Resistance Mechanism to Metsulfuron-Methyl in Polypogon fugax

Polypogon fugax is a common winter weed in China and other Asia countries. We have previously found a P. fugax biotype (R) resistant to acetyl co-enzyme A carboxylase (ACCase) herbicides also cannot be effectively controlled by some acetolactate synthase (ALS) herbicides. This study evaluated the level of resistance to four ALS herbicides (metsulfuron-methyl, chlorsulfuron, monosulfuron, pyribambenz isopropyl) in the R biotype and the associated resistance mechanism. The R biotype exhibited moderate level of resistance to metsulfuron-methyl (6.0-fold) compared with the sensitive biotype (S). Sequence analysis of ALS gene revealed that two ALS genes existed in P. fugax. However, no substitution associated with ALS resistance mechanism were found in ALS genes between the S and R biotypes. The activity of ALS enzyme isolated from the R biotype was inherently higher and less sensitive to metsulfuron-methyl than the S biotype. Glutathione S-transferases (GST) activity was also less sensitive to metsulfuron-methyl in the R than as the S biotypes. Malathion, a cytochrome P450 (CYP) monooxygenase inhibitor, had much greater synergistic effect with metsulfuron-methyl on the R than as the S plants, reducing the ED50 value (herbicide dose to inhibit growth by 50%) of metsulfuron-methyl by 23- and 6-fold, respectively, suggesting that CYP mediated enhanced metabolism might contribute to the resistance to ALS herbicides. These results suggest that metsulfuron-methyl resistance in the R biotype was associated with the up-regulated ALS enzymatic activity and the GST and CYP-mediated enhanced herbicide metabolism.

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Rat liver glutathione S-transferases. DNA sequence analysis of a Yb2 cDNA clone and regulation of the Yb1 and Yb2 mRNAs by phenobarbital.

Journal of Biological Chemistry ◽

10.1016/s0021-9258(19)57495-6 ◽

1986 ◽

Vol 261 (17) ◽

pp. 7952-7957 ◽

Cited By ~ 2

Author(s):

G J Ding ◽

V D Ding ◽

J A Rodkey ◽

C D Bennett ◽

A Y Lu ◽

...

Keyword(s):

Sequence Analysis ◽

Dna Sequence ◽

Rat Liver ◽

Cdna Clone ◽

Dna Sequence Analysis ◽

Liver Glutathione ◽

Glutathione S Transferases

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Sequence analysis of mutations that affect the synthesis, assembly and enzymatic activity of the unc-54 myosin heavy chain of Caenorhabditis elegans

Journal of Molecular Biology ◽

10.1016/0022-2836(85)90170-6 ◽

1985 ◽

Vol 183 (4) ◽

pp. 543-551 ◽

Cited By ~ 74

Author(s):

Nick J. Dibb ◽

Daniel M. Brown ◽

Jonathan Karn ◽

Donald G. Moerman ◽

Suzanne L. Bolten ◽

...

Keyword(s):

Caenorhabditis Elegans ◽

Sequence Analysis ◽

Enzymatic Activity ◽

Myosin Heavy Chain ◽

Heavy Chain

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Mechanisms of insecticide resistance in a temephos selected Culex quinquefasciatus (Diptera: Culicidae) strain from Sri Lanka

Bulletin of Entomological Research ◽

10.1017/s0007485300050719 ◽

1990 ◽

Vol 80 (4) ◽

pp. 453-457 ◽

Cited By ~ 20

Author(s):

H.T.R. Peiris ◽

J. Hemingway

Keyword(s):

Cytochrome P450 ◽

Sri Lanka ◽

Culex Quinquefasciatus ◽

Resistant Strain ◽

Resistance Mechanism ◽

Transferase Activity ◽

Glutathione S Transferase ◽

Biochemical Assays ◽

Significant Difference ◽

Naphthyl Acetate

AbstractCulex quinquefasciatus Say from Peliyagoda, Sri Lanka, has larval resistance to temephos, malathion, fenitrothion and chlorpyrifos. Biochemical assays on individual resistant and susceptible mosquitoes of this strain showed that there was a good correlation between this resistance and increased esterase activity with both 1-and 2-naphthyl acetate, which appears to be the major resistance mechanism in this multiple organophosphate resistant strain. There was no significant difference in malaoxon, bendiocarb or propoxur sensitivity of the acetylcholinesterase from the resistant and susceptible strains, indicating that the sensitivity of the target site has not been altered. Biochemical assays on mass homogenates of the resistant and susceptible strains showed no correlation between resistance and the level of glutathione s-transferase activity, or the amount of cytochrome P450 present.

