Multiple resistant Phalaris minor from South Africa

International Survey of Herbicide-Resistant Weeds

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Thursday, April 18, 2024

MULTIPLE RESISTANT LITTLE SEED CANARY GRASS
(Phalaris minor)

Multiple Resistance: 2 Sites of Action
Inhibition of Acetyl CoA Carboxylase HRAC Group 1 (Legacy A)
Inhibition of Acetolactate Synthase HRAC Group 2 (Legacy B)

South Africa

INTRODUCTION		LITTLE SEED CANARY GRASS
Little seed Canary grass (Phalaris minor) is a monocot weed in the Poaceae family. In South Africa this weed first evolved multiple resistance (to 2 herbicide sites of action) in 1999 and infests Pastures, and Wheat. Multiple resistance has evolved to herbicides in the Groups 1 (Legacy A), and Inhibition of Acetolactate Synthase HRAC Group 2 (Legacy B). These particular biotypes are known to have resistance to clodinafop-propargyl, diclofop-methyl, fenoxaprop-ethyl, haloxyfop-methyl, iodosulfuron-methyl-Na, mesosulfuron-methyl, propaquizafop, quizalofop-ethyl, and sulfosulfuron and they may be cross-resistant to other herbicides in the Groups 1 (Legacy A), and Inhibition of Acetolactate Synthase HRAC Group 2 (Legacy B). 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 Aug 04, 2003 )
Common Name	Little seed Canary grass
Species	Phalaris minor
Group	Inhibition of Acetyl CoA Carboxylase HRAC Group 1 (Legacy A) Inhibition of Acetolactate Synthase HRAC Group 2 (Legacy B)
Herbicides	clodinafop-propargyl, diclofop-methyl, fenoxaprop-ethyl, haloxyfop-methyl, iodosulfuron-methyl-Na, mesosulfuron-methyl, propaquizafop, quizalofop-ethyl, and sulfosulfuron
Location	South Africa
Year	1999
Situation(s)	Pastures, and Wheat
Contributors - (Alphabetically)	Pj Pieterse
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ACADEMIC ASPECTS

Confirmation Tests

Greenhouse trials comparing a known susceptible Little seed Canary grass biotype with this Little seed Canary grass 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 1, 2 resistant Little seed Canary grass 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 multiple resistant Little seed Canary grass from South Africa please update the database.

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CONTRIBUTING WEED SCIENTISTS

PJ PIETERSE

Lecturer University Of Stellenbosch Dept Of Agronomy 115 Weed Research Lab Stellenbosch, 7602 South Africa Email Pj Pieterse

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

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Herbicide Resistant Little seed Canary grass Globally
(Phalaris minor)

Country

FirstYear

Situation

Active Ingredients

Site of Action

Australia (Victoria)

2012

Wheat

clodinafop-propargyl

Inhibition of Acetyl CoA Carboxylase ( HRAC Group 1 (Legacy A)

India

1991

Wheat

isoproturon

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

India

1994

Wheat

diclofop-methyl, and pinoxaden

Inhibition of Acetyl CoA Carboxylase ( HRAC Group 1 (Legacy A)

India

2006

Wheat

clodinafop-propargyl, fenoxaprop-ethyl, isoproturon, mesosulfuron-methyl, pinoxaden, pyroxsulam, and sulfosulfuron

Multiple Resistance: 3 Sites of Action
Inhibition of Acetyl CoA Carboxylase ( HRAC Group 1 (Legacy A)
Inhibition of Acetolactate Synthase ( HRAC Group 2 (Legacy B)
PSII inhibitors - Serine 264 Binders ( HRAC Group 5 (Legacy C1 C2)

India

2013

Wheat

iodosulfuron-methyl-Na, and mesosulfuron-methyl

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

Iran

2004

Winter wheat

clodinafop-propargyl, diclofop-methyl, fenoxaprop-ethyl, pinoxaden, and tralkoxydim

