HRAC Group 2 (Legacy B) resistant Raphanus raphanistrum from Australia, New South Wales

INTERNATIONAL HERBICIDE-RESISTANT WEED DATABASE

HRAC GROUP 2 (LEGACY B) RESISTANT WILD RADISH
(Raphanus raphanistrum)

Inhibition of Acetolactate Synthase HRAC Group 2 (Legacy B)

Australia, New South Wales

INTRODUCTION		WILD RADISH
Wild Radish (Raphanus raphanistrum) is a dicot weed in the Brassicaceae family. In New South Wales this weed first evolved resistance to Group 2 (Legacy B) herbicides in 2004 and infests Cereals. Group 2 (Legacy B) herbicides are known as Inhibition of Acetolactate Synthase (Inhibition of Acetolactate Synthase ). Research has shown that these particular biotypes are resistant to chlorsulfuron, metsulfuron-methyl, and triasulfuron and they may be cross-resistant to other Group 2 (Legacy B) 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 10, 2009 )
Common Name	Wild Radish
Species	Raphanus raphanistrum
Group	Inhibition of Acetolactate Synthase HRAC Group 2 (Legacy B)
Herbicides	chlorsulfuron, metsulfuron-methyl, and triasulfuron
Location	Australia, New South Wales
Year	2004
Situation(s)	Cereals
Contributors - (Alphabetically)	Andrew Storrie
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ACADEMIC ASPECTS

Confirmation Tests

Field trials comparing a known susceptible Wild Radish biotype with this Wild Radish 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 2 resistant Wild Radish indicate that the inheritance is determined by a dominant 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 2 (Legacy B) resistant Wild Radish from New South Wales 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 2 (Legacy B) resistant Wild Radish from New South Wales please update the database.

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CONTRIBUTING WEED SCIENTISTS

ANDREW STORRIE

Principal Agronomo Po Box 5444 Albany, 6332, Western Australia Australia Email Andrew Storrie Web : Web Site Link

ACKNOWLEDGEMENTS
The Herbicide Resistance Action Committee, The Weed Science Society of America, and weed scientists in New South Wales have been instrumental in providing you this information. Particular thanks is given to Andrew Storrie for providing detailed information.

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Herbicide Resistant Wild Radish Globally
(Raphanus raphanistrum)

Country

FirstYear

Situation

Active Ingredients

Site of Action

Australia (Western Australia)

1997

Cereals, and Wheat

chlorsulfuron, and metosulam

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

Australia (Western Australia)

1998

Cropland

chlorsulfuron, diflufenican, and metosulam

Multiple Resistance: 2 Sites of Action
Inhibition of Acetolactate Synthase ( HRAC Group 2 (Legacy B)
Phytoene Desaturase inhibitors ( HRAC Group 12 (Legacy F1)

Australia (South Australia)

1998

Spring Barley, and Wheat

chlorsulfuron, iodosulfuron-methyl-Na, and metosulam

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

Australia (Western Australia)

1999

Lupins, and Triazine-tolerant canola

atrazine, and simazine

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

Australia (Western Australia)

1999

Cereals

2,4-D

Auxin Mimics ( HRAC Group 4 (Legacy O)

Australia (New South Wales )

2004

Cereals

chlorsulfuron, metsulfuron-methyl, and triasulfuron

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

Australia (South Australia)

2006

Cereals

2,4-D, diflufenican, MCPA, and triasulfuron

Multiple Resistance: 3 Sites of Action
Inhibition of Acetolactate Synthase ( HRAC Group 2 (Legacy B)
Phytoene Desaturase inhibitors ( HRAC Group 12 (Legacy F1)
Auxin Mimics ( HRAC Group 4 (Legacy O)

Australia (Victoria)

2009

Spring Barley, and Wheat

2,4-D, chlorsulfuron, and metosulam

Multiple Resistance: 2 Sites of Action
Inhibition of Acetolactate Synthase ( HRAC Group 2 (Legacy B)
Auxin Mimics ( HRAC Group 4 (Legacy O)

Australia (Western Australia)

2010

Fallow

2,4-D, chlorsulfuron, diflufenican, glyphosate, imazethapyr, MCPA, metosulam, and sulfometuron-methyl

Multiple Resistance: 4 Sites of Action
Inhibition of Acetolactate Synthase ( HRAC Group 2 (Legacy B)
Phytoene Desaturase inhibitors ( HRAC Group 12 (Legacy F1)
Inhibition of Enolpyruvyl Shikimate Phosphate Synthase ( HRAC Group 9 (Legacy G)
Auxin Mimics ( HRAC Group 4 (Legacy O)

Australia (Victoria)

2011

Spring Barley, and Wheat

2,4-D

Auxin Mimics ( HRAC Group 4 (Legacy O)

Australia (New South Wales )

2013

Oats, Spring Barley, and Wheat

2,4-D

Auxin Mimics ( HRAC Group 4 (Legacy O)

