<b>HRAC Group 1</b> <font size='2'> (Legacy A) </font> resistant Phalaris paradoxa from Israel

INTERNATIONAL HERBICIDE-RESISTANT WEED DATABASE

HRAC GROUP 1 (LEGACY A) RESISTANT HOOD CANARYGRASS
(Phalaris paradoxa)

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

Israel

INTRODUCTION		HOOD CANARYGRASS
Hood Canarygrass (Phalaris paradoxa) is a monocot weed in the Poaceae family. In Israel this weed first evolved resistance to Group 1 (Legacy A) herbicides in 2004 and infests Peas, and Wheat. Group 1 (Legacy A) herbicides are known as Inhibition of Acetyl CoA Carboxylase (Inhibition of Acetyl CoA Carboxylase ). Research has shown that these particular biotypes are resistant to clethodim, clodinafop-propargyl, cycloxydim, diclofop-methyl, fenoxaprop-ethyl, fluazifop-butyl, haloxyfop-methyl, and tralkoxydim and they may be cross-resistant to other Group 1 (Legacy A) 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 Jul 10, 2007 )
Common Name	Hood Canarygrass
Species	Phalaris paradoxa
Group	Inhibition of Acetyl CoA Carboxylase HRAC Group 1 (Legacy A)
Herbicides	clethodim, clodinafop-propargyl, cycloxydim, diclofop-methyl, fenoxaprop-ethyl, fluazifop-butyl, haloxyfop-methyl, and tralkoxydim
Location	Israel
Year	2004
Situation(s)	Peas, and Wheat
Contributors - (Alphabetically)	Ofer Hochberg, and Baruch Rubin
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ACADEMIC ASPECTS

Confirmation Tests

Field, Greenhouse, and Laboratory trials comparing a known susceptible Hood Canarygrass biotype with this Hood Canarygrass 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 resistant Hood Canarygrass indicate that the inheritance is determined by a dominant, nuclear 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 1 (Legacy A) resistant Hood Canarygrass from Israel 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 1 (Legacy A) resistant Hood Canarygrass from Israel please update the database.

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CONTRIBUTING WEED SCIENTISTS

OFER HOCHBERG

M.sc Student The Hebrew University Of Jerusalem Rh Smith Institute Of Plant Sciences And Genetics In Agricul 9335 Hazard Way Ste 201 Rehovot, 76100 Israel Email Ofer Hochberg

BARUCH RUBIN

Professor Hebrew University Of Jerusalem Inst. Plant Sci. & Genetics In Agriculture Faculty Of Agric. Food & Environm. Rehovot, 76100, Israel Israel Email Baruch Rubin

ACKNOWLEDGEMENTS
The Herbicide Resistance Action Committee, The Weed Science Society of America, and weed scientists in Israel have been instrumental in providing you this information. Particular thanks is given to Ofer Hochberg, and Baruch Rubin for providing detailed information.

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Herbicide Resistant Hood Canarygrass Globally
(Phalaris paradoxa)

Country

FirstYear

Situation

Active Ingredients

Site of Action

Australia (New South Wales )

1997

Wheat, and Winter pulses

fenoxaprop-ethyl, and sethoxydim

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

Australia (New South Wales )

2012

Spring Barley, and Wheat

clodinafop-propargyl, and mesosulfuron-methyl

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)

Iran

2007

Winter wheat

diclofop-methyl

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

Israel

1979

Railways, and Roadsides

atrazine

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

Israel

2004

Peas, and Wheat

clethodim, clodinafop-propargyl, cycloxydim, diclofop-methyl, fenoxaprop-ethyl, fluazifop-butyl, haloxyfop-methyl, and tralkoxydim

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

Italy

1998

Wheat

clodinafop-propargyl, diclofop-methyl, pinoxaden, and sethoxydim

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

Mexico

1996

Wheat

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

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

Syria

2015

Faba beans, Potatoes, and Wheat

clodinafop-propargyl, and fenoxaprop-ethyl

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

Literature about Similar Cases

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Cruz-Hipolito, H. ; Domínguez-Valenzuela, J. A. ; Osuna, M. D. ; Prado, R. de. 2012. Resistance mechanism to acetyl coenzyme A carboxylase inhibiting herbicides in Phalaris paradoxa collected in Mexican wheat fields. Plant and Soil 355 : 121 - 130.

