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A novel W1999S mutation and non-target site resistance impact on acetyl-CoA carboxylase inhibiting herbicides to varying degrees in a UK Lolium multiflorum population.

Kaundun SS, Bailly GC, Dale RP, Hutchings SJ, McIndoe E - PLoS ONE (2013)

Bottom Line: Additionally population UK21 is characterised by other resistance mechanisms, very likely non non-target site based, affecting several aryloxyphenoxyproprionate (FOP) herbicides but not the practical field rate of pinoxaden.The positive identification of wild type tryptophan and mutant serine alleles at ACCase position 1999 could be readily achieved with an original DNA based derived cleaved amplified polymorphic sequence (dCAPS) assay that uses the same PCR product but two different enzymes for positively identifying the wild type tryptophan and mutant serine alleles identified here.This paper highlights intrinsic differences between ACCase inhibiting herbicides that could be exploited for controlling ryegrass populations such as UK21 characterised by compound-specific target site and non-target site resistance.

View Article: PubMed Central - PubMed

Affiliation: Syngenta, Jealott's Hill International Research Centre, Bracknell, United Kingdom. deepak.kaundun@syngenta.com

ABSTRACT

Background: Acetyl-CoA carboxylase (ACCase) inhibiting herbicides are important products for the post-emergence control of grass weed species in small grain cereal crops. However, the appearance of resistance to ACCase herbicides over time has resulted in limited options for effective weed control of key species such as Lolium spp. In this study, we have used an integrated biological and molecular biology approach to investigate the mechanism of resistance to ACCase herbicides in a Lolium multiflorum Lam. from the UK (UK21).

Methodology/principal findings: The study revealed a novel tryptophan to serine mutation at ACCase codon position 1999 impacting on ACCase inhibiting herbicides to varying degrees. The W1999S mutation confers dominant resistance to pinoxaden and partially recessive resistance to cycloxydim and sethoxydim. On the other hand, plants containing the W1999S mutation were sensitive to clethodim and tepraloxydim. Additionally population UK21 is characterised by other resistance mechanisms, very likely non non-target site based, affecting several aryloxyphenoxyproprionate (FOP) herbicides but not the practical field rate of pinoxaden. The positive identification of wild type tryptophan and mutant serine alleles at ACCase position 1999 could be readily achieved with an original DNA based derived cleaved amplified polymorphic sequence (dCAPS) assay that uses the same PCR product but two different enzymes for positively identifying the wild type tryptophan and mutant serine alleles identified here.

Conclusion/significance: This paper highlights intrinsic differences between ACCase inhibiting herbicides that could be exploited for controlling ryegrass populations such as UK21 characterised by compound-specific target site and non-target site resistance.

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Related in: MedlinePlus

Haloxyfop-P-methyl dose response tests on four plant groups: homozygous wild type WW1999, heterozygous WS1999 and homozygous mutant SS1999 from the mixed resistant population UK21 and standard sensitive STD1 plants (WW1999) for comparison.Observed values represent dry weight relative to untreated (%) averaged across biological and technical replicates.
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pone-0058012-g004: Haloxyfop-P-methyl dose response tests on four plant groups: homozygous wild type WW1999, heterozygous WS1999 and homozygous mutant SS1999 from the mixed resistant population UK21 and standard sensitive STD1 plants (WW1999) for comparison.Observed values represent dry weight relative to untreated (%) averaged across biological and technical replicates.

Mentions: Whole plant dose response tests on characterised UK21 genotypes were carried out to determine the precise levels of resistance conferred by target site and non-target site resistance to two FOPs, two DIMs and pinoxaden in UK21 (Tables 3 and 4). Dose response curves were obtained for all plant groups and herbicides except for diclofop-methyl on all three different UK21 genotypes (Figure 3). At the highest rate tested (15 kg ai/ha) all the plants survived the diclofop-methyl treatment. On average, the heterozygous and homozygous mutant plants (<20% biomass reduction) were less controlled than the homozygous wild type plants (42% biomass reduction) implying that the target site resistance at position 1999 did contribute to higher levels of resistance to diclofop-methyl in UK21. Compared to diclofop-methyl, lower levels of resistance were observed for haloxyfop-p-methyl with respect to the W1999S target site resistance and non-target site resistance contained in UK21 (Figure 4). One or two copies of the mutant serine allele amounted to a resistance factor (Rf) of around 3 in both cases. However this was sufficient to cause survivorship to the FOP herbicide at the recommended field rate. A higher level of resistance was identified between the wild type UK21-WW1999 and STD1-WW1999 plants. Resistance to pinoxaden was confirmed with the W1999S mutation resulting in resistance factors of 11 and 33 for one and two mutant serine alleles respectively (Figure 5). The shift between the wild type UK21-WW1999 and STD1-WW1999 plants was small (Rf of 3) with average GR50 values of 2.1 g ai/ha and 8.3 g ai/ha only, thus confirming the non-significance of non-target site resistance at the recommended field rate of pinoxaden. The W1999S mutation had a lesser effect on sethoxydim compared to pinoxaden reflecting the partially recessive and dominant nature of this mutation on the DIM and DEN herbicide respectively (Figure 6). And finally, the dose response assay ascertained the minimal impact of the W1999S mutation on tepraloxydim with almost overlapping curves for UK21-WW1999 and UK21-WS1999 (Figure 7). GR50 values for any one wild and mutant UK21 genotypes were well below the recommended field rate of the herbicide (Table 3).