Australia (Western Australia)

2015

Wheat

2,4-D, atrazine, chlorsulfuron, diflufenican, fluridone, isoxaflutole, mesotrione, and tembotrione

Multiple Resistance: 5 Sites of Action
Inhibition of Acetolactate Synthase ( HRAC Group 2 (Legacy B)
PSII inhibitors - Serine 264 Binders ( HRAC Group 5 (Legacy C1 C2)
Phytoene Desaturase inhibitors ( HRAC Group 12 (Legacy F1)
Inhibition of Hydroxyphenyl Pyruvate Dioxygenase ( HRAC Group 27 (Legacy F2)
Auxin Mimics ( HRAC Group 4 (Legacy O)

Australia (Western Australia)

2020

Wheat

2,4-D, dicamba, mesotrione, metsulfuron-methyl, pyrasulfotole, and topramezone

Multiple Resistance: 3 Sites of Action
Inhibition of Acetolactate Synthase ( HRAC Group 2 (Legacy B)
Inhibition of Hydroxyphenyl Pyruvate Dioxygenase ( HRAC Group 27 (Legacy F2)
Auxin Mimics ( HRAC Group 4 (Legacy O)

Brazil

2013

Spring Barley, and Wheat

chlorimuron-ethyl, cloransulam-methyl, imazapic, imazapyr, iodosulfuron-methyl-Na, metsulfuron-methyl, and sulfometuron-methyl

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

South Africa

1997

Spring Barley, and Wheat

chlorsulfuron, iodosulfuron-methyl-Na, metsulfuron-methyl, thifensulfuron-methyl, triasulfuron, and tribenuron-methyl

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

Literature about Similar Cases

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COSTA, L.O. and RIZZARDI, M.A.. 2014. Raphanus raphanistrumResistance to the Herbicide Metsulfuron-Methyl. In Press : .

The ALS-inhibiting herbicides, especially metsulfuron-methyl, are widely used for weed control, mainly wheat and barley in southern Brazil. Raphanus raphanistrum is a major weed of winter crops. However, in recent years, R. raphanistrum, after being treated with metsulfuron, has shown no symptoms of toxicity, possibly due to herbicide resistance. Aiming to evaluate the existence of R. raphanistrum biotypes resistant to metsulfuron, an experiment was conducted in a greenhouse, in a completely randomized design with four replications. The plots consisted of pots with six plants. The treatments consisted of the interaction of resistant R. raphanistrum (biotype R) and susceptible R. raphanistrum (biotypes S) with ten doses of the herbicide (0.0; 0.6; 1.2; 2.4; 4.8; 9.6; 19.2; 38.4; 76.8 and 153.6 g i.a. ha-1). The application of the test herbicides occurred when the crop was at the stage of 3 to 4 true leaves. The variables analyzed were control and dry matter accumulation. Statistical analysis of dose-response curves was performed by non linear regression. Biotype S was susceptible to the herbicide even at doses below the recommended. Biotype R was insensitive to the herbicide obtaining values of resistance factor (F) higher than 85. The dose-response curve confirmed the existence of R. raphanistrum biotypes with high level of resistance to metsulfuron-methyl..

Jugulam, M. ; DiMeo, N. ; Veldhuis, L. J. ; Walsh, M. ; Hall, J. C.. 2013. Investigation of MCPA (4-chloro-2-ethylphenoxyacetate) resistance in wild radish (Raphanus raphanistrum L.). Journal of Agricultural and Food Chemistry 61 : 12516 - 12521.

The phenoxy herbicides (e.g., 2,4-D and MCPA) are used widely in agriculture for the selective control of broadleaf weeds. In Western Australia, the reliance on phenoxy herbicides has resulted in the widespread evolution of phenoxy resistance in wild radish (Raphanus raphanistrum) populations. In this research the inheritance and mechanism of MCPA resistance in wild radish were determined. Following classical breeding procedures, F₁, F₂, and backcross progeny were generated. The F₁ progeny showed an intermediate response to MCPA, compared to parents, suggesting that MCPA resistance in wild radish is inherited as an incompletely dominant trait. Segregation ratios observed in F₂ (3:1; resistant:susceptible) and backcross progeny (1:1; resistant to susceptible) indicated that the MCPA resistance is controlled by a single gene in wild radish. Radiolabeled MCPA studies suggested no difference in MCPA uptake or metabolism between resistant and susceptible wild radish; however, resistant plants rapidly translocated more ¹⁴C-MCPA to roots than susceptible plants, which may have been exuded from the plant. Understanding the genetic basis and mechanism of phenoxy resistance in wild radish will help formulate prudent weed management strategies to reduce the incidence of phenoxy resistance..

