Multiple resistant Lolium rigidum from Australia, Victoria

1982

Canola, Spring Barley, and Wheat

chlorsulfuron, diclofop-methyl, fluazifop-butyl, sethoxydim, tralkoxydim, and trifluralin

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)
Inhibition of Microtubule Assembly ( HRAC Group 3 (Legacy K1)

1982

Spring Barley, and Wheat

chlorpropham, chlorsulfuron, clomazone, diclofop-methyl, ethalfluralin, fluazifop-butyl, imazapyr, metolachlor, metsulfuron-methyl, quizalofop-ethyl, sethoxydim, tralkoxydim, tri-allate, triasulfuron, and trifluralin

Multiple Resistance: 6 Sites of Action
Inhibition of Acetyl CoA Carboxylase ( HRAC Group 1 (Legacy A)
Inhibition of Acetolactate Synthase ( HRAC Group 2 (Legacy B)
Inhibition of Deoxy-D-Xylulose Phosphate Synthase ( HRAC Group 13 (Legacy F4)
Inhibition of Microtubule Assembly ( HRAC Group 3 (Legacy K1)
Inhibition of Microtubule Organization ( HRAC Group 23 (Legacy K2)
Very Long-Chain Fatty Acid Synthesis inhibitors ( HRAC Group 15 (Legacy K3 N)

1984

Cropland, Spring Barley, and Wheat

chlorsulfuron, and metsulfuron-methyl

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

1984

Cropland, and Pasture seed

trifluralin

Inhibition of Microtubule Assembly ( HRAC Group 3 (Legacy K1)

1984

Cropland

metolachlor

Very Long-Chain Fatty Acid Synthesis inhibitors ( HRAC Group 15 (Legacy K3 N)

Australia (New South Wales )

1984

Pastures, Spring Barley, and Wheat

chlorsulfuron, diclofop-methyl, fluazifop-butyl, metsulfuron-methyl, quizalofop-ethyl, sethoxydim, and trifluralin

1985

Canola, Chickpea, Faba beans, Lentils, Lupins, Peas, Spring Barley, and Wheat

chlorsulfuron, diclofop-methyl, fluazifop-butyl, haloxyfop-methyl, metsulfuron-methyl, quizalofop-ethyl, sethoxydim, tralkoxydim, triasulfuron, and trifluralin

1988

Railways, and Roadsides

amitrole

Inhibition of Lycopene Cyclase ( HRAC Group 34 (Legacy F3)

1988

Cropland, Pasture seed, Railways, Roadsides, and Triazine-tolerant canola

atrazine, and simazine

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

1994

Cereals

trifluralin

Inhibition of Microtubule Assembly ( HRAC Group 3 (Legacy K1)

Australia (New South Wales )

1996

Canola, Cereals, Fencelines, and Wheat

glyphosate

Inhibition of Enolpyruvyl Shikimate Phosphate Synthase ( HRAC Group 9 (Legacy G)

1997

Apples, Around Buildings, Canola, Cereals, Fencelines, Irrigation Channels, Roadsides, and Wheat

glyphosate

Inhibition of Enolpyruvyl Shikimate Phosphate Synthase ( HRAC Group 9 (Legacy G)

1999

Alfalfa, Cereals, Clover, Fencelines, Grapes, Irrigation Channels, and Roadsides

glyphosate

Inhibition of Enolpyruvyl Shikimate Phosphate Synthase ( HRAC Group 9 (Legacy G)

1999

Wheat

chlorsulfuron, diclofop-methyl, glyphosate, and trifluralin

Multiple Resistance: 4 Sites of Action
Inhibition of Acetyl CoA Carboxylase ( HRAC Group 1 (Legacy A)
Inhibition of Acetolactate Synthase ( HRAC Group 2 (Legacy B)
Inhibition of Enolpyruvyl Shikimate Phosphate Synthase ( HRAC Group 9 (Legacy G)
Inhibition of Microtubule Assembly ( HRAC Group 3 (Legacy K1)

2003

Cereals, Fencelines, Grapes, Railways, and Roadsides

glyphosate

Inhibition of Enolpyruvyl Shikimate Phosphate Synthase ( HRAC Group 9 (Legacy G)

2008

Grapes

amitrole, and glyphosate

Multiple Resistance: 2 Sites of Action
Inhibition of Lycopene Cyclase ( HRAC Group 34 (Legacy F3)
Inhibition of Enolpyruvyl Shikimate Phosphate Synthase ( HRAC Group 9 (Legacy G)

