<b>HRAC Group 2</b> <font size='2'> (Legacy B) </font> resistant Monochoria vaginalis from Japan

INTERNATIONAL HERBICIDE-RESISTANT WEED DATABASE

HRAC GROUP 2 (LEGACY B) RESISTANT ARROWLEAFED MONOCHORIA
(Monochoria vaginalis)

Inhibition of Acetolactate Synthase HRAC Group 2 (Legacy B)

Japan, Ibaraki, Akita

INTRODUCTION		ARROWLEAFED MONOCHORIA
Arrowleafed Monochoria (Monochoria vaginalis) is a monocot weed in the Pontederiaceae family. In Japan this weed first evolved resistance to Group 2 (Legacy B) herbicides in 1998 and infests Rice. 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 bensulfuron-methyl 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 Jan 08, 2014 )
Common Name	Arrowleafed Monochoria
Species	Monochoria vaginalis
Group	Inhibition of Acetolactate Synthase HRAC Group 2 (Legacy B)
Herbicides	bensulfuron-methyl
Location	Japan, Ibaraki, Akita
Year	1998
Situation(s)	Rice
Contributors - (Alphabetically)	Satoshi Iwakami, Tohru Tominaga, and Akira Uchino
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NOTES ABOUT THIS BIOTYPE

GENERAL

Tohru Tominaga

Takanori Ohsako and Tohru Tominaga. Nucleotide substitutions in the acetolactate synthase genes of sulfonylurea-resistant biotypes of Monochoria vaginalis (Pontederiaceae). Genes Genet. Syst. (2007) 82, p. 207–215

Some point mutations in acetolactate synthase (ALS) confer resistance to ALSinhibiting herbicides in weeds. To clarify the evolution of the herbicide resistance of Monochoria vaginalis, a weed in rice fields in Japan, the nucleotide sequences of four genes encoding ALS were surveyed in five sulfonylurea-resistant (SU-R) and five sulfonylurea-susceptible (SU-S) biotypes. In the ALS1 gene, two SU-R biotypes showed nucleotide substitutions changing Pro₁₉₇ to Ser and Leu, respectively. In a different gene, ALS3, three other SU-R biotypes showed either of the two nonsynonymous nucleotide substitutions seen in ALS1. Only two biotypes geographically located distantly from each other shared the same mutation conferring SU resistance in the same gene. These patterns of nucleotide substitutions indicate that the SU-R phenotype was acquired independently by different biotypes. Nucleotide diversity values of the genes showing SU-R mutations were higher than those of ALS2 lacking any SU-R mutation and of a putative pseudogene, ALS4. This result suggests that the maintenance of nucleotide variability within target genes provides an opportunity for the evolution of SU-R phenotypes by herbicide-driven selection for mutations conferring resistance.

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ACADEMIC ASPECTS

Confirmation Tests

Field, and Greenhouse trials comparing a known susceptible Arrowleafed Monochoria biotype with this Arrowleafed Monochoria 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 Arrowleafed Monochoria 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 2 (Legacy B) resistant Arrowleafed Monochoria from Japan please update the database.

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CONTRIBUTING WEED SCIENTISTS

SATOSHI IWAKAMI

Weed Scientist University of Tsukuba Faculty of Life and Environmental Sciences 1-1-1 Tennoudai Tsukuba, 305-8577, Ibaraki Japan Email Satoshi Iwakami

TOHRU TOMINAGA

Professor Kyoto University Graduate School of Agriculture Kitashirakawa-Oiwakecho Sakyo Kyoto, 606-8502, Kyoto Japan Email Tohru Tominaga

AKIRA UCHINO

Weed Scientist NARO Agricultural Research Center Graduate School of Agriculture 3-1-1 Kannondai Tsukuba, 305-8666, Ibaraki Japan Email Akira Uchino

ACKNOWLEDGEMENTS
The Herbicide Resistance Action Committee, The Weed Science Society of America, and weed scientists in Japan have been instrumental in providing you this information. Particular thanks is given to Satoshi Iwakami, Tohru Tominaga, and Akira Uchino for providing detailed information.

