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P.B. Sweetser

Bio: P.B. Sweetser is an academic researcher from DuPont. The author has contributed to research in topics: Metabolite. The author has an hindex of 2, co-authored 2 publications receiving 268 citations.
Topics: Metabolite

Papers
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Journal ArticleDOI
TL;DR: This metabolite has been characterized as the O -glycoside of chlorsulfuron in which the phenyl ring has undergone hydroxylation followed by conjugation with a carbohydrate moiety.

207 citations

Journal ArticleDOI
TL;DR: It is suggested that metabolism may be the basis of selectivity to chlorsulfuron for tolerant broadleaf plants as well as for grasses.

62 citations


Cited by
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Journal ArticleDOI
Hugh M. Brown1
TL;DR: The sulfonylurea herbicides are characterized by broad-spectrum weed control at very low use rates, good crop selectivity, and very low acute and chronic animal toxicity.
Abstract: The sulfonylurea herbicides are characterized by broad-spectrum weed control at very low use rates (c. 2–75 g ha−1), good crop selectivity, and very low acute and chronic animal toxicity. This class of herbicides acts through inhibition of acetolactate synthase (EC 4.1.3.18; also known as acetohydroxyacid synthase), thereby blocking the biosynthesis of the branched-chain amino acids valine, leucine and isoleucine. This inhibition leads to the rapid cessation of plant cell division and growth. Crop-selective sulfonylurea herbicides have been commercialized for use in wheat, barley, rice, corn, soybeans and oilseed rape, with additional crop-selective compounds in cotton, potatoes, and sugarbeet having been noted. Crop selectivity results from rapid metabolic inactivation of the herbicide in the tolerant crop. Under growth-room conditions, metabolic half-lives in tolerant crop plants range from 1–5 h, while sensitive plant species metabolize these herbicides much more slowly, with half-lives > 20 h. Pathways by which sulfonylurea herbicides are inactivated among these plants include aryl and aliphatic hydroxylation followed by glucose conjugation, sulfonylurea bridge hydrolysis and sulfonamide bond cleavage, oxidative O-demethylation and direct conjugation with (homo)glutathione. Sulfonylurea herbicides degrade in soil through a combination of bridge hydrolysis and microbial degradation. Hydrolysis is significantly faster under acidic (pH 5) than alkaline (pH 8) conditions, allowing the use of soil pH as a predictor of soil residual activity. Chemical and microbial processes combine to give typical field dissipation half-lives of 1–6 weeks, depending on the soil type, location and compound. Very short residual sulfonylurea herbicides with enhanced susceptibility to hydrolysis (DPX-L5300) and microbial degradation (thifensulfuron-methyl) have been developed.

530 citations

Journal ArticleDOI
TL;DR: This Update presents an historical review to current understanding of metabolic herbicide resistance evolution in weedy plant species and reveals the genes endowing metabolic herbicides resistance in plants.
Abstract: Weedy plant species that have evolved resistance to herbicides due to enhanced metabolic capacity to detoxify herbicides (metabolic resistance) are a major issue. Metabolic herbicide resistance in weedy plant species first became evident in the 1980s in Australia (in Lolium rigidum) and the United Kingdom (in Alopecurus myosuroides) and is now increasingly recognized in several crop-weed species as a looming threat to herbicide sustainability and thus world crop production. Metabolic resistance often confers resistance to herbicides of different chemical groups and sites of action and can extend to new herbicide(s). Cytochrome P450 monooxygenase, glycosyl transferase, and glutathione S-transferase are often implicated in herbicide metabolic resistance. However, precise biochemical and molecular genetic elucidation of metabolic resistance had been stalled until recently. Complex cytochrome P450 superfamilies, high genetic diversity in metabolic resistant weedy plant species (especially cross-pollinated species), and the complexity of genetic control of metabolic resistance have all been barriers to advances in understanding metabolic herbicide resistance. However, next-generation sequencing technologies and transcriptome-wide gene expression profiling are now revealing the genes endowing metabolic herbicide resistance in plants. This Update presents an historical review to current understanding of metabolic herbicide resistance evolution in weedy plant species.

