imazapic applied alone or in combination with picloram, and smooth brome (B. inermis) tolerance to these treatments in Genesee, Idaho, during 1999 and 2000. Sixty days after treatment (DAT) imazapic applied at 70 and 140 g a.i./ha reduced annual grass (downy brome (B. tectorum), medusahead (Taeniatherum caput-medusae) and annual bluegrass (Poa annua)) plant density and biomass by 66-76% compared with the untreated control. Picloram applied at 280 and 420 g a.i./ha reduced yellow starthistle plant density and biomass by over 93%. Imazapic applied at 70 and 140 g/ha reduced smooth brome biomass by 79-95% at 60 DAT. Picloram did not affect the density or the biomass of annual grasses or smooth brome, whereas imazapic did not markedly affect the density or the biomass of yellow starthistle. Downy brome control increased to a maximum of 97% with increasing imazapic dose (maximum of 280 g/ha) at 30, 60, and 90 DAT..

Valenzuela-Valenzuela, J. M. ; Lownds, N. K. ; Sterling, T. M.. 2002. Ethylene is not involved in clopyralid action in yellow starthistle (Centaurea solstitialis L.). Pesticide Biochemistry and Physiology 72 : 142 - 152.

Auxinic herbicides often increase ethylene production in susceptible but not resistant plants. Thus, a role for ethylene biosynthesis in the resistance to, and mode of action of, auxinic herbicides has been suggested. Experiments were conducted to determine the role of ethylene production induced by clopyralid (3,6-dichloro-2-pyridine carboxylic acid) in the mode of action of, and cross-resistance to, this herbicide in picloram (4-amino-3,5,6-trichloro-2-pyridinecarboxylic acid)-susceptible (S) and -resistant (R) yellow starthistle (C. solstitialis) plants. Foliar-applied clopyralid induced ethylene production, epinasty, and necrosis in S but had no effect on R. Wounding induced ethylene production in both S and R, so R possesses a functional ethylene biosynthesis pathway. Aminoethoxyvinylglycine (AVG), an ethylene synthesis inhibitor, inhibited ethylene production in S; however, clopyralid-induced epinasty, necrosis, and shoot weight reduction were not prevented. Therefore, herbicide damage was not attributable to induced ethylene. In addition, silver thiosulfate (STS), an ethylene action inhibitor, did not alter herbicide damage. Foliar-applied ethephon, an ethylene-releasing compound, increased ethylene released from S and R, but did not visibly affect plants. Exogenous-applied ethylene in a flow-through system for 48 h did not induce morphological symptoms in plants at 0 or 250 µlitre litre^-1; at 500 µlitre litre^-1 and greater ethylene induced slight leaf rolling and wilting in both accessions although there was no effect on plant weight 3 weeks after treatment. The low sensitivity to exogenously applied ethylene and the inability of AVG and STS to block any symptoms induced by clopyralid suggest that ethylene is a symptom, not a mediator, of auxinic herbicide action and resistance in yellow starthistle..

Valenzuela-Valenzuela, J. M. ; Lownds, N. K. ; Sterling, T. M.. 2001. Clopyralid uptake, translocation, metabolism, and ethylene induction in picloram-resistant yellow starthistle (Centaurea solstitialis L.). Pesticide Biochemistry and Physiology 71 : 11 - 19.

Clopyralid uptake, translocation, metabolism, and clopyralid-induced ethylene production were compared in picloram-resistant (R) and -susceptible (S) yellow starthistle accessions to study the mechanism of cross-resistance in picloram-resistant yellow starthistle. Clopyralid (11.7 mM) applied to the foliage induced ethylene production on the S accession only. Regardless of the accession, clopyralid was rapidly absorbed, with about 75% of the applied radiolabel absorbed within the first 2 h following treatment, and there was no additional uptake over the following 46 h. Radiolabel translocated from treated leaves in both accessions and the amount translocated increased with time. Metabolism of [¹⁴C]clopyralid was determined 2, 24, and 96 h following herbicide application. Radioactivity in the insoluble fraction increased with time in both accessions while about 90% of the radioactivity remained in the soluble fraction after 96 h in both R and S accessions. Picloram-resistant and -susceptible accessions metabolized clopyralid to 2 major metabolites. The metabolite more polar than clopyralid (metabolite 1), clopyralid, and the metabolite less polar than clopyralid (metabolite 2) had retention times of 2.4, 3.3 and 6.1 minutes, respectively. At 96 h after herbicide treatment, 50% of the clopyralid was metabolized by the resistant accession and 24% by the susceptible accession with an equal distribution of metabolites 1 and 2 in both accessions..

Miller, T. W. ; Shinn, S. L. ; Thill, D. C.. 2001. Cross-resistance in and chemical control of auxinic herbicide-resistant yellow starthistle (Centaurea solstitialis). Weed Technology 15 : 293 - 299.

An accession of auxinic herbicide-resistant yellow starthistle found near Dayton, Washington, USA was tested to evaluate cross resistance to growth regulator herbicides and susceptibility to herbicides with different modes of action. Picloram at 0.43 kg a.i./ha removed susceptible (S) yellow starthistle plants from a field plot, and surviving resistant (R) plants were dug and moved to the greenhouse. Known S plants were transplanted from a pasture near the R population. The R biotype was reconfirmed as resistant to picloram in greenhouse tests, with resistance ratios of 5.6 and 3.8 for vegetative and reproductive biomass, respectively, and 10.2 for LD₅₀ (lethal dose for 50% of the treated population) data. The R biotype was also cross-resistant to clopyralid and dicamba in all responses and to 2,4-D and triclopyr in vegetative biomass and LD₅₀ data. In field trials, eight herbicides were applied alone and in various combinations with and without addition of picloram. The yellow starthistle population was apparently comprised of differing percentages of R and S plants in 1997 and 1998, as picloram alone controlled 65 to 76% of the yellow starthistle in 1997 and 96 to 97% in 1998. BAS 662 01H (dicamba + SAN 836) at 0.28 or 0.42 kg ae/ha, respectively, or dicamba at 0.56 kg ae/ha were the best alternative treatments in either trial in either year, but only in 1998 did control exceed 85%. Picloram and other auxinic herbicides should continue to be useful for control of mixed R and S yellow starthistle populations. However, effective herbicides with different mode(s) of action integrated with range improvement practices and biological control must be identified for long-term yellow starthistle management..

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