Triazines resistance mechanisms

Radosevich, S.R. and O.T. DeVilliers (1976). Studies on the mechanism of s-triazine resistance in common groundsel. Weed Sci. 24 229-232. 

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. 

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). 

Excellent progress has been made in the understanding of the cause, nature, genetics, mechanism and solutions of herbicide-resistant weeds since the first triazine-resistant common groundsel was reported more than 35 years ago. Resistance management programs have been extremely successful in controlling most weeds that have developed resistance to the triazine herbicides. However, research is critical to better understand the rapid increase and spread of many new weed biotypes resistant to several classes of herbicides. 

Triazine Resistance We attempted to answer the previous four questions using data and examples derived from the study of the best documented case of herbicide resistance, triazine resistance. Two kinds of mechanisms may be responsible for this triazine resistance first is the presence of detoxification metabolic pathways, as seen in corn (11). This also may occur in weed populations, especially Panicoideae, but a low heritability makes its study complex. The second mechanism of triazine resistance is the loss of herbicide binding at the level of the chloroplast. 

In the field, natural selection acts to optimize the adaptations of a plant so as to maximize individual fitness. In triazine resistant weeds, coevolution of the less productive chloroplast with the nuclear genome could have resulted in compensatory mechanisms not present in susceptible plants. These mechanisms could optimize productivity and maximize the fitness of those individuals, within the constraints imposed by impaired PSII. Even slight differences in the chloroplast genome between susceptible and resistant biotypes could result in different responses to the same selection pressures in the environment, perhaps in the direction of overcoming limitations caused by the resistance mutation. Thus, after several generations of selection, many nuclear-genome controlled traits are likely to appear that could mask intrinsic differences between biotypes due to the chloroplast mutation. It is also possible that the alteration in PSII in resistant plants triggers developmental events that compensate in some way. Effects of the resistance mutation may be compensated for by other aspects of plant performance such as carbon allocation or rate of development. Resistant plants may not necessarily be less productive than susceptible ones when traits not directly linked with triazine resistance are considered. 

An understanding of the biochemical characteristics of the PS II localized herbicide receptor domain is particularly relevant because of the appearance of triazine-resistant weed biotypes in the United States, Canada, and Europe (3). Initial attempts at understanding the mechanism(s) of resisTance directed investigators to evaluate alterations in uptake, translocation, or metabolism of triazines. Only small differences between susceptible and resistant biotypes were established, these being insufficient to explain the mechanism of extreme herbicide resistance. 

The appearance of weeds that showed considerable resistance to the triazine herbicides eventually led to detailed biochemical studies that identified resistance mechanisms at the level of a D1 protein amino acid change. Hirschberg and Mclntosh showed that in Amaranthus hybridus this was due to a replacement of serine 264 by glycine. Remarkably, this particular amino acid change did not greatly affect the inhibitory properties of the phenylurea diuron. Subsequent work has shown, however, that changes at amino acids 219 and 275 will give resistance to diuron but have... 

Shimabukuro et al. (1966) identified 2-chloro-4-amino-6-isopropylamino-i-triazine (G-30033) as a major metabolite in shoots of mature pea plants. These results indicated that a second mechanism for tolerance to atrazine existed in some moderately susceptible plants. Later, Shimabukuro (1967a) was able to demonstrate that atrazine could be metabolized independently in both roots and shoots of young pea plants to 2-chloro-4-amino-6-isopropylamino-.t-triazine. This metabolite was much less phytotoxic than the parent compound. The metabolism of atrazine in resistant com and sorghum, in intermediately susceptible pea, and in highly susceptible wheat was reported by Shimabukuro (1967b). This study revealed two possible pathways for metabolism of atrazine in higher plants. All species studied were able to metabolize atrazine by TV-deal kyI ation of either of the two alkyl groups present. Com and wheat that contain the cyclic hydroxyamate (2,4-dihydroxy-7-methoxy-l,4-benzoxazine-3-one) also metabolized atrazine by conversion to hydroxy-atrazine (G-34048). Subsequent metabolism was postulated to be by conversion to more polar compounds. 

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. 

Before Radosevich and De Villiers found in 1975 that isolated chloroplasts of resistant common groundsel were insensitive to atrazine and simazine (2), it had been erroneously assumed that all living plants would die if the herbicides could reach their target site intact. We now know that mechanisms of selectivity in crops can be due to differences in metabolism rates, uptake, translocation, site of action or avoidance mechanisms. However, the mechanisms of herbicide resistance that have evolved in weeds are usually different from the mechanisms of herbicide selectivity in most crops. This is certainly true with the most prevalent and thoroughly studied cases of herbicide resistance, including the triazines, dinitroanilines, and AHAS inhibitors. 

As the primary mechanism of action of the. -triazines involves inhibition of PS II electron transport, attention was also directed at analysis of chloroplast reactions in resistant weed biotypes (10, 11, 12). These studies can be summarized as follows (a) in aTl cases studied to date, there is a modification in the chloroplast membranes of resistant biotypes that changes the characteristics of s-triazine binding (b) this modification results in altered bincfTng characteristics of other classes of herbicides, (i.e., only slight resistance to ureas, but increased sensitivity to phenols) (see for review), and (c) the alteration of the herbicide receptor in resistant weeds is accompanied... 

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