Background and aims: In this study, we describe the molecular, physiological and agronomic aspects involved in the resistance to acetyl coenzyme A carboxylase inhibiting herbicides (ACCase) observed in one biotype of Phalaris paradoxa from Mexico. Methods: Dose-response Assays: The herbicide rate inhibiting plant growth of each biotype by 50% with respect to the untreated control, ED₅₀. Enzyme purification and ACCase assays to determine herbicide rate inhibiting the enzyme of each biotype by 50% with respect to the untreated control, I₅₀. Absorption and Translocation Assays with [¹⁴C]diclofop-methyl. Metabolism of diclofop-methyl and its metabolites were identified by thin-layer chromatography. Study of target site resistance mechanism at enzyme and molecular levels. Results: In this work, it has been studied the whole-plant response of Phalaris paradoxa biotypes from Mexico resistant (R) and susceptible (S) to ACCase-inhibiting herbicides: aryloxyphenoxypropionate (APP), cyclohexanedione (CHD) and phenylpyrazoline (PPZ), and the mechanism behind their resistance were studied. To analyse the resistance mechanism, the enzyme ACCase activity was investigated. Results from biochemical assays indicated a target-site resistance as the cause of reduced susceptibility to ACCase inhibitors. The absorption, translocation and metabolism were similar between R and S biotypes. A point mutation never described before was detected within the triplet of glycine at the amino acid position 2096 (referring to EMBL accession no. AJ310767) and resulted in the triplet of serine. This new mutation could explain the loss of affinity for the ACCase-inhibiting herbicides. Conclusions: We found a new mutation, which had never been described before. This mutation was detected within the triplet of glycine at the amino acid position 2096. This new mutation confers cross-resistance to three different chemical groups of ACCase-inhibiting herbicides..

Collavo, A. ; Panozzo, S. ; Lucchesi, G. ; Scarabel, L. ; Sattin, M.. 2011. Characterisation and management of Phalaris paradoxa resistant to ACCase-inhibitors. Crop Protection 30 : 293 - 299.

Phalaris paradoxa is a competitive grass commonly found in durum wheat crops of central and southern Italy. Among the 85 populations screened from 1998 to 2008 for resistance to ACCase-inhibitors and graminicide sulfonylureas, 17 resulted as being resistant to at least one ACCase inhibitor while none of the populations showed resistance to sulfonylureas. ACCase resistance in hood canary-grass seems to be spreading rather slowly in Italy. Out of the 17 populations, seven were characterised through outdoor dose-response pot experiments to investigate resistance levels and cross-resistance patterns to ACCase-inhibitors and multiple resistance to other mode of action. Molecular bases of resistance to the recently introduced DEN herbicide pinoxaden were also investigated. Six populations were confirmed to be ACCase-resistant with various cross-resistance patterns. Two populations were resistant to all tested ACCase herbicides, with pinoxaden resistance indexes (RI) based on survival ranging from 22 to 50. The two populations have been molecularly characterised for resistance to pinoxaden. A single point-mutation in the ACCase gene was identified in each population, causing the amino-acid substitutions of Ile₁₇₈₁Val and Asp₂₀₇₈Gly in 0478L and 0025, respectively. The results suggest that resistance of P. paradoxa to pinoxaden is due to an altered target site and different mutations cause different resistance levels. The biological characteristics of the species, mainly self-pollinated, and the absence of multiple resistance allow herbicides with different modes of action to be used for controlling ACCase-resistant populations. Chemical tools should be carefully used within integrated weed management strategies..

Bhowmik, P. C.. 2010. Current status of herbicide resistant weeds around the Globe. Journal of Crop and Weed 6 : 33 - 43.