339 citations

Journal ArticleDOI
TL;DR: A central role for specific GSTFs in MHR in weeds that has parallels with similar roles for unrelated GSTs in MDR in humans and shows their potential as targets for chemical intervention in resistant weed management is demonstrated.
Abstract: Multiple-herbicide resistance (MHR) in black-grass (Alopecurus myosuroides) and annual rye-grass (Lolium rigidum) is a global problem leading to a loss of chemical weed control in cereal crops. Although poorly understood, in common with multiple-drug resistance (MDR) in tumors, MHR is associated with an enhanced ability to detoxify xenobiotics. In humans, MDR is linked to the overexpression of a pi class glutathione transferase (GSTP1), which has both detoxification and signaling functions in promoting drug resistance. In both annual rye-grass and black-grass, MHR was also associated with the increased expression of an evolutionarily distinct plant phi (F) GSTF1 that had a restricted ability to detoxify herbicides. When the black-grass A. myosuroides (Am) AmGSTF1 was expressed in Arabidopsis thaliana, the transgenic plants acquired resistance to multiple herbicides and showed similar changes in their secondary, xenobiotic, and antioxidant metabolism to those determined in MHR weeds. Transcriptome array experiments showed that these changes in biochemistry were not due to changes in gene expression. Rather, AmGSTF1 exerted a direct regulatory control on metabolism that led to an accumulation of protective flavonoids. Further evidence for a key role for this protein in MHR was obtained by showing that the GSTP1- and MDR-inhibiting pharmacophore 4-chloro-7-nitro-benzoxadiazole was also active toward AmGSTF1 and helped restore herbicide control in MHR black-grass. These studies demonstrate a central role for specific GSTFs in MHR in weeds that has parallels with similar roles for unrelated GSTs in MDR in humans and shows their potential as targets for chemical intervention in resistant weed management.

247 citations

Journal ArticleDOI
01 Jan 1993
TL;DR: The present study focuses on the component parts of the mechanism of action of the enzyme Acetolactate Synthase, which acts as a “spatially aggregating force” to form the polypeptide “base” of herbicide.
Abstract: CONTENTS INTRODUCTION 204 RESISTANCE TO AMINO ACID SYNTHESIS INHIBITORS .. . . .... ... ...... 204 Acetolactate Synthase (ALS) Inhibitors .... . . ... 204 5E(?Jl;h;;;��:j.��'!:: ����.�.����������.��.�.��.���.�������.��.�!.�.����� 207 Glu tamine Synthetase (GS) Inhibitors ... . ...... ........ 208 RESISTANCE TO PHOTOSYSTEM II (PSII) INHIBITORS... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 208 RESISTANCE TO LIPID SYNTHESIS INHIBITORS .. . ... ... ... ... ........ ....... 211 Acetyl Coenzyme A Carboxylase (ACCase) Inhibitors . 211 RESISTANCE TO AUXIN-TYPE HERBICIDES 213 Phenoxyacetic Acids ......... .. ... ... ..... , 213 RESISTANCE TO MITOTIC INHIBITORS ... ... ... ... . 215 Dinitroanilines . . . . .. .... . . . . . . .. ... .. . .. ......... .. .. ...... 215 RESISTANCE TO PHOTOSYSTEM I (PSI) INHIBITORS 217 Bipyridiliums 217 CROSSAND MULTIPLE-HERBICIDE RESISTANCE 219 AGRONOMIC IMPLICATIONS OF HERBICIDE RESISTANCE ........ ...... 221

233 citations

Journal ArticleDOI
TL;DR: The tobacco ALS gene was isolated from a line of tobacco which is resistant to the sulfonylurea herbicides due to an alteration in ALS, and codes for an ALS that is sensitive to the herbicides, as assayed by transformation of the gene into sensitive tobacco cells.
Abstract: Acetolactate synthase (ALS) is the first common enzyme in the biosynthetic pathways to valine, isoleucine, and leucine. It is the target of two structurally unrelated classes of herbicides, the sulfonylureas and the imidazolinones. Genomic clones encoding ALS have been isolated from the higher plants Arabidopsis thaliana and Nicotiana tabacum, using a yeast ALS gene as a heterologous hybridization probe. Clones were positively identified by the homology of their deduced amino acid sequences with those of yeast and bacterial ALS isozymes. The tobacco and Arabidopsis ALS genes have approximately 70% nucleotide homology, and encode mature proteins which are approximately 85% homologous. Little homology is seen between the amino acid sequences of the presumptive N-terminal chloroplast transit peptides. Both plant genes lack introns. The tobacco ALS gene was isolated from a line of tobacco which is resistant to the sulfonylurea herbicides due to an alteration in ALS. The tobacco gene which was isolated codes for an ALS that is sensitive to the herbicides, as assayed by transformation of the gene into sensitive tobacco cells.

229 citations