Lopes Ovejero, R. F. ; Soares, D. J. ; Oliveira, W. S. ; Fonseca, L. B. ; Berger, G. U. ; Soteres, J. K. ; Christoffoleti, P. J.. 2013. Residual herbicides in weed management for glyphosate-resistant soybean in Brazil. Planta Daninha 31 : 947 - 959.

In agricultural production systems where the glyphosate-resistant soybean crop (Glycine max) is grown and the practice of crop rotation with alternative herbicides is not adopted, the exclusive and continuous use of glyphosate has led to the occurrence of resistant weed populations that may limit or compromise the benefits of this technology. Thus, the efficacy of weed management programs, including the use of residual herbicides (sulfentrazone, flumioxazin, imazethapyr, diclosulan, chlorimuron and s-metolachlor) applied in preemergence and followed by in-crop postemergence applications of glyphosate (PRE-POST) were compared to glyphosate postemergence only programs - POST. The study was conducted across nine locations during the 2009/2010 and 2010/2011 growing seasons. PRE-POST programs were efficient in the control of Amaranthus viridis, Brachiaria plantaginea, Bidens pilosa, Commelina benghalensis, Eleusine indica, Euphorbia heterophylla and Raphanus raphanistrum, with the level of control being similar when comparing the program with two applications of glyphosate POST. Some PRE-POST programs were not efficient in controlling Cenchrus echinatus, Ipomoea hederifolia and Ipomoea triloba. Sulfentrazone and diclosulam PRE-POST programs improved the control of Ipomoea triloba compared to sequential applications of glyphosate alone. No significant differences in soybean yield were observed between any of the herbicide treatments or study locations. The use of residual herbicides in preemergence followed by glyphosate in-crop postemergence provides consistent weed control and reducing early season weed competition. Furthermore, these programs utilize at least two herbicide modes of action for herbicide use diversity, which will be needed to stay ahead of resistance build-up, regardless of when weeds may appear..

Li Mei ; Yu Qin ; Han HePing ; Vila-Aiub, M. ; Powles, S. B.. 2013. ALS herbicide resistance mutations in Raphanus raphanistrum: evaluation of pleiotropic effects on vegetative growth and ALS activity. Pest Management Science 69 : 689 - 695.

Background: Gene mutations that endow herbicide resistance may cause pleiotropic effects on plant ecology and physiology. This paper reports on the effect of a number of known and novel target-site resistance mutations of the ALS gene (Ala-122-Tyr, Pro-197-Ser, Asp-376-Glu or Trp-574-Leu) on vegetative growth traits of the weed Raphanus raphanistrum. Results: The results from a series of experiments have indicated that none of these ALS resistance mutations imposes negative pleiotropic effects on relative growth rate (RGR), photosynthesis and resource-competitive ability in R. raphanistrum plants. The absence of pleiotropic effects on plant growth occurs in spite of increased (Ala-122-Tyr, Pro-197-Ser, Asp-376-Glu) and decreased (Trp-574-Leu) extractable ALS activity. Conclusion: The absence of detrimental pleiotropic effects on plant growth associated with the ALS target-site resistance mutations reported here is a contributing factor in resistance alleles being at relatively high frequencies in ALS-herbicide-unselected R. raphanistrum populations..

Walsh, M. J. ; Stratford, K. ; Stone, K. ; Powles, S. B.. 2012. Synergistic effects of atrazine and mesotrione on susceptible and resistant wild radish (Raphanus raphanistrum) populations and the potential for overcoming resistance to triazine herbicides. Weed Technology 26 : 341 - 347.

The synergistic interaction between mesotrione, a hydroxyphenylpyruvate dioxygenase (HPPD)-inhibiting herbicide, and atrazine, a photosystem II (PS II)-inhibiting herbicide, has been identified in the control of several weed species. A series of dose-response studies examined the synergistic effect of these herbicides on a susceptible (S) wild radish population. The potential for this interaction to overcome target-site psbA gene-based atrazine resistance in a resistant (R) wild radish population was also investigated. Control of S wild radish with atrazine was enhanced by up to 40% when low rates (1.0 to 1.5 g ha^-1) of mesotrione were applied in combination. This synergistic response was demonstrated across a range of atrazine-mesotrione rate combinations on this S wild radish population. Further, the efficacy of 1.5 g ha^-1 mesotrione increased control of the R population by a further 60% when applied in combination with 400 g ha^-1 of atrazine. This result clearly demonstrated the synergistic interaction of these herbicides in overcoming the target-site resistance mechanism. The mechanism responsible for the observed synergistic interaction between mesotrione and atrazine remains unknown. However, it is speculated that an alternate atrazine binding site may be responsible. Regardless of the biochemical nature of this interaction, evidence from whole-plant bioassays clearly demonstrated that synergistic herbicide combinations improve herbicide efficiency, with lower application rates required to control weed populations. This, combined with the potential to overcome psbA gene-based triazine resistance, and, thereby, regain the use of these herbicides, will result in more sustainable herbicide use..

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