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Effects of Hexachlorobenzene Feeding and Iron Overload on Enzymes of Haem Biosynthesis and Cytochrome P450 in Rat Liver

Clinical Science ◽

10.1042/cs0530111 ◽

1977 ◽

Vol 53 (2) ◽

pp. 111-115 ◽

Cited By ~ 2

Author(s):

M. Louw ◽

A. C. Neethling ◽

V. A. Percy ◽

M. Carstens ◽

B. C. Shanley

Keyword(s):

Cytochrome P450 ◽

Synergistic Effect ◽

Progressive Increase ◽

Decarboxylase Activity ◽

Progressive Decrease ◽

Uroporphyrinogen Decarboxylase ◽

Time Intervals ◽

Liver Cytochrome ◽

Haem Biosynthesis ◽

P450 Concentration

1. The effect of hexachlorobenzene feeding on liver δ-aminolaevulinate synthase, uroporphyrinogen decarboxylase and cytochrome P450 was studied at various time-intervals in siderotic and non-siderotic rats. 2. In the non-siderotic group hexachlorobenzene feeding led to a progressive decrease in liver uroporphyrinogen decarboxylase activity, accompanied by a progressive increase in δ-aminolaevulinate synthase activity. Cytochrome P450 concentrations were above normal throughout but fell toward the end of the experiment. 3. Similar but more marked changes were found in the siderotic animals. The fall in uroporphyrinogen decarboxylase activity occurred earlier and was significantly greater in these animals, whereas the increase in δ-aminolaevulinate synthase activity was consistently larger. Liver cytochrome P450 concentration also rose but to a lesser extent than that in the non-siderotic rats. 4. Hexachlorobenzene-induced porphyria would seem to be attributable to inhibition or inactivation of hepatic uroporphyrinogen decarboxylase. Hepatic siderosis has a synergistic effect with hexachlorobenzene on this enzyme and may exert additional effects by promoting cytochrome P450 turnover.

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Cytochrome P450 Endowed Herbicide Metabolism

Weed and Crop Resistance to Herbicides ◽

10.1007/978-94-011-5538-0_10 ◽

1997 ◽

pp. 101-108 ◽

Cited By ~ 3

Author(s):

F. Durst ◽

J. P. Salaün ◽

D. Werck-Reichhart ◽

F. Zimmerlin

Keyword(s):

Cytochrome P450 ◽

Herbicide Metabolism

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Evolution of target and non-target based multiple herbicide resistance in a single Palmer amaranth (Amaranthus palmeri) population from Kansas

Weed Technology ◽

10.1017/wet.2020.32 ◽

2020 ◽

Vol 34 (3) ◽

pp. 447-453

Author(s):

Sushila Chaudhari ◽

Vijay K. Varanasi ◽

Sridevi Nakka ◽

Prasanta C. Bhowmik ◽

Curtis R. Thompson ◽

...

Keyword(s):