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Herbicide Resistant Arrowleafed Monochoria Globally
(Monochoria vaginalis)

Country

FirstYear

Situation

Active Ingredients

Site of Action

China

2010

Rice

bensulfuron-methyl

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

Indonesia

2022

Rice

bensulfuron-methyl, bispyribac-sodium, and penoxsulam

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

Japan

1998

Rice

bensulfuron-methyl

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

South Korea

1999

Rice

bensulfuron-methyl

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

Literature about Similar Cases

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Tanigaki, S. et al. . 2021. Gene expression shapes the patterns of parallel evolution of herbicide resistance in the agricultural weed Monochoria vaginalis. New Phytologist 232 : 928 - 940.

Summary

The evolution of herbicide resistance in weeds is an example of parallel evolution, throughwhich genes encoding herbicide target proteins are repeatedly represented as evolutionarytargets. The number of herbicide target-site genes differs among species, and little is knownregarding the effects of duplicate gene copies on the evolution of herbicide resistance.

We investigated the evolution of herbicide resistance in Monochoria vaginalis, which car-ries ﬁve copies of sulfonylurea target-site acetolactate synthase (ALS) genes. Suspected resis-tant populations collected across Japan were investigated for herbicide sensitivity and ALSgene sequences, followed by functional characterization and ALS gene expression analysis.

We identiﬁed over 60 resistant populations, all of which carried resistance-conferring aminoacid substitutions exclusively in MvALS1 or MvALS3. All MvALS4 alleles carried a loss-of-function mutation. Although the enzymatic properties of ALS encoded by these genes werenot markedly different, the expression of MvALS1 and MvALS3 was prominently higheramong all ALS genes.

The higher expression of MvALS1 and MvALS3 is the driving force of the biased represen-tation of genes during the evolution of herbicide resistance in M. vaginalis. Our ﬁndings high-light that gene expression is a key factor in creating evolutionary hotspots

Takanori Ohsako and Tohru Tominaga. 2013. Nucleotide substitutions in the acetolactate synthase genes of sulfonylurea-resistant biotypes ofMonochoria vaginalis(Pontederiaceae). Genes and Genetic Systems 82 : 207–215.

Some point mutations in acetolactate synthase (ALS) confer resistance to ALSinhibiting herbicides in weeds. To clarify the evolution of the herbicide resistance of Monochoria vaginalis , a weed in rice fields in Japan, the nucleotide sequences of four genes encoding ALS were surveyed in five sulfonylurea-resistant (SU-R) and five sulfonylurea-susceptible (SU-S) biotypes. In the ALS1 gene, two SU-R biotypes showed nucleotide substitutions changing Pro197 to Ser and Leu, respectively. In a different gene, ALS3 , three other SU-R biotypes showed either of the two nonsynonymous nucleotide substitutions seen in ALS1 . Only two biotypes geographically located distantly from each other shared the same mutation conferring SU resistance in the same gene. These patterns of nucleotide substitutions indicate that the SU-R phenotype was acquired independently by different biotypes. Nucleotide diversity values of the genes showing SU-R mutations were higher than those of ALS2 lacking any SU-R mutation and of a putative pseudogene, ALS4 . This result suggests that the maintenance of nucleotide variability within target genes provides an opportunity for the evolution of SU-R phenotypes by herbicide-driven selection for mutations conferring resistance. .

Song HaYoung ; Cho SooJin ; Lim HeeKyung ; Park NoJoong ; Hwang InTaek. 2010. Transformation a mutant Monochoria vaginalis acetolactate synthase (ALS) gene renders Arabidopsis thaliana resistant to ALS inhibitors. Pesticide Biochemistry and Physiology 97 : 223 - 228.

