Herbicide target-site resistance

Richter, J. and S.B. Powles (1993). Pollen expression of herbicide target site resistance genes in annual ryegrass (Lolium rigidum). Plant Physiol., 102 1037-1041. 

REDUCTION IN THE SENSITIVITY OF HERBICIDE TARGET SITES. Crossresistance may involve changes in the sensitivity of herbicide target sites. However, if this is the only mechanism for resistance in Lolium there must be changes in more than one target site since there is resistance to more than one herbicide class. 

Target-site resistance is due to reduced or lost ability of the herbicide to bind to its target protein. This is usually an enzyme with a crucial function in metabolic pathways or the component of an electron transport system. As a further possibility, target-site resistance could also be caused by an overproduction of the herbicide-binding protein. 

Cases analyzed to date show that herbicide resistance is very frequently based on a target-site mutation. Within the past 35 years weed species have developed target-site resistance to most known herbicide chemistries. Those of major importance are discussed below. 

In many cases, mutants of weed species with target-site resistance to triazines showed lower growth rate and ecological fitness than the susceptible wild type, when analyzed in absence of a triazine herbicide as selection agent. The quantum yield of CO2 reduction in resistant biotypes was decreased. Furthermore, the electron transfer between the primary and secondary quinones in the PS II reaction center was slowed, which may have been the cause of increased susceptibility to photoinhibition in the resistant biotypes [23, 24]. 

First biotypes of LoUum ri um with target-site resistance to ACCase inhibitors were identified in the early 1990s in Australia. Sdection either with an APP or a CHD herbicide resulted in target-site cross-resistance to both herbicide groups. But, regardless of whether selection was by an APP or a CHD compound, the level of resistance in these biotypes was higher to APP than to CHD herbicides. ACCase resistance factors were 30-85 for diclofop, >10-216 for haloxyfop and 1-8 for sethoxydim [31, 35, 36]. 

Weeds can develop resistance to herbicides. Because of this, herbicides are often rotated from season to season. For example, target site resistance... 

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. 

Devine, M.D. and C.V. Eberlein (1997). Physiological, biochemical and molecular aspects of herbicide resistance based on altered target sites, pp. 