Inhibition of Acetyl CoA Carboxylase ( HRAC Group 1 (Legacy A)

Israel

1993

Wheat

fenoxaprop-ethyl

Inhibition of Acetyl CoA Carboxylase ( HRAC Group 1 (Legacy A)

Mexico

1996

Wheat

clodinafop-propargyl, fenoxaprop-ethyl, fluazifop-butyl, pinoxaden, sethoxydim, and tralkoxydim

Inhibition of Acetyl CoA Carboxylase ( HRAC Group 1 (Legacy A)

Pakistan

2015

Wheat

fenoxaprop-ethyl

Inhibition of Acetyl CoA Carboxylase ( HRAC Group 1 (Legacy A)

South Africa

1999

Pastures, and Wheat

clodinafop-propargyl, diclofop-methyl, fenoxaprop-ethyl, haloxyfop-methyl, iodosulfuron-methyl-Na, mesosulfuron-methyl, propaquizafop, quizalofop-ethyl, and sulfosulfuron

Multiple Resistance: 2 Sites of Action
Inhibition of Acetyl CoA Carboxylase ( HRAC Group 1 (Legacy A)
Inhibition of Acetolactate Synthase ( HRAC Group 2 (Legacy B)

United States (California)

2001

Onions

clethodim, fenoxaprop-ethyl, fluazifop-butyl, and sethoxydim

Inhibition of Acetyl CoA Carboxylase ( HRAC Group 1 (Legacy A)

Literature about Similar Cases

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Javid Gherekhloo, Ricardo Alcántara de la Cruz, Maria D Osuna, Sima Sohrabi,Rafael De Prado. 2020. ASSESSING GENETIC VARIATION AND SPREAD OF Phalarisminor RESISTANT TO ACCASE INHIBITING HERBICIDES INIRAN. Planta Daninha 38 : .

Littleseed canarygrass (Phalaris minor) is the second most serious and problematic grass weed in wheat fields in Iran, and has developed resistance to ACCase inhibiting herbicides. Inter-simple sequence repeat (ISSR) analysis was used to assess genetic variation between and within ACCase inhibitor-resistant and susceptible P. minor populations in Iran and to determine the origin of resistance and its dispersal. Sixteen P. minor populations from different regions in Iran were analysed using seven primers. Genetic relationships generated using UPGMA analysis indicated the presence of more than one genotype among the herbicide resistant populations. The results indicated that the high genetic similarity and physical proximity among the resistant P. minor populations in the different regions is mainly due to cross pollination, mechanical seed dispersion and local ecological factors. These findings suggested that independent selection as well as movement of resistant seeds had occurred, which could explain the presence and dispersion of ACCase inhibitor-resistance in these populations.
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Singh, D. V. ; Kuruba Adeppa ; Krishna Misra. 2012. Mechanism of isoproturon resistance in Phalaris minor: in silico design, synthesis and testing of some novel herbicides for regaining sensitivity. Journal of Molecular Modeling 18 : 1431 - 1445.

Isoproturon, 3-p-cumenyl-1 dimethylurea was the only herbicide controlling Phalaris minor, a major weed growing in wheat fields till the early 1980s. Since it has acquired resistance against isoproturon, like other substituted urea herbicides, where the identified target site for isoproturon is in the photosynthetic apparatus at D1 protein of Photosystem-II (PS-II). Nucleotide sequence of susceptible and resistant psbA gene of P. minor has been reported to have four point mutations. During the present work D1 protein of both susceptible and resistant biotypes of P. minor has been modeled. Transmembrane segments of amino acids were predicted by comparing with the nearest homolog of bacterial D1 protein. Volume and area of active site of both susceptible and resistant biotypes has been simulated. Isoproturon was docked at the active site of both, susceptible and resistant D1 proteins. Modeling and simulation of resistance D1 protein indicates that the resistance is due to alteration in secondary structure near the binding site, resulting in loss in cavity area, volume and change in binding position, loss of hydrogen bonds, hydrophobic interaction and complete loss of hydrophobic sites. To regain sensitivity in resistant biotype new derivatives of isoproturon molecules have been proposed, synthesized and tested. Among the 17 derivatives we found that the N-methyl triazole substituted isoproturon is a potential substitute for isoproturon..