Acetolactate synthase (ALS) genes from Monochoria vaginalis resistant (R) and susceptible (S) biotypes against ALS inhibitors found in Korea revealed a single amino acid substitution of Proline (CCT), at 169th position based on the M. vaginalis ALS sequence numbering, to serine (TCT) in conserved domain A of the gene (equal to the proline 197 in Arabidopsis thaliana ALS gene sequence). A. thaliana plants transformed with the single mutated (Pro₁₆₉ to Ser) M. vaginalis ALS gene (including transit signal peptide) showed cross-resistance patterns to ALS-inhibiting herbicides, like as sulfonylurea-herbicide bensulfuron methyl (R/S factor of 9.5), imidazolinone-herbicide imazapyr (R/S factor of 5.1), and triazolopyrimidine-herbicide flumetsulam (R/S factor of 17.6) when measuring hypocotyls' length of A. thaliana. The ALS activity from the transgenic A. thaliana plants confirmed the cross-resistance pattern to these herbicides like as R/S factor of 8.3 to bensulfuron methyl, 2.3 to imazapyr, and 13.2 to flumetsulam..

Inagaki, H. ; Imaizumi, T. ; Wang GuangXi ; Tominaga, T. ; Kato, K. ; Iyozumi, H. ; Nukui, H.. 2009. Sulfonylurea-resistant biotypes of Monochoria vaginalis generate higher ultraweak photon emissions than the susceptible ones. Pesticide Biochemistry and Physiology 95 : 117 - 120.

All living organisms spontaneously generate ultraweak photon emissions, which originate from biochemical reactions in cells. Current research uses the ultraweak photon emission from organisms as a novel indicator in nondestructive analyses of an organisms living state. This study indicates that ultraweak photon emissions from Monochoria vaginalis are different between resistant biotypes (R) to sulfonylurea (SU) and susceptible biotypes (S). In SU-R biotypes, distinct increases in photon emissions were observed, but there was little increase in SU-S biotypes. In addition, photon emissions from the resistant biotypes of M. vaginalis were suppressed by treatment with P450 inhibitors. This suggests that cytochrome P450 monooxygenase, which plays a crucial role in the metabolic detoxification of SUs, could be associated with the generation of ultraweak photon emissions. Ultraweak photon emissions have a potential use in a novel diagnosis system as an indicator in a nondestructive testing of weeds resistant to SUs..

Imaizumi, T. ; Wang, G. X. ; Tominaga, T.. 2008. Inheritance of sulfonylurea resistance in Monochoria vaginalis. Weed Research (Oxford) 48 : 448 - 454.

The inheritance of sulfonylurea (SU) resistance in Monochoria vaginalis was investigated based on the bensulfuron-methyl response phenotypes of F₁ plants between SU-resistant (R) and -susceptible (S) and segregation analysis in F₂ progenies. Differences of SU resistance between SU-R biotypes and F₁ plants at the recommended field dose were also investigated by comparing shoot dry weight. All F₁ plants survived the treatment with 25 g a.i. ha^-1 bensulfuron-methyl, one-third of the recommended field dose, and showed similar responses to SU-R plants. Conversely, all F₁ plants died or showed extreme necrosis at 225 g a.i. ha^-1, three times the recommended field dose, as SU-S plants. F₂ plants were classified as either R or S phenotype. Segregation for resistance to bensulfuron-methyl in F₂ families did not differ from the expected 3:1 (R:S) ratio at 25 g a.i. ha^-1. At 225 g a.i. ha^-1, the F₂ families segregated in a 1:3 (R:S) ratio. These results suggest that SU resistance in M. vaginalis is controlled by a single nuclear allele with resistance being dominant at low dose and susceptibility dominant at high dose. Moreover, F₁ plants died or were extremely injured after application of bensulfuron-methyl at the recommended field dose, although SU-R biotypes grew normally..

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