A novel W1999S mutation and non-target site resistance impact on acetyl-CoA carboxylase inhibiting herbicides to varying degrees in a UK Lolium multiflorum population.

Kaundun SS, Bailly GC, Dale RP, Hutchings SJ, McIndoe E - PLoS ONE (2013)

Haloxyfop-P-methyl dose response tests on four plant groups: homozygous wild type WW1999, heterozygous WS1999 and homozygous mutant SS1999 from the mixed resistant population UK21 and standard sensitive STD1 plants (WW1999) for comparison.Observed values represent dry weight relative to untreated (%) averaged across biological and technical replicates.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3585232&req=5

pone-0058012-g004: Haloxyfop-P-methyl dose response tests on four plant groups: homozygous wild type WW1999, heterozygous WS1999 and homozygous mutant SS1999 from the mixed resistant population UK21 and standard sensitive STD1 plants (WW1999) for comparison.Observed values represent dry weight relative to untreated (%) averaged across biological and technical replicates.
Mentions: Whole plant dose response tests on characterised UK21 genotypes were carried out to determine the precise levels of resistance conferred by target site and non-target site resistance to two FOPs, two DIMs and pinoxaden in UK21 (Tables 3 and 4). Dose response curves were obtained for all plant groups and herbicides except for diclofop-methyl on all three different UK21 genotypes (Figure 3). At the highest rate tested (15 kg ai/ha) all the plants survived the diclofop-methyl treatment. On average, the heterozygous and homozygous mutant plants (<20% biomass reduction) were less controlled than the homozygous wild type plants (42% biomass reduction) implying that the target site resistance at position 1999 did contribute to higher levels of resistance to diclofop-methyl in UK21. Compared to diclofop-methyl, lower levels of resistance were observed for haloxyfop-p-methyl with respect to the W1999S target site resistance and non-target site resistance contained in UK21 (Figure 4). One or two copies of the mutant serine allele amounted to a resistance factor (Rf) of around 3 in both cases. However this was sufficient to cause survivorship to the FOP herbicide at the recommended field rate. A higher level of resistance was identified between the wild type UK21-WW1999 and STD1-WW1999 plants. Resistance to pinoxaden was confirmed with the W1999S mutation resulting in resistance factors of 11 and 33 for one and two mutant serine alleles respectively (Figure 5). The shift between the wild type UK21-WW1999 and STD1-WW1999 plants was small (Rf of 3) with average GR50 values of 2.1 g ai/ha and 8.3 g ai/ha only, thus confirming the non-significance of non-target site resistance at the recommended field rate of pinoxaden. The W1999S mutation had a lesser effect on sethoxydim compared to pinoxaden reflecting the partially recessive and dominant nature of this mutation on the DIM and DEN herbicide respectively (Figure 6). And finally, the dose response assay ascertained the minimal impact of the W1999S mutation on tepraloxydim with almost overlapping curves for UK21-WW1999 and UK21-WS1999 (Figure 7). GR50 values for any one wild and mutant UK21 genotypes were well below the recommended field rate of the herbicide (Table 3).

Bottom Line: Additionally population UK21 is characterised by other resistance mechanisms, very likely non non-target site based, affecting several aryloxyphenoxyproprionate (FOP) herbicides but not the practical field rate of pinoxaden.The positive identification of wild type tryptophan and mutant serine alleles at ACCase position 1999 could be readily achieved with an original DNA based derived cleaved amplified polymorphic sequence (dCAPS) assay that uses the same PCR product but two different enzymes for positively identifying the wild type tryptophan and mutant serine alleles identified here.This paper highlights intrinsic differences between ACCase inhibiting herbicides that could be exploited for controlling ryegrass populations such as UK21 characterised by compound-specific target site and non-target site resistance.

View Article: PubMed Central - PubMed

Affiliation: Syngenta, Jealott's Hill International Research Centre, Bracknell, United Kingdom. deepak.kaundun@syngenta.com

ABSTRACT

Background: Acetyl-CoA carboxylase (ACCase) inhibiting herbicides are important products for the post-emergence control of grass weed species in small grain cereal crops. However, the appearance of resistance to ACCase herbicides over time has resulted in limited options for effective weed control of key species such as Lolium spp. In this study, we have used an integrated biological and molecular biology approach to investigate the mechanism of resistance to ACCase herbicides in a Lolium multiflorum Lam. from the UK (UK21).

Methodology/principal findings: The study revealed a novel tryptophan to serine mutation at ACCase codon position 1999 impacting on ACCase inhibiting herbicides to varying degrees. The W1999S mutation confers dominant resistance to pinoxaden and partially recessive resistance to cycloxydim and sethoxydim. On the other hand, plants containing the W1999S mutation were sensitive to clethodim and tepraloxydim. Additionally population UK21 is characterised by other resistance mechanisms, very likely non non-target site based, affecting several aryloxyphenoxyproprionate (FOP) herbicides but not the practical field rate of pinoxaden. The positive identification of wild type tryptophan and mutant serine alleles at ACCase position 1999 could be readily achieved with an original DNA based derived cleaved amplified polymorphic sequence (dCAPS) assay that uses the same PCR product but two different enzymes for positively identifying the wild type tryptophan and mutant serine alleles identified here.

Conclusion/significance: This paper highlights intrinsic differences between ACCase inhibiting herbicides that could be exploited for controlling ryegrass populations such as UK21 characterised by compound-specific target site and non-target site resistance.

Show MeSH
Related in: MedlinePlus