The incidence and wide spread of herbicide resistant weeds is a global problem. Over the past 65 years, repeated use of herbicides has resulted in the evolution of resistant weed species. The first resistant species to triazine was discovered in 1970 in the United States. Since then, a large number of weed species has evolved resistance to several classes of herbicide. Currently, there are 334 resistant biotypes, including 190 weed species (113 dicots and 77 monocots) in over 310, 000 fields around the world Common resistant species are Chenopodium album and Amaranthus retroflexus resistant to triazine, Phalaris minor resistant to isoproturon, P. minor and P. paradoxa resistant to diclofop, Echinochloa colona resistant to propanil, Echinochloa crusgalli resistant to butachlor, Eleusine indica resistant to trifluralin, Lolium rigidum resistant to diclofop, Lactuca serriola resistant to metsuljuron, glyphosate resistance to Eleusine indica, Conyza canadensis, Lolium rigidum, and Lolium multiflorum. Multiple weed resistance to more than one class of herbicides with different modes of action has also been documented with many species. Currently there has been increased herbicide resistance to various weed species around the globe. Most common species are Lolium rigidum, Avena fatua, Amaranthus retroflexus, Chenopodium album, Setaria viridis, Echinochloa crusgalli, Eleusine indica, Kochia scoparia, Conyza canadensis, and Amaranthus hybridus..

O Hochberg, M Sibony, and B Rubin. 2009. The response of ACCase-resistant Phalaris paradoxa populations involves two different target site mutations. Weed Research 49 : 37.

Phalaris paradoxa (awned canary-grass) is an aggressive annual winter weed in wheat and other arable crops that is controlled mainly by ACCase-inhibiting herbicides: cyclohexanediones (DIMs), aryloxyphenoxypropionates (FOPs) and phenylpyrazolines (DENs, e.g. pinoxaden). The selection pressure imposed on the weed populations by repeated use of these herbicides has resulted in the evolution of increased numbers of ACCase-resistant populations of P. paradoxa in Israel and other countries. Two populations, Revadim (RV) and Mishmar Ha’emek (MH) that were exposed to differing weed and crop management tactics were investigated. Both populations were highly resistant to all FOPs, pinoxaden and cycloxydim, but responded differently to some DIMs. RV plants exhibited much higher resistance to tralkoxydim than MH plants, while showing similar low levels of resistance to tepraloxydim and clethodim. Both populations were equally susceptible to graminicides with other modes of action. The mutations responsible for the observed resistance were identified using PCR-RFLP and by sequencing the carboxyl transferase domain of the chloroplastic ACCase gene. RV plants possess a substitution of Asp2078 to Gly, whereas in MH population a mixture of Ile2041 to Asn or Asp2078 to Gly was found. Our study demonstrates that lack of herbicide and crop rotation may result in the evolution of diverse target site mutations and differential response of the whole plant to ACCase inhibitors..

Gherekhloo, J. ; Zand, E. ; Gonzáles-Torralva, F. ; Prado, R. de. 2009. Herbicide-resistant weeds in Iran: a short review. : 376 - 380.

More than 70% of arable land in Iran is given over to cultivation of wheat, barley and rice which are major crops in the country, while wheat alone covers nearly 52%. During last four decades, 86 herbicides belonging to different families such as synthetic auxins, triazines, phenylureas, aryloxyphenoxypropanoates (APP), cyclohexadiones (CHD), sulphonylureas, imidazolinones, and glycines have been registered in Iran, 24 of which are for selective control of weeds in wheat and barley. Consecutive use of acetyl Coenzyme A carboxylase (ACCase) inhibiting herbicides for control grasses which are troublesome weeds in wheat in Iran, has resulted in resistance of some grass species to ACCase inhibitors in some parts of the country. To date, resistance of Avena ludoviciana, A. fatua, Phalaris minor, P. paradoxa, Lolium rigidum to APP herbicides has been reported. To date there is no document about the appearance of resistant weeds in fields of other crops in Iran..

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Heap, I. The International Herbicide-Resistant Weed Database. Online. Friday, November 22, 2024 . Available www.weedscience.org Copyright © 1993- 2024 WeedScience.org All rights reserved. Fair use of this material is encouraged. Proper citation is requested.