2010

Pasture seed

clethodim, and paraquat

Multiple Resistance: 2 Sites of Action
Inhibition of Acetyl CoA Carboxylase ( HRAC Group 1 (Legacy A)
PS I Electron Diversion ( HRAC Group 22 (Legacy D)

2010

Pasture seed

atrazine, chlorsulfuron, clethodim, glyphosate, haloxyfop-methyl, imazapyr, iodosulfuron-methyl-Na, and paraquat

Multiple Resistance: 5 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)
PS I Electron Diversion ( HRAC Group 22 (Legacy D)
Inhibition of Enolpyruvyl Shikimate Phosphate Synthase ( HRAC Group 9 (Legacy G)

2013

Grapes

glyphosate, and paraquat

Multiple Resistance: 2 Sites of Action
PS I Electron Diversion ( HRAC Group 22 (Legacy D)
Inhibition of Enolpyruvyl Shikimate Phosphate Synthase ( HRAC Group 9 (Legacy G)

Australia (New South Wales )

2015

Wheat

tri-allate

Very Long-Chain Fatty Acid Synthesis inhibitors ( HRAC Group 15 (Legacy K3 N)

2015

Wheat

tri-allate

Very Long-Chain Fatty Acid Synthesis inhibitors ( HRAC Group 15 (Legacy K3 N)

Chile

1997

Canola, Cereals, Lupins, Spring wheat, and Winter wheat

clethodim, clodinafop-propargyl, diclofop-methyl, haloxyfop-methyl, sethoxydim, and tralkoxydim

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

Chile

2003

Wheat

clethodim, clodinafop-propargyl, diclofop-methyl, flucarbazone-Na, haloxyfop-methyl, iodosulfuron-methyl-Na, pinoxaden, and tepraloxydim

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)

France

1993

Wheat

diclofop-methyl

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

France

2005

Cereals, Grapes, Orchards, and Rapeseed

glyphosate

Inhibition of Enolpyruvyl Shikimate Phosphate Synthase ( HRAC Group 9 (Legacy G)

France

2006

Wheat

flupyrsulfuron-methyl-Na, iodosulfuron-methyl-Na, mesosulfuron-methyl, and propoxycarbazone-Na

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

1997

Winter wheat

diclofop-methyl

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

2009

Winter wheat

chlorsulfuron

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

2016

Orchards

glyphosate

Inhibition of Enolpyruvyl Shikimate Phosphate Synthase ( HRAC Group 9 (Legacy G)

2017

Grapes, Olive, and Orchards

glufosinate-ammonium

Inhibition of Glutamine Synthetase ( HRAC Group 10 (Legacy H)

Iran

2007

Winter wheat

clodinafop-propargyl, diclofop-methyl, and pinoxaden

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

1979

Orchards, and Roadsides

atrazine, and simazine

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

1998

Alfalfa, and Wheat

clodinafop-propargyl, diclofop-methyl, pinoxaden, and quizalofop-ethyl

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

2007

Wheat

chlorsulfuron, clodinafop-propargyl, florasulam, flumetsulam, glyphosate, imazapyr, iodosulfuron-methyl-Na, mesosulfuron-methyl, metosulam, pinoxaden, propoxycarbazone-Na, sulfometuron-methyl, and tribenuron-methyl

2013

Carrots, and Wheat

clethodim, clodinafop-propargyl, cycloxydim, haloxyfop-methyl, iodosulfuron-methyl-Na, mesosulfuron-methyl, pinoxaden, propoxycarbazone-Na, and sulfometuron-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)

Italy

2007

Grapes, and Orchards

glyphosate

Inhibition of Enolpyruvyl Shikimate Phosphate Synthase ( HRAC Group 9 (Legacy G)

Saudi Arabia

1992

Cereals, and Wheat

clodinafop-propargyl, diclofop-methyl, and tralkoxydim

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

1993

Wheat

clodinafop-propargyl, diclofop-methyl, fluazifop-butyl, haloxyfop-methyl, imazamox, sethoxydim, and tralkoxydim

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)

2001

Grapes

glyphosate

Inhibition of Enolpyruvyl Shikimate Phosphate Synthase ( HRAC Group 9 (Legacy G)

2002

Fruit, and Grapes

paraquat

PS I Electron Diversion ( HRAC Group 22 (Legacy D)

