Metabolic Resistance to Acetolactate Synthase Inhibiting Herbicide Tribenuron-Methyl in <i>Descurainia sophia</i> L. Mediated by Cytochrome P450 Enzymes

Yang, Qian; Li, Jinyao; Shen, Jing; Xu, Yufang; Liu, Hongjie; Deng, Wei; Li, Xuefeng; Zheng, Mingqi

doi:10.1021/acs.jafc.7b05825

Cited by 43 publications

(47 citation statements)

References 50 publications

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“…and overexpression of these genes in Arabidopsis resulted in resistance to group B herbicides bensulfuron-methyl and penoxsulam [203] and group F4 clomazone [204]. The isolation of CYP genes responsible for HR from other weed species will likely occur in the near future as chemical inhibition of P450 indicate that these genes are involved in HR for flixweed ( Descurainia sophia L.) [205], water hemp ( Amaranthus tuberculatus (Moq.) Sauer var.…”

Section: Current Application: What Genes Underlie Herbicide Resistmentioning

confidence: 99%

Population Genomic Approaches for Weed Science

Martin

Parent

Laforest

et al. 2019

Plants

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Genomic approaches are opening avenues for understanding all aspects of biological life, especially as they begin to be applied to multiple individuals and populations. However, these approaches typically depend on the availability of a sequenced genome for the species of interest. While the number of genomes being sequenced is exploding, one group that has lagged behind are weeds. Although the power of genomic approaches for weed science has been recognized, what is needed to implement these approaches is unfamiliar to many weed scientists. In this review we attempt to address this problem by providing a primer on genome sequencing and provide examples of how genomics can help answer key questions in weed science such as: (1) Where do agricultural weeds come from; (2) what genes underlie herbicide resistance; and, more speculatively, (3) can we alter weed populations to make them easier to control? This review is intended as an introduction to orient weed scientists who are thinking about initiating genome sequencing projects to better understand weed populations, to highlight recent publications that illustrate the potential for these methods, and to provide direction to key tools and literature that will facilitate the development and execution of weed genomic projects.

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Section: Current Application: What Genes Underlie Herbicide Resistmentioning

confidence: 99%

Population Genomic Approaches for Weed Science

Martin

Parent

Laforest

et al. 2019

Plants

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“…Enhanced metabolism is a mechanism for herbicide resistance. Water starwort [Myosoton aquaticum (L.) Moench] and flixweed [Descurainia sophia (L.) Webb ex Prantl] from China are resistant to tribenuron-methyl via enhanced herbicide metabolism (Bai et al 2018;Yang et al 2018). A resistant blackgrass (Alopecurus myosuroides Huds.)…”

Section: Difference In the Metabolic Rate To Mesosulfuron-methylmentioning

confidence: 99%

Non–target site based resistance to the ALS-inhibiting herbicide mesosulfuron-methyl in American sloughgrass (Beckmannia syzigachne)

Wang

Liu

et al. 2019

Weed Sci

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American sloughgrass [Beckmannia syzigachne (Steud.) Fernald] is one of the most predominant and troublesome weeds in wheat (Triticum aestivum L.) fields rotated with rice (Oryza sativa L.) in China. Mesosulfuron-methyl is one of the main herbicides used to selectively control B. syzigachne in winter wheat fields in China. After many years of application, mesosulfuron-methyl failed to control B. syzigachne in Yutai County. The objectives of this study were to determine the resistance level to mesosulfuron-methyl and other acetolactate synthase (ALS) inhibitors in the B. syzigachne population collected from Yutai County (R) and identify the mechanism of resistance. The results indicated that the R population was 4.1-fold resistant to mesosulfuron-methyl and was cross-resistant to pyroxsulam (600-fold), imazethapyr (4.1-fold), flucarbazone (12-fold), and bispyribac-sodium (12-fold). In vitro assays revealed that ALS in the R population was as sensitive as that in a susceptible (S) population. Gene sequence analysis identified no known resistant mutations in the ALS gene of the R population. Furthermore, real-time quantitative reverse transcriptase PCR experiments indicated that the expression level of the ALS gene in the R population was not different from that of the S population. However, the cytochrome P450 inhibitor malathion reversed the R population's resistance to mesosulfuron-methyl. The result of ultraperformance liquid chromatography–tandem mass spectrometry (UPLC-MS-MS) spectral analysis indicated that the metabolic rates of mesosulfuron-methyl in the R population were significantly faster than in the S population. Therefore, non-target resistance to mesosulfuron-methyl has been demonstrated in the R population. The resistance was very likely caused by enhanced herbicide metabolism.

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“…A widely accepted mechanism for safeners is that they accelerate herbicide metabolism in crops by upregulating glycosyltransferases, cytochrome P 450 monooxygenases, GST, GSH, and adenosine triphosphate (ATP)binding cassette transporter proteins that detoxify herbicides. [21][22][23] Sun et al reported that isoxadifen-ethyl alleviated nicosulfuron injury in maize by enhancing GST activity. 24 Substituted oxazole isoxazole carboxamides protected maize from chlorsulfuron by increasing GST activity and GSH content.…”

Section: Introductionmentioning

confidence: 99%

“…Enhancement of the detoxifying activity of enzymes by safeners is vital in herbicide metabolism. A widely accepted mechanism for safeners is that they accelerate herbicide metabolism in crops by upregulating glycosyltransferases, cytochrome P 450 monooxygenases, GST, GSH, and adenosine triphosphate (ATP)‐binding cassette transporter proteins that detoxify herbicides 21–23 . Sun et al .…”

Section: Introductionmentioning

confidence: 99%

Protective efficacy of phenoxyacetyl oxazolidine derivatives as safeners against nicosulfuron toxicity in maize

Zhang

Gao

Hoang

et al. 2020

Pest Management Science

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BACKGROUND: Herbicide safeners mitigate crop damage without reducing herbicide efficacy. Here, the protective effects of phenoxyacetyl oxazolidine derivatives as potential safeners were evaluated with a view toward reducing injury caused by sulfonylurea herbicide nicosulfuron to sensitive maize varieties. RESULTS: Growth indices demonstrated that the bioactivity of compound 9 (N-phenoxyacety-2-methyl-2,4-diethyl-1,3-oxazolidine) was superior to that of R-28725 and all other compounds tested. Compound 9 induced endogenous glutathione and upregulated glutathione-S-transferase (GST) in maize. Thus, it could enhance maize tolerance to nicosulfuron. Compared with the untreated water control group, the maximum reaction rate of GST was increased by 37.62%, while the maximum velocity of GST was decreased by 61.93% after treatment with compound 9. Acetolactate synthase relative activity was significantly enhanced in the case of treatment with compound 9, indicating the excellent protective effects of compound 9 against nicosulfuron in maize. CONCLUSIONS: The present work demonstrates that phenoxyacetyl oxazolidine derivatives are potentially efficacious as herbicide safeners and merit further investigation.

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Metabolic Resistance to Acetolactate Synthase Inhibiting Herbicide Tribenuron-Methyl in Descurainia sophia L. Mediated by Cytochrome P450 Enzymes

Cited by 43 publications

References 50 publications

Population Genomic Approaches for Weed Science

Population Genomic Approaches for Weed Science

Non–target site based resistance to the ALS-inhibiting herbicide mesosulfuron-methyl in American sloughgrass (Beckmannia syzigachne)

Protective efficacy of phenoxyacetyl oxazolidine derivatives as safeners against nicosulfuron toxicity in maize

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