Resistance Mechanism ◽

Acetolactate Synthase ◽

Palmer Amaranth ◽

Target Site ◽

Epsp Synthase ◽

High Incidence ◽

Evolution Of Resistance ◽

Target Site Resistance ◽

Herbicide Atrazine ◽

Sites Of Action

AbstractThe evolution of resistance to multiple herbicides in Palmer amaranth is a major challenge for its management. In this study, a Palmer amaranth population from Hutchinson, Kansas (HMR), was characterized for resistance to inhibitors of photosystem II (PSII) (e.g., atrazine), acetolactate synthase (ALS) (e.g., chlorsulfuron), and EPSP synthase (EPSPS) (e.g., glyphosate), and this resistance was investigated. About 100 HMR plants were treated with field-recommended doses (1×) of atrazine, chlorsulfuron, and glyphosate, separately along with Hutchinson multiple-herbicide (atrazine, chlorsulfuron, and glyphosate)–susceptible (HMS) Palmer amaranth as control. The mechanism of resistance to these herbicides was investigated by sequencing or amplifying the psbA, ALS, and EPSPS genes, the molecular targets of atrazine, chlorsulfuron, and glyphosate, respectively. Fifty-two percent of plants survived a 1× (2,240 g ai ha−1) atrazine application with no known psbA gene mutation, indicating the predominance of a non–target site resistance mechanism to this herbicide. Forty-two percent of plants survived a 1× (18 g ai ha−1) dose of chlorsulfuron with proline197serine, proline197threonine, proline197alanine, and proline197asparagine, or tryptophan574leucine mutations in the ALS gene. About 40% of the plants survived a 1× (840 g ae ha−1) dose of glyphosate with no known mutations in the EPSPS gene. Quantitative PCR results revealed increased EPSPS copy number (50 to 140) as the mechanism of glyphosate resistance in the survivors. The most important finding of this study was the evolution of resistance to at least two sites of action (SOAs) (~50% of plants) and to all three herbicides due to target site as well as non–target site mechanisms. The high incidence of individual plants with resistance to multiple SOAs poses a challenge for effective management of this weed.

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Confirmation of S-metolachlor resistance in Palmer amaranth (Amaranthus palmeri)

Weed Technology ◽

10.1017/wet.2019.44 ◽

2019 ◽

Vol 33 (5) ◽

pp. 720-726 ◽

Cited By ~ 4

Author(s):

Chad Brabham ◽

Jason K. Norsworthy ◽

Michael M. Houston ◽

Vijay K Varanasi ◽

Tom Barber

Keyword(s):

Dose Response ◽

Resistance Mechanism ◽

Acetolactate Synthase ◽

Chain Fatty Acid ◽

Palmer Amaranth ◽

Cross Resistance ◽

Amaranthus Palmeri ◽

Glutathione S Transferase ◽

Long Chain Fatty Acid ◽

Long Chain

AbstractS-Metolachlor is commonly used by soybean and cotton growers, especially with POST treatments for overlapping residuals, to obtain season-long control of glyphosate- and acetolactate synthase (ALS)–resistant Palmer amaranth. In Crittenden County, AR, reports of Palmer amaranth escapes following S-metolachlor treatment were first noted at field sites near Crawfordsville and Marion in 2016. Field and greenhouse experiments were conducted to confirm S-metolachlor resistance and to test for cross-resistance to other very-long-chain fatty acid (VLCFA)–inhibiting herbicides in Palmer amaranth accessions from Crawfordsville and Marion. Palmer amaranth control in the field (soil <3% organic matter) 14 d after treatment (DAT) was ≥94% with a 1× rate of acetochlor (1,472 g ai ha–1; emulsifiable concentrate formulation) and dimethenamid-P (631 g ai ha–1). However, S-metolachlor at 1,064 g ai ha–1 provided only 76% control, which was not significantly different from the 1/2× and 1/4× rates of dimethenamid-P and acetochlor (66% to 85%). In the greenhouse, Palmer amaranth accessions from Marion and Crawfordsville were 9.8 and 8.3 times more resistant to S-metolachlor compared with two susceptible accessions based on LD50 values obtained from dose–response experiments. Two-thirds and 1.5 times S-metolachlor at 1,064 g ha–1 were the estimated rates required to obtain 90% mortality of the Crawfordsville and Marion accessions, respectively. Data collected from the field and greenhouse confirm that these accessions have evolved a low level of resistance to S-metolachlor. In an agar-based assay, the level of resistance in the Marion accession was significantly reduced in the presence of a glutathione S-transferase (GST) inhibitor, suggesting that GSTs are the probable resistance mechanism. With respect to other VLCFA-inhibiting herbicides, Marion and Crawfordsville accessions were not cross-resistant to acetochlor, dimethenamid-P, or pyroxasulfone. However, both accessions, based on LD50 values obtained from greenhouse dose–response experiments, exhibited reduced sensitivity (1.5- to 3.6-fold) to the tested VLCFA-inhibiting herbicides.

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