2003

Grapes

glyphosate, haloxyfop-methyl, paraquat, and tepraloxydim

Multiple Resistance: 3 Sites of Action
Inhibition of Acetyl CoA Carboxylase ( HRAC Group 1 (Legacy A)
PS I Electron Diversion ( HRAC Group 22 (Legacy D)
Inhibition of Enolpyruvyl Shikimate Phosphate Synthase ( HRAC Group 9 (Legacy G)

1992

Wheat

chlorotoluron, and diclofop-methyl

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

1992

Wheat

diclofop-methyl

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

1992

Orchards

simazine

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

2006

Orchards

glyphosate

Inhibition of Enolpyruvyl Shikimate Phosphate Synthase ( HRAC Group 9 (Legacy G)

United States (California)

2016

Olive

glyphosate, and oxyfluorfen

Multiple Resistance: 2 Sites of Action
Inhibition of Protoporphyrinogen Oxidase ( HRAC Group 14 (Legacy E)
Inhibition of Enolpyruvyl Shikimate Phosphate Synthase ( HRAC Group 9 (Legacy G)

Tunisia

1996

Cereals

diclofop-methyl

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

1998

Almonds, and Orchards

glyphosate

Inhibition of Enolpyruvyl Shikimate Phosphate Synthase ( HRAC Group 9 (Legacy G)

Specific Papers about this Case

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Boutsalis, P. ; Gill, G. S. ; Preston, C.. 2012. Incidence of herbicide resistance in rigid ryegrass (Lolium rigidum) across southeastern Australia. Weed Technology 26 : 391 - 398.

Herbicide resistance in rigid ryegrass is an escalating problem in grain-cropping fields of southeastern Australia due to increased reliance on herbicides as the main method for weed control. Weed surveys were conducted between 1998 and 2009 to identify the extent of herbicide-resistant rigid ryegrass across this region to dinitroaniline, and acetolactate synthase- and acetyl coenzyme A (CoA) carboxylase-inhibiting herbicides. Rigid ryegrass was collected from cropped fields chosen at random. Outdoor pot studies were conducted during the normal winter growing season for rigid ryegrass with PRE-applied trifluralin and POST-applied diclofop-methyl, chlorsulfuron, tralkoxydim, pinoxaden, and clethodim. Herbicide resistance to trifluralin in rigid ryegrass was identified in one-third of the fields surveyed from South Australia, whereas less than 5% of fields in Victoria exhibited resistance. In contrast, resistance to chlorsulfuron was detected in at least half of the cropped fields across southeastern Australia. Resistance to the cereal-selective aryloxyphenoxypropionate-inhibiting herbicides diclofop-methyl, tralkoxydim, and pinoxaden ranged between 30 and 60% in most regions, whereas in marginal cropping areas less than 12% of fields exhibited resistance. Resistance to clethodim varied between 0 and 61%. Higher levels of resistance to clethodim were identified in the more intensively cropped, higher-rainfall districts where pulse and canola crops are common. These weed surveys demonstrated that a high incidence of resistance to most tested herbicides was present in rigid ryegrass from cropped fields in southeastern Australia, which presents a major challenge for crop producers..

Tan, M. K. ; Preston, C. ; Wang, G. X.. 2007. Molecular basis of multiple resistance to ACCase-inhibiting and ALS-inhibiting herbicides in Lolium rigidum. Weed Research (Oxford) 47 : 534 - 541.

Herbicide resistance in Lolium rigidum is widespread across much of the agricultural land in Australia. As the incidence of herbicide resistance has increased, so has the incidence of multiple herbicide resistance. This reduces the herbicide options available for control of this weed. This study reports on the successful amplification and sequencing of the acetolactate synthase (ALS) gene of L. rigidum using primers designed from sequence information of related taxa. This enables, for the first time, the successful determination of a mutation in the ALS gene of this species that provides resistance to ALS-inhibiting herbicides. This mutation causes amino acid substitution at Trp574 (numbering standardised to Arabidopsis thaliana) to Leu which had been reported to confer a high level of resistance against all classes of ALS inhibitor herbicides. In addition, multiple resistance to ALS-inhibiting and acetyl-coenzyme A carboxylase-inhibiting herbicides is acquired through the independent accumulation of mutant alleles for the target sites. This may thus explain some of the irregular, mosaic resistance patterns that occur in this predominantly outcrossing species..

