Resistance enhanced herbicide metabolism

Weed Resistance Based on Enhanced Herbicide Metabolism... 

In summary, triazine resistance in weeds is most commonly due to a target site alteration that confers a very high level of resistance to. y-triazinc herbicides. Although a Ser264 to Gly mutation in the D1 protein is most common, additional alterations have been identified that confer resistance to triazines and other classes of PS II inhibitors. Enhanced herbicide metabolism plays a major role in conferring resistance in only a few weed biotypes. In these biotypes, the pattern of resistance may be broader, with some cross-resistance to av-trazinones, uracils, heterocyclic ureas and phenyl ureas. The level and pattern of resistance to various herbicides in these biotypes depend, presumably, on the activity and specificity of the enzyme(s) responsible for the enhanced herbicide metabolism. 

Resistant biotypes being reported in the early 1990s were selected by chlorsul-furon or metsulfuron-methyl in wheat-growing areas or by sulfometuron-methyl in non-crop areas. While resistance of Lolium rigidum to ALS-inhibitors was attributed to enhanced herbicide metabolism [50] it was shown, for Lolium perenne and dicotyledonous species like Stellaria media, Kochia scoparia, Scdsola iberica and Lactuca serriola, that resistant biotypes had a mutated ALS with reduced susceptibility to ALS-inhibitmg herbicides [51-53]. The IC50S for sulfonylureas, which were determined in vitro with ALS isolated from Stellaria media, Salsola iberica and Lolium perenne, increased 4- to 50-fold in the resistant biotypes. Smaller increases, about 2- to 7-fold, were determined in the same biotypes for the imidazo-linone herbicide imazapyr [53]. 

In other weed biotypes, resistance to triazine herbicides is likely conferred by rapid metabolism of the herbicides to inactive compounds. A chlorotoluron-resistant biotype of blackgrass (slender foxtail) was cross-resistant to various other groups of herbicides, including triazines (Kemp et al., 1990). The mechanism of chlorotoluron resistance was Cyt P450-based enhanced oxidative metabolism through /V-demethylation and ring-methyl hydroxylation (Moss and Cussans, 1991). Consequently, it is likely that resistance to triazines in this blackgrass biotype is also due to enhanced herbicide detoxification. 

Adapted species may have developed, however, strategies which enable them to survive allelopathic attacks. One of those strategies certainly includes detoxification of absorbed allelochemicals by constitutive or inducible pathways. Metabolization and detoxification are known reactions in a number of crops upon application of diverse synthetic herbicides.38 Enhanced herbicide detoxification is an important factor in the development of nontarget-site cross-resistance and multiple resistance. It is reasonable to expect comparable strategies in plants that are relatively resistant to allelochemicals such as DIBOA, DIMBOA, and their derivatives. Especially in ecosystems where co-existing species have to be adapted to each other, detoxification of absorbed allelochemicals may play a crucial role under defined circumstances. 

PBO is known to enhance the activity of several herbicides, but when this action was first described detailed studies on the metabolic fate of PBO in plants had not been undertaken, nor had a full evaluation been made of its environmental fate, all essential for commercial use. Consideration has also been given to using PBO to overcome resistance in herbicides. 

The mixed-function oxidase inhibitors aminobenzotriazole and piperonyl butoxide can synergize herbicide activity in resistant Lolium growing in a hydroponic system. This indicates that at least one aspect of cross-resistance in Lolium rigidum may be related to enhanced metabolic activity of mixed-function oxidazes acting to detoxify herbicides. We are now concentrating on direct studies of herbicide metabolism in resistant biotypes. 

Cross-resistance means that a single resistance mechanism causes resistance to several herbicides. The term target-site cross-resistance is used when these herbicides bind to the same target site, whereas nontarget-site cross-resistance is due to a single nontarget-site mechanism (e.g., enhanced metabolic detoxification) that entails resistance across herbicides with different modes of action. 

Plants have active and passive mechanisms for resistance to most microorganisms. Since chemicals used for weed control interfere with metabolic processes of plants, interactions between herbicides and plant pathogens are to be expected. Interactions commonly, although not always, result in increased disease associated with herbicide use. Several examples of disease enhancement by herbicides were described in the preceding chapter. We describe here a less common phenomenon where certain fungi that colonize plant roots enhance the efficacy of a herbicide. 

Nontarget-site resistance is caused by mechanisms that reduce the amount of herbicidally active compound reaching the target site. An important mechanism is enhanced metabolic detoxification of the herbicide in the weed, with the effect that only insufficient amounts of herbicidally active substance will reach the target site. Furthermore, reduced uptake and translocation or sequestration of the herbicide may lead to insufficient herbicide transport to the target site. 

Enhanced metabolism resistance (EMR). This is the most conunon mechanism and develops slowly over mar years. Herbicides affected by enhanced metabolism are broken down (detoxified) mote rapidly in resistant than susceptible plants. Each time the same herbicide is sprayed more of the resistant plants will remain so that gradually the weed population will be dominated by the more resistant plants. 

While progress is being made in this area of plant metabolism, difficulties associated with the isolation of plant microsomal preparations active in the utilization of other herbicide substrates, and with the purification of the active mfo enzymes themselves, are still to be resolved. Consequently, only slow progress has been made on the identification of specific mfo polypeptides suitable as candiates for gene transfer studies. Such studies are aimed at manipulating crop plants for herbicide resistance based on enhanced oxidative detoxification. 

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