Non‐target‐site resistance to PDS‐inhibiting herbicides in a wild radish (<scp><i>Raphanus raphanistrum</i></scp>) population

Lu, Huan; Yu, Qin; Han, Heping; Owen, Mechelle; Powles, Stephen B.

doi:10.1002/ps.5733

Cited by 20 publications

(16 citation statements)

References 37 publications

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“…Sauer 35 and Raphanus raphanistrum. 36 Generally, P450 genes can confer resistance to herbicides belonging to different chemical groups, and it was found to be one of the main mechanisms for ALS-and ACCase-inhibiting herbicides. For example, CYP71AK2 and CYP72A254 were significantly transcribed in E. phyllopogon of the bispyribacresistant line.…”

Section: ■ Discussionmentioning

confidence: 99%

“…Similar findings were also documented in many other metabolic herbicide-resistant weeds, such as Amaranthus tuberculatus (Moq.) Sauer and Raphanus raphanistrum . Generally, P450 genes can confer resistance to herbicides belonging to different chemical groups, and it was found to be one of the main mechanisms for ALS- and ACCase-inhibiting herbicides.…”

Section: Discussionmentioning

confidence: 99%

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Investigating the Mechanism of Metabolic Resistance to Tribenuron-Methyl in Capsella bursa-pastoris (L.) Medik. by Full-Length Transcriptome Assembly Combined with RNA-Seq

Zhang

Wang

Bei

et al. 2021

J. Agric. Food Chem.

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Capsella bursa-pastoris (L.) Medik. has evolved resistance to ALS-inhibiting herbicides on a large scale. Previous studies primarily focused on the target-site resistance (TSR), and the non-TSR (NTSR) is not well characterized. In this study, pre-treatment with the cytochrome P450 monooxygenase (P450) inhibitor malathion clearly reduced the tribenuron-methyl resistance in the resistant (R) population. After tribenuron-methyl treatment, the glutathione S-transferase (GST) activity of R plants was significantly higher than that of susceptible (S) plants. The higher tribenuron-methyl metabolism in R plants was also confirmed by using LC–MS/MS analysis. Isoform sequencing (Iso-Seq) combined with RNA sequencing (RNA-Seq) was used to identify candidate genes involved in non-target metabolic resistance in this population. A total of 37 differentially expressed genes were identified, 11 of them constitutively upregulated in R plants, including three P450s, one GST, two glycosyltransferases, two ATP-binding cassette transporters, one oxidase, and two peroxidases. This study confirmed the metabolic tribenuron-methyl resistance in C. bursa-pastoris, and the transcriptome data obtained by Iso-Seq combined with RNA-Seq provide gene resources for understanding the molecular mechanism of NTSR in C. bursa-pastoris.

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Section: ■ Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Investigating the Mechanism of Metabolic Resistance to Tribenuron-Methyl in Capsella bursa-pastoris (L.) Medik. by Full-Length Transcriptome Assembly Combined with RNA-Seq

Zhang

Wang

Bei

et al. 2021

J. Agric. Food Chem.

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“…Pre-treatment with piperonyl butoxide (PBO), but not malathion, increased control of resistant P. annua with fenoxaprop (109), indicating that PBO inhibited specific P450 enzymes critical for fenoxaprop metabolism. Although P450 genes found in the past decade were mostly related to metabolism of ACCase, ALS, and PSII inhibitors, more recently P450 inhibitors have inhibited the P450 metabolism of several classes of herbicides (i.e., HPPD, PPO, synthetic auxins, and carotenoid synthesis inhibitors) (110)(111)(112)(113). Critically, P450s have potential to metabolize herbicides from different mode of action groups, creating unpredictable patterns of cross-resistance.…”