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Literature about Similar Cases

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Zakia El-Mastouri, Pavlina Kosnarova, Katerina Hamouzova, Ezzedine Alimi, Josef Soukup. 2024. Insight into the herbicide resistance patterns in Lolium rigidum populations in Tunisian and Moroccan wheat regions. Front. Plant Sci. 15 : 1 - 12.

Rigid ryegrass (Lolium rigidum Gaud.) is one of the most troublesome weeds in Moroccan and Tunisian cereal crop fields. In total, 19 rigid ryegrass field populations were randomly selected in northern wheat crop areas of Morocco and Tunisia to examine the patterns of herbicide resistance to acetolactate synthase (ALS)- and acetyl-CoA carboxylase (ACCase)-inhibiting herbicides. Greenhouse experiments confirmed reduced sensitivity to ALS- and/or ACCase-inhibiting herbicides in all L. rigidum populations. The occurrence of target-site resistance (TSR) was tested using high-throughput genotyping. The advent of next-generation sequencing (NGS) has enabled easy identification of causal mutations and confirmed the presence of ALS and ACCase mutations at specific codons conferring TSR. Thirteen populations showed resistance to ALS inhibiting herbicides associated with point mutations in positions Pro-197-Thr, Pro-197 Ser, Pro-197-Leu, Pro-197-Gln and Trp-574-Leu, while resistance to ACCase-inhibiting herbicides was detected in 18 populations in positions Asp-2078-Val, Trp-2027-Cys, Ile-1781-Leu, Gly-2096-Ala, and Ile 2041-Asn of the enzymes conferring TSR. Additionally, dose–response experiments with pyroxsulam applied after the inhibition of cytochrome P450 monooxygenase by malathion showed an increase in sensitivity in two out of seven highly resistant (HR) rigid ryegrass populations. This demonstrates the presence of non target site resistance (NTSR) in some ryegrass populations. Further evidence of NTSR was investigated in dose–response experiments with pyroxsulam, following pretreatment with the glutathione S-transferase (GST) inhibitor 4-chloro-7-nitrobenzoxadiazole (NBD-Cl), which partially reversed resistance in only a few individuals of two L. rigidum populations. Hence, our study confirms the existence of multiple and cross resistance to ALS- and ACCase-inhibiting herbicides in L. rigidum from Morocco and Tunisia with both TSR and NTSR mechanisms. These results emphasize local resistance management as an important tool to detect and mitigate gene flow from rigid ryegrass populations where resistance has evolved..

Zakia El-Mastouri, Katerina Hamouzova, Tudor Trifan, Pavlina Kosnarova, Ezzedine Alimi, Josef Soukup. 2024. Resistance to ACCase and ALS-inhibiting herbicides detected in targeted sampling of Lolium rigidum (rigid ryegrass) populations from cereal crops in Morocco, Algeria, and Tunisia. Crop Protection 186 : 1 - 9.

Lolium rigidum Gaud. (rigid ryegrass) is one of the most widespread weeds in cereal crops in Morocco, Algeria and Tunisia. This weed has evolved resistance to various herbicide modes of action in this region. ACCase and ALS inhibiting herbicides are mainly used in the major-cereal growing regions to control rigid ryegrass. Through a questionnaire, regions where farmers reported less control of herbicide treatments were registered in the three Maghreb countries. Registered fields were visited for collection and 75 field populations were screened with two ACCase and two ALS herbicides. Target site resistance (TSR) was diagnosed using Illumina Next Generation Sequencing (NGS) technology. The sensitivity bioassay results revealed over 60% of sampled populations to be resistant to pinoxaden and/or clodinafop and about 40% to be resistant to iodosulfuron + mesosulfuron and/or pyroxsulam. In addition, 53% of populations displayed resistance (R) to the two herbicide modes of action tested among the regions. In total, 16 ACCase and 11 ALS mutant alleles were identified, carrying out an amino-acid substitution and conferring herbicide resistance in 3700 of the analyzed plants. Most ACCase and ALS mutations were detected at codons Ile1781 and Pro197, respectively. Not only does this study demonstrate the presence of both cross and multiple resistance, it also highlights the non-ACCase and non-ALS -based resistance mechanisms that could confer resistance to herbicides with different modes of action which complicates the resistance management strategies. In the three Maghreb countries, this challenge is even more prominent due to few modes of action being available for rigid ryegrass control due to low-cost market and the prevalence of generic herbicides..

