Herbicide triazine resistance

Cross-Resistance to Other Herbicides in Triazine Resistance... 

Vermass, W.F.J. and C.J. Arntzen (1984). Synthetic quinones influencing herbicide binding and photosystem II electron transport. The effects of triazine-resistance on quinone binding properties in thylakoid membranes. Biochim. Biophys. Acta., 725 483 -91. 

Triazines were one of the first family of herbicides where weed resistance was widely recognized and documented in the literature. A simazine-resistant biotype of common groundsel was identified in Washington, United States, in 1968. Since then biotypes of at least 66 triazine-resistant weed species have been reported, mostly in the United States, Canada, and Europe (Heap, 2006). 

Triazine herbicides provide selective weed control in crops such as corn, sorghum, and sugarcane. In addition, some members of the triazine family are used for weed control in orchards, horticultural, and perennial crops, etc. A unique selective use of triazine herbicides is in triazine-tolerant rapeseed. Although triazine herbicides provide control of a wide variety of grass and broadleaf weeds, the long-term, widespread, and repetitive use of triazine herbicides in crop and noncrop situations has led to the selection of many triazine-resistant weeds. The physiological and biochemical basis of triazine selectivity between crops and weeds and of resistance to triazine herbicides in weeds is well understood. 

Weed resistance to the triazine herbicides was first identified in the late 1960s, with a biotype of common groundsel that was resistant to simazine (Ryan, 1970). Since then, resistance to triazine herbicides has been reported in many weed species (Holt and LeBaron, 1990 LeBaron and McFarland, 1990 Gronwald, 1994). Most cases of triazine resistance have been reported in the US, Canada, and Europe, where triazine herbicides have been used extensively in corn monocultures (LeBaron and McFarland, 1990 Stephenson et al., 1990 LeBaron, 1991). Most of the. v-triazinc-resistant weed species have been selected against atrazine and usually show a high level of cross-resistance to other. v-triazine herbicides. In most cases, these weeds also show a low level of resistance to as-triazinones (e.g., metribuzin). Triazine-resistant weeds are often less vigorous than nonresistant weeds, which facilitates their management. 

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. 

The high efficacy of triazine herbicides and their repetitive use in crops and noncrop situations has resulted in the selection of weeds that are resistant to these herbicides or are not well controlled at the lower rates now being used. In most instances, triazine resistance is due to an alteration in the herbicide-binding site in PS II. Despite the widespread occurrence of triazine resistance, these herbicides are still widely used, even in fields in which triazine-resistant biotypes are known to occur. The rate of increase in the selection for triazine-resistant weed species depends in part on the integration of alternative weed control strategies, in addition to the use of triazine herbicides, for control of these weed species. Due to their resistance mechanism, many triazine-resistant weeds are less competitive than their susceptible counterparts. 

Fuerst, E.P., C.J. Arntzen, K. Pfister, and D. Penner (1986). Herbicide cross-resistance in triazine-resistant biotypes of four species. Weed Sci., 34 344-353. 

Hall, J.C., M.J. Donnelly-Vanderloo, and D.J. Hume (1996). Triazine-resistant crops The agronomic impact and physiological consequences, pp. 107-126. In Duke, S.O. ed., Herbicide-Resistant Crops. Boca Raton, FL Lewis Publishers. 

Soon after the discovery of triazine-resistant common groundsel, another equally important discovery was made. Radosevich and DeVilliers (1976) found that the mechanism of resistance in this weed was due to insensitive chloro-plasts that were capable of photosynthesis, even in the presence of simazine or atrazine. This was surprising because earlier research had confirmed that there were no differences in plant selectivity or susceptibility due to the origin of chloroplasts. Moreland (1969) had reported that isolated chloroplasts were equally inhibited to simazine whether they came from tolerant com or susceptible spinach. Radosevich and Appleby (1973) had confirmed there were no differences between the susceptible and resistant biotypes of common groundsel due to herbicide uptake, distribution, or metabolism, whereas it is known that com metabolizes triazine herbicides (Shimabukuro, 1985). 

The levels of infestations or seriousness of triazine resistance within each species varies gready. The author is aware of 19 cases where the resistant weed is no longer present or cannot be identified as resistant to triazine herbicides. In other cases, the current status is unknown. Several triazine-resistant biotypes are likely to be of little or no agronomic importance within a geographical area. 

A major limitation of global surveys and confirmations of herbicide-resistant weeds has been the variability in the methods used in identifying resistance. Unless the cases of resistance have been confirmed by laboratory or greenhouse studies and include information on the degree of resistance, the reports of resistance should not be recognized as being confirmed. Van Oorschot (1991) Truelove and Hensley (1982) and others have conducted and reported on extensive research on the best methods for confirming triazine-resistant weeds. 

In almost all cases of triazine-resistant weeds, it has been documented that they are discovered in fields after years of repeated use of triazine herbicides without mixing or rotating with herbicides that have an alternate mode of action. However, a few exceptions have been reported. For example, Lior et al. (1996) found that various populations... 

Yerkes et al. (1996) reported that although chlorophyll fluorescence measurements and C02 assimilation in resistant jimsonweed leaves were affected within 1 day of atrazine application, they returned to normal (at rates and levels equivalent to those in untreated leaves) within 5 days. Atrazine-resistant jimsonweed was cross-resistant to simazine, but was susceptible to prometryn, metribuzin, terbacil, and other herbicides. Chlorophyll fluorescence was unaffected in triazine-resistant pigweed, which showed cross-resistance to some triazines, moderate resistance to metribuzin and terbacil, and negative cross-resistance to bentazon and pyridate. 

In some triazine-resistant species where resistance is due to more rapid metabolism of the herbicide, the weeds develop resistance gradually and may be only slightly resistant. This is especially true with some of the monocot or grass weeds that are already partially inherently resistant to atrazine (Thompson et al. 1971 Gressel et al., 1982, 1983). DePrado et al. (1995) found that fall panicum has the capacity for rapid detoxification, which is slightly greater in plants from fields that have been repeatedly treated with atrazine. 

Ritter and Menbere (1997) have reviewed the history and control of triazine-resistant weeds - especially common lamb s-quarters, smooth pigweed, bamyardgrass, velvetleaf, and giant foxtail - in the mid-Atlantic region of the United States. They concluded that the factors influencing the presence of the resistant weeds included lack of crop rotation and lack of herbicide rotation. 

Target site cross-resistance, in which a change at the site of action of one herbicide also confers resistance to herbicides from a different class (e.g., selection by triazine-resistant D1 protein that is also less sensitive to triazinones). 

Until the mid-1990s, multiple-resistance (i.e., resistance to more than one herbicide mode of action within the same biotype) had not been reported within North America. However, Foes et al. (1996) found a kochia biotype from western Illinois resistant to atrazine and several ALS-inhibiting herbicides. Lopez-Martinez et al. (1996) reported that a triazine-resistant Echinochloa species found in atrazine-treated com also showed cross-resistance to quinclorac. Clay and Underwood (1989) and Clay (1989) reported that one triazine-resistant biotype of American willowherb was also resistant to paraquat from a hop garden in the United Kingdom treated annually for 25 years with simazine and paraquat. 

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