Author
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Gronwald, John |
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Submitted to: International Symposium on Weed & Crop Resistance to Herbicides Proceedings
Publication Type: Proceedings Publication Acceptance Date: 9/5/1996 Publication Date: N/A Citation: N/A Interpretive Summary: Technical Abstract: Approximately 25 years ago, the first case of triazine resistance in weeds was reported. Today, triazine resistance is the most prevalent type of herbicide resistance found in weeds. With few exceptions, resistance to PSII-inhibiting herbicides is due to a modification at the target site, the D1 protein of the PSII complex. It is well established that modification of amino acid residues in the QB-binding niche on the D1 protein reduces the affinity of triazine herbicides at this site so that they can no longer effectively compete for the exchangeable plastoquinone QB. For all cases of target site resistance that have been identified in the field and investigated, resistance is due to a point mutation of the psbA gene resulting in the substitution of Gly for Ser at residue 264. The appearance of weed biotypes exhibiting resistance to PSII-inhibiting herbicides due to enhanced herbicide metabolism has been a relatively recent development. This resistance mechanism is not as widespread as resistance due to a modified target site and has been found in only a few species. Resistance to the phenylureas and triazines in biotypes of Alopecurus myosuroides and Lolium rigidum appears to be due to enhanced oxidative metabolism mediated by cytochrome P-450s. In contrast, atrazine resistance in biotypes of Abutilon theophrasti is due to enhanced detoxification via glutathione conjugation. The level of resistance associated with enhanced detoxification is generally lower than that associated with modification at the target site. Although currently limited in scope, resistance to PSII-inhibiting herbicides due to enhanced detoxification has the potential of becoming a more serious problem than resistance due to a modified target site. |