Singh, D. V. ; Shikha Agarwal ; Kesharwani, R. K. ; Krishna Misra. 2012. Molecular modeling and computational simulation of the photosystem-II reaction center to address isoproturon resistance in Phalaris minor. Journal of Molecular Modeling 18 : 3903 - 3913.

Isoproturon is the only herbicide that can control Phalaris minor, a competitive weed of wheat that developed resistance in 1992. Resistance against isoproturon was reported to be due to a mutation in the psbA gene that encodes the isoproturon-binding D1 protein. Previously in our laboratory, a triazole derivative of isoproturon (TDI) was synthesized and found to be active against both susceptible and resistant biotypes at 0.5 kg/ha but has shown poor specificity. In the present study, both susceptible D1_(S), resistant D1_(R) and D2 proteins of the PS-II reaction center of P. minor have been modeled and simulated, selecting the crystal structure of PS-II from Thermosynechococcus elongatus (2AXT.pdb) as template. Loop regions were refined, and the complete reaction center D1/D2 was simulated with GROMACS in lipid (1-palmitoyl-2-oleoylglycero-3-phosphoglycerol, POPG) environment along with ligands and cofactor. Both S and R models were energy minimized using steepest decent equilibrated with isotropic pressure coupling and temperature coupling using a Berendsen protocol, and subjected to 1,000 ps of MD simulation. As a result of MD simulation, the best model obtained in lipid environment had five chlorophylls, two plastoquinones, two phenophytins and a bicarbonate ion along with cofactor Fe and oxygen evolving center (OEC). The triazole derivative of isoproturon was used as lead molecule for docking. The best worked out conformation of TDI was chosen for receptor-based de novo ligand design. In silico designed molecules were screened and, as a result, only those molecules that show higher docking and binding energies in comparison to isoproturon and its triazole derivative were proposed for synthesis in order to get more potent, non-resistant and more selective TDI analogs..

Gherekhloo, J. ; Osuna, M. D. ; Prado, R. de. 2012. Biochemical and molecular basis of resistance to ACCase-inhibiting herbicides in Iranian Phalaris minor populations. Weed Research (Oxford) 52 : 367 - 372.

Phalaris minor is a common weed in wheat and barley fields of Iran. Repeated use of ACCase inhibiting herbicides during the last two decades to control this weed has resulted in the appearance of populations of P. minor that are resistant to the aryloxyphenoxy propionates (APP) in some wheat fields of the country. Dose-response assays were conducted to investigate the level of resistance in two P. minor populations (AR and MR4) which have developed resistance to three APP herbicides, including diclofop-methyl, fenoxaprop-P ethyl and clodinafop propargyl. A high level of resistance in these populations may be due to the presence of an altered ACCase enzyme in these plants, and we hypothesised that one or more mutations in the gene encoding ACCase enzyme are responsible for insensitivity of the enzyme. Results confirmed that resistance in both populations was target site-based, and molecular studies revealed that substitutions of Trp-2027-Cys and Asp-2078-Gly, respectively in AR and MR4, are responsible for insensitivity of the enzyme in these populations. This is the first report to show that these substitutions endow resistance to APP herbicides in P. minor, though other resistant biotypes are reported from elsewhere. These mutations may result in resistance of P. minor to some DIM and DEN herbicides. It seems that lack of adequate herbicide and crop rotation has selected plants with different target site mutations, which cause differential responses of the ACCase enzyme to ACCase inhibitors. Additional resistance management practices may be necessary to prevent ACCase-inhibiting herbicides from becoming ineffective over wide areas..

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