Section: Cytochrome P450-mediated Herbicide Metabolismmentioning

confidence: 99%

Mechanisms of evolved herbicide resistance

Gaines

Duke

Morran

et al. 2020

Journal of Biological Chemistry

434

493

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The widely successful use of synthetic herbicides over the past 70 years has imposed strong and widespread selection pressure, leading to the evolution of herbicide resistance in hundreds of weed species. Both target-site resistance (TSR) and non-target-site resistance (NTSR) mechanisms have evolved to most herbicide classes. TSR often involves mutations in genes encoding the protein targets of herbicides, affecting the binding of the herbicide either at or near catalytic domains or in regions affecting access to them. Most of these mutations are non-synonymous single-nucleotide polymorphisms, but polymorphisms in more than one codon or entire codon deletions have also evolved. Some herbicides bind multiple proteins, making TSR mechanisms more difficult to evolve. Increased amounts of protein target, by increased gene expression or by gene duplication, is an important, albeit less common, TSR mechanism. NTSR mechanisms include reduced absorption or translocation and increased sequestration or metabolic degradation. The mechanisms that can contribute to NTSR are complex and often involve genes that are members of large gene families. For example, enzymes involved in herbicide metabolism–based resistances include cytochromes P450, glutathione-S-transferases, glucosyl and other transferases, aryl acylamidase, and others. Both TSR and NTSR mechanisms can combine at the individual level to produce higher resistance levels. The vast array of herbicide-resistance mechanisms for generalist (NTSR) and specialist (TSR and some NTSR) adaptations that have evolved over a few decades illustrate the evolutionary resilience of weed populations to extreme selection pressures. These evolutionary processes drive herbicide and herbicide-resistant crop development and resistance management strategies.

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“…in Israel. Resistance to diflufenican in R. raphanistrum was reported to be due to its metabolism involving cytochrome P450s (Lu et al 2020b). Three of the four diflufenican-resistant weed species (all except S. orientale) were also resistant to at least one additional SOA (Heap 2022).…”

Section: Resultsmentioning

confidence: 99%

A nonnative Palmer amaranth (Amaranthus palmeri) population in the Republic of South Africa is resistant to herbicides with different sites of action

et al. 2022

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Palmer amaranth (Amaranthus palmeri S. Watson) is not native to Africa. Based on the presence and persistence of A. palmeri populations, its invasive status in southern Africa is classified as “naturalized”. Globally, A. palmeri is one of the most troublesome weed species in several crops including soybean [Glycine max (L.) Merr.], maize (Zea mays L.), and cotton (Gossypium hirsutum L.). Certain populations of A. palmeri in various countries were reported to be resistant to herbicides with different sites-of-action (SOAs). Two biotypes of A. palmeri in the United States of America reportedly each have resistance to herbicides representing five different SOAs, and between them a total of eight different SOAs are involved. Resistance mechanisms in these biotypes involve target site and/or non-target site resistance. Here we characterize a specific A. palmeri population that was found in Douglas district in South Africa and showed resistance to various herbicide SOAs. Initially, this A. palmeri population was discovered in a glyphosate-tolerant cotton field, where it survived glyphosate treatment. Subsequently, greenhouse experiments were conducted to characterize this A. palmeri population for potential resistance to herbicides of additional SOAs, and molecular analyses were conducted to reveal the mechanisms of herbicide resistance. Results indicated resistance to chlorimuron ethyl and glyphosate in this population, while <90% control (decreased sensitivity) was observed at the label rate for mesotrione, atrazine, saflufenacil, and s-metolachlor. However, glufosinate, tembotrione, acifluorfen, dicamba, 2,4-D, metribuzin, acetochlor, isoxaflutole, diflufenican and pyroxasulfone were effective at controlling this population. This profiling of herbicide sensitivity has allowed development of programs to control and potentially minimize the spread of this weed. In addition, molecular analysis of EPSPS revealed the role of higher copy number as a mechanism for glyphosate resistance in this population, and a Ser-653-Asn target site mutation likely conferring resistance to the ALS-inhibitor chlorimuron-ethyl. No known target site mutations were identified for the PPO-inhibitor group.

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

Cited by 20 publications

References 37 publications

Investigating the Mechanism of Metabolic Resistance to Tribenuron-Methyl in Capsella bursa-pastoris (L.) Medik. by Full-Length Transcriptome Assembly Combined with RNA-Seq

Investigating the Mechanism of Metabolic Resistance to Tribenuron-Methyl in Capsella bursa-pastoris (L.) Medik. by Full-Length Transcriptome Assembly Combined with RNA-Seq

Mechanisms of evolved herbicide resistance

A nonnative Palmer amaranth (Amaranthus palmeri) population in the Republic of South Africa is resistant to herbicides with different sites of action

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