Fernández-Moreno PT, Bastida F, De Prado R. 2015. First case of glyphosate resistance in France. Agronomy for Sustainable Development 35 : 1469 - 1476.

Glyphosate is a broad-spectrum systemic herbicide used to kill weeds, especially annual broadleaf weeds and grasses known to compete with commercial crops grown around the globe. However, weeds evolve and develop resistance to glyphosate. Until recently, no case of glyphosate resistance had been detected in France. Glyphosate resistance was indeed recently recorded in a Lolium rigidum weed population from a vineyard in the South of France. Here, we studied the mechanisms of this resistance case. Seed samples of L. rigidum were collected from the vineyard where resistance had been detected, as well as from a nearby area that had no known history of exposure to glyphosate. We studied the effect of retention of glyphosate spray, shikimic acid accumulation, glyphosate absorption and translocation, glyphosate metabolism, and the sequence of the enzyme that glyphosate targets in plants, 5-enolpyruvylshikimate-3-phosphate synthase. Our results show that glyphosate absorption decreased by 30 % in the resistant L. rigidum weed. In addition, glyphosate translocation out of the treated leaves was reduced by 52 %. Finally, the resistant biotype had a serine amino acid substitution at position 106 of the predicted protein, instead of the proline amino acid present in the susceptible population. Our results suggest that the resistant population of L. rigidumpresents three different mechanisms of resistance to glyphosate, namely reduced absorption, reduced mobility in the plants, and a mutation in the gene coding for the enzyme targeted by glyphosate..

Adu-Yeboah, P. ; Malone, J. M. ; Gill, G. ; Preston, C.. 2014. Reduced glyphosate translocation in two glyphosate-resistant populations of rigid ryegrass (Lolium rigidum) from fence lines in South Australia. Weed Science 62 : 4 - 10.

Populations of rigid ryegrass with resistance to glyphosate have started to become a problem on fence lines of cropping fields of southern Australian farms. Seed of rigid ryegrass plants that survived glyphosate application were collected from two fence line locations in Clare, South Australia. Dose-response experiments confirmed resistance of these fence line populations to glyphosate. Both populations required 9- to 15-fold higher glyphosate dose to achieve 50% mortality in comparison to a standard susceptible population. The mechanism of resistance in these populations was investigated. Sequencing a conserved region of the gene encoding 5-enolpyruvyl-shikimate-3-phosphate synthase identified no differences between the resistant and susceptible populations. Absorption of glyphosate into leaves of the resistant populations was not different from the susceptible population. However, the resistant plants retained significantly more herbicide in the treated leaf blades than did the susceptible plants. Conversely, susceptible plants translocated significantly more herbicide to the leaf sheaths and untreated leaves than the resistant plants. The differences in translocation pattern for glyphosate between the resistant and susceptible populations of rigid ryegrass suggest resistance is associated with altered translocation of glyphosate in the fence line populations..

Busi, R. ; Gaines, T. A. ; Vila-Aiub, M. M. ; Powles, S. B.. 2014. Inheritance of evolved resistance to a novel herbicide (pyroxasulfone). Plant Science 217/218 : 127 - 134.

Agricultural weeds have rapidly adapted to intensive herbicide selection and resistance to herbicides has evolved within ecological timescales. Yet, the genetic basis of broad-spectrum generalist herbicide resistance is largely unknown. This study aims to determine the genetic control of non-target-site herbicide resistance trait(s) that rapidly evolved under recurrent selection of the novel lipid biosynthesis inhibitor pyroxasulfone in Lolium rigidum. The phenotypic segregation of pyroxasulfone resistance in parental, F₁ and back-cross (BC) families was assessed in plants exposed to a gradient of pyroxasulfone doses. The inheritance of resistance to chemically dissimilar herbicides (cross-resistance) was also evaluated. Evolved resistance to the novel selective agent (pyroxasulfone) is explained by Mendelian segregation of one semi-dominant allele incrementally herbicide-selected at higher frequency in the progeny. In BC families, cross-resistance is conferred by an incompletely dominant single major locus. This study confirms that herbicide resistance can rapidly evolve to any novel selective herbicide agents by continuous and repeated herbicide use. The results imply that the combination of herbicide options (rotation, mixtures or combinations) to exploit incomplete dominance can provide acceptable control of broad-spectrum generalist resistance-endowing monogenic traits. Herbicide diversity within a set of integrated management tactics can be one important component to reduce the herbicide selection intensity..

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