Target site mutations and cytochrome P450s confer resistance to fenoxaprop‐<i>P</i>‐ethyl and mesosulfuron‐methyl in <i>Alopecurus aequalis</i>

Zhao, Ning; Yan, Yanyan; Luan, Ge; Zhu, Baolin; Liu, Weitang; Wang, Jinxin

doi:10.1002/ps.5089

Cited by 64 publications

(75 citation statements)

References 45 publications

(116 reference statements)

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“…Dose–response bioassays were performed to examine the sensitivities of S and R plants to different herbicides as described previously . Seven ACCase inhibitors, one photosystem II (PSII) inhibitor, and one 4‐hydroxyphenylpyruvate dioxygenase (HPPD) inhibitor were used in this study (Table ).…”

Section: Methodsmentioning

confidence: 99%

“…Single‐dose testing was conducted as described in Zhao et al with minor modification. Briefly, 100 seeds were randomly selected from each population and grown in a controlled greenhouse setting (natural light, 25° C/15° C, and ∼75% relative humidity).…”

Section: Methodsmentioning

confidence: 99%

“…), [9][10][11][12] shortawn foxtail (Alopecurus aequalis Sobol. ), [13][14][15] water chickweed (Myosoton aquaticum L.), 16 rigid brome (Bromus rigidus Roth. ), 17 and wild oat species (Avena fatua L. and Avena sterilis L.).…”

Section: Introductionmentioning

confidence: 99%

“…To date, most AASs on the known mutation sites of ACCase are not yet characterized in this species, nor the NTSR. Considering also that TSR and NTSR coexistence has been frequently identified in different resistant weeds, it is important to investigate the unknown or unreported target‐site mutations along with the TSR coupled to NTSR in specific species for improving herbicide resistance management.…”

Section: Introductionmentioning

confidence: 99%

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Trp‐1999‐Ser mutation of acetyl‐CoA carboxylase and cytochrome P450s‐involved metabolism confer resistance to fenoxaprop‐P‐ethyl in Polypogon fugax

Zhao

Luan

Yan

et al. 2019

Pest Management Science

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BACKGROUND Asia minor bluegrass (Polypogon fugax Nees ex Steud.) is an invasive grass species severely infesting wheat and canola fields in China. In May 2017, a suspected resistant P. fugax population AHHY that survived fenoxaprop‐P‐ethyl applied at its field‐recommended rate was collected from a wheat field in Huaiyuan County, Anhui Province, China. This study aimed to determine the resistance profile of AHHY to acetyl‐CoA carboxylase (ACCase) inhibitors and to investigate its mechanisms of resistance to fenoxaprop. RESULTS Single‐dose testing indicated that the AHHY population had evolved resistance to fenoxaprop. The partial carboxyltransferase domain of ACCase in P. fugax was amplified and compared. Four loci encoding plastidic ACCase were isolated from both the resistant and sensitive individuals. Combining gene sequencing with the derived cleaved amplified polymorphic sequence assay, we found that 100% of the plants of AHHY carried Trp‐1999‐Ser mutation in their ACCase1,1–2 allele. Whole‐plant dose–response bioassay indicated that AHHY was highly resistant to fenoxaprop and pinoxaden (resistance index (RI) ≥ 10) with low resistance to clodinafop‐propargyl, sethoxydim, and clethodim (2 ≤ RI < 5). Pre‐treatment with piperonyl butoxide largely reduced (55%) the weed's resistance to fenoxaprop. Both basal and fenoxaprop‐induced glutathione S‐transferases activities toward 1‐chloro‐2, 4‐dinitrobenzene were significantly higher in resistant plants than in susceptible plants. CONCLUSION This study revealed that P. fugax had multiple alleles encoding plastidic ACCase, and reported for the first time the occurrence of Trp‐1999‐Ser mutation and non‐target‐site resistance in this species. Fenoxaprop resistance in AHHY plants was conferred by target‐site mutation and P450s‐involved enhanced metabolism. © 2019 Society of Chemical Industry

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Trp‐1999‐Ser mutation of acetyl‐CoA carboxylase and cytochrome P450s‐involved metabolism confer resistance to fenoxaprop‐P‐ethyl in Polypogon fugax

Zhao

Luan

Yan

et al. 2019

Pest Management Science

Self Cite

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“…Cummins, Cole, & Edwards, 1999;Duhoux, Carrère, Duhoux, & Délye, 2017;Duhoux, Carrère, Gouzy, Bonin, & Délye, 2015;Küpper, Peter, et al, 2018;W. Liu et al, 2018;Nakka et al, 2017;Pan et al, 2019;Peng et al, 2010;Varanasi, Brabham, & Norsworthy, 2018;N. Zhao et al, 2019)).…”

Section: Introductionmentioning

confidence: 99%

The genetic architecture and genomic context of glyphosate resistance inAmaranthus tuberculatus

Kreiner

Tranel

Weigel

et al. 2020

Preprint

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Although much of what we know about the genetic basis of herbicide resistance has come from detailed investigations of monogenic adaptation at known target-sites, the importance of polygenic resistance has been increasingly recognized. Despite this, little work has been done to characterize the genomic basis of herbicide resistance, including the number and distribution of involved genes, their effect sizes, allele frequencies, and signatures of selection. Here we implement genome-wide association (GWA) and population genomic approaches to examine the genetic architecture of glyphosate resistance in the problematic agricultural weed, Amaranthus tuberculatus. GWA correctly identifies the gene targeted by glyphosate, and additionally finds more than 100 genes across all 16 chromosomes associated with resistance. The encoded proteins have relevant non-target-site resistance and stress-related functions, with potential for pleiotropic roles in resistance to other herbicides and diverse life history traits. Resistance-related alleles are enriched for large effects and intermediate frequencies, implying that strong selection has shaped the genetic architecture of resistance despite potential pleiotropic costs. The range of common and rare allele involvement implies a partially shared genetic basis of non-target-site resistance across populations, complemented by population-specific alleles. Resistance-related alleles show evidence of balancing selection, and suggest a long-term maintenance of standing variation at stress-response loci that have implications for plant performance under herbicide pressure. By our estimates, genome-wide SNPs explain a near comparable amount of the total variation in glyphosate resistance to monogenic mechanisms, indicating the potential for an underappreciated polygenic contribution to the evolution of herbicide resistance in weed populations.

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Esomeprazole overcomes paclitaxel‐resistance and enhances anticancer effects of paclitaxel by inducing autophagy in A549/Taxol cells

Bai

Ding

et al. 2020

Cell Biology International

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Non‐small‐cell lung cancer (NSCLC) is one of the most common malignancies, and the occurrence of drug‐resistance severely limits the efficacy of anticancer drugs in the treatment of NSCLC. Identification of new agents to reverse drug‐resistance in NSCLC treatment is of great importance and urgency both clinically and scientifically. In the present study, we found that A549/Taxol cells displayed a high level of resistance to paclitaxel with the resistance index up to 231. Importantly, esomeprazole could potentiate the antiproliferative effect of paclitaxel in A549/Taxol cells, but not in A549 cells. Further exploration on the underlying mechanisms revealed that esomeprazole decreased the intracellular pH via inhibiting V‐ATPase expression in A549/Taxol cells. Meanwhile, esomeprazole pretreatment significantly promoted paclitaxel‐induced polymerization of tubulin and enhanced the proportion of G2/M‐arrested cells in A549/Taxol cells. Unfortunately, esomeprazole could only result in a slight decrease in the expression of P‐gp in A549/Taxol cells. Interestingly, esomeprazole significantly increased paclitaxel‐induced apoptosis, which was impeded by the autophagy inhibitor 3‐MA in A549/Taxol cells. Taken together, our data suggest that esomeprazole is a promising chemosensitizer against paclitaxel‐resistant NSCLC by inducing autophagy. Our study also offers a new strategy to solve the paclitaxel‐resistance problem during NSCLC treatment.

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Target site mutations and cytochrome P450s confer resistance to fenoxaprop‐P‐ethyl and mesosulfuron‐methyl in Alopecurus aequalis

Cited by 64 publications

References 45 publications

Trp‐1999‐Ser mutation of acetyl‐CoA carboxylase and cytochrome P450s‐involved metabolism confer resistance to fenoxaprop‐P‐ethyl in Polypogon fugax

Trp‐1999‐Ser mutation of acetyl‐CoA carboxylase and cytochrome P450s‐involved metabolism confer resistance to fenoxaprop‐P‐ethyl in Polypogon fugax

The genetic architecture and genomic context of glyphosate resistance inAmaranthus tuberculatus

Esomeprazole overcomes paclitaxel‐resistance and enhances anticancer effects of paclitaxel by inducing autophagy in A549/Taxol cells

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