Cross‐resistance to diflufenican and picolinafen and its inheritance in oriental mustard (<scp><i>Sisymbrium orientale</i></scp> L.)

Dang, Hue Thi; Malone, Jenna; Gill, Gurjeet; Preston, Christopher

doi:10.1002/ps.5087

Cited by 12 publications

(10 citation statements)

References 45 publications

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“…The results demonstrated that resistance to PDS‐inhibiting herbicides in this R population is not due to mutation or amplification of the target‐site PDS gene. Thus, this R wild radish population does not have target‐site resistance, in contrast to other PDS‐inhibiting herbicide R weed populations that exhibit target‐site based resistance mechanisms …”

Section: Discussionmentioning

confidence: 89%

“…For example, resistance to the PDS‐inhibiting herbicide fluridone was reported in H. verticillata due to target PDS gene mutations (Arg304‐Ser, Arg304‐Cys and Arg304‐His) . Most recently, high levels of resistance (up to 237‐fold) to diflufenican and picolinafen were reported in Sisymbrium orientale , which are endowed by the PDS gene mutations Leu498‐Val alone and Glu425‐Asp plus Leu498‐Val, respectively …”

Section: Introductionmentioning

confidence: 99%

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Non‐target‐site resistance to PDS‐inhibiting herbicides in a wild radish (Raphanus raphanistrum) population

Han

et al. 2020

Pest Management Science

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BACKGROUND: Diflufenican resistance has been reported in wild radish populations since 1998, but the resistance mechanisms have not been investigated. Recently, we identified a wild radish population (H2/10) from the Western Australian grain belt that is resistant (R) to the phytoene desaturase (PDS)-inhibiting herbicide diflufenican.RESULTS: Dose-response results showed this R population is 4.9-fold more resistant than the susceptible (S) population based on the LD 50 R/S ratio. In addition, the R population also exhibits cross-resistance to the PDS-inhibiting herbicide fluridone. The cytochrome P450 inhibitor malathion reversed diflufenican resistance and partially reversed fluridone resistance in the R population. The full coding sequences of the PDS gene were cloned from the S and R plants and there are natural variations in the PDS gene transcripts/alleles with no correlation to resistance. In addition, the R plants had a level of PDS gene expression that is not significantly different from the S plants.CONCLUSION: These results demonstrated that diflufenican resistance in this R wild radish population is likely due to non-target-site based enhanced herbicide metabolism involving cytochrome P450s.

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Section: Discussionmentioning

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Non‐target‐site resistance to PDS‐inhibiting herbicides in a wild radish (Raphanus raphanistrum) population

Han

et al. 2020

Pest Management Science

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“…In this study, malathion application ruled out Cyt-P450 metabolic-based resistance to diflufenican in the R C. bonariensis population. Most cases of resistance to PDS inhibitors have involved target site mutations in the PDS gene, , suggesting that the diflufenican resistance of the R C. bonariensis population might be based on TSR mechanisms.…”

Section: Discussionmentioning

confidence: 99%

“…In this study, malathion application ruled out Cyt-P450 metabolicbased resistance to diflufenican in the R C. bonariensis population. Most cases of resistance to PDS inhibitors have involved target site mutations in the PDS gene, 47,48 suggesting that the diflufenican resistance of the R C. bonariensis population might be based on TSR mechanisms. Because the R C. bonariensis population showed a response to 2,4-D similar to that of the S population after treatment with malathion, it was clear that metabolic resistance mediated by Cyt-P450 was the only mechanism against the phytotoxic action of 2,4-D.…”

Section: Discussionmentioning

confidence: 99%

Non-Target-Site Resistance Mechanisms Endow Multiple Herbicide Resistance to Five Mechanisms of Action in Conyza bonariensis

Palma-Bautista

Vázquez-García

Domínguez-Valenzuela

et al. 2021

J. Agric. Food Chem.

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The repeated use of herbicides can lead to the selection of multiple resistance weeds. Some populations of Conyza bonariensis occurring in olive groves from southern Spain have developed resistance to various herbicides. This study determined the resistance levels to 2,4-D, glyphosate, diflufenican, paraquat, and tribenuron-methyl in a putative resistant (R) C. bonariensis population, and the possible non-target-site resistance (NTSR) mechanisms involved were characterized. Resistance factors varied as follows: glyphosate (8.9), 2,4-D (4.8), diflufenican (5.0), tribenuron-methyl (19.6), and paraquat (85.5). Absorption of 14 Cglyphosate was up to 25% higher in the susceptible (S) population compared to the R one, but 14 C-paraquat absorption was similar (up to 70%) in both populations. S plants translocated more than 60% of both 14 C-glyphosate and 14 C-paraquat toward shoots and roots, while R plants translocated less than 10%. The R population was able to metabolize 57% of the 2,4-D into nontoxic metabolites and 68% of the tribenuron-methyl into metsulfuron-methyl (10%), metsulfuron-methyl-hydroxylate (18%), and conjugate-metsulfuron-methyl (40%). Among the NTSR mechanisms investigated, absorption and translocation could be involved in glyphosate resistance, but only translocation for paraquat. Proofs of the presence of enhanced metabolism as a resistance mechanism were found for tribenuron-methyl and 2,4-D, but not for diflufenican. This research informs the first occurrence of multiple resistance to five herbicide classes (acetolactate synthase inhibitors, 5-enolpyruvylshikimate-3-phosphate synthase inhibitors, photosystem I electron diverters, photosystem II inhibitors, and synthetic auxin herbicides) in C. bonariensis.

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“…A double-substitution Glu-425-Asp + Leu-498-Val was first observed in S. orientale from Australia [83]. Dose–response revealed a resistant phenotype to diflufenican and picolinafen, which are both pyridinecarboxamides.…”

Section: Summary By Herbicide Groupmentioning

confidence: 99%

Target-Site Mutations Conferring Herbicide Resistance

Murphy

Tranel

2019

Plants

109

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Mutations conferring evolved herbicide resistance in weeds are known in nine different herbicide sites of action. This review summarizes recently reported resistance-conferring mutations for each of these nine target sites. One emerging trend is an increase in reports of multiple mutations, including multiple amino acid changes at the glyphosate target site, as well as mutations involving two nucleotide changes at a single amino acid codon. Standard reference sequences are suggested for target sites for which standards do not already exist. We also discuss experimental approaches for investigating cross-resistance patterns and for investigating fitness costs of specific target-site mutations.

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Cross‐resistance to diflufenican and picolinafen and its inheritance in oriental mustard (Sisymbrium orientale L.)

Abstract: Resistance to diflufenican and picolinafen in the P40 population is likely conferred by Leu-498-Val and Glu-425-Asp mutations in the PDS gene. Inheritance of resistance to these herbicides is managed by a single dominant gene. © 2018 Society of Chemical Industry.

Cited by 12 publications

References 45 publications

Non‐target‐site resistance to PDS‐inhibiting herbicides in a wild radish (Raphanus raphanistrum) population

Non‐target‐site resistance to PDS‐inhibiting herbicides in a wild radish (Raphanus raphanistrum) population

Non-Target-Site Resistance Mechanisms Endow Multiple Herbicide Resistance to Five Mechanisms of Action in Conyza bonariensis

Target-Site Mutations Conferring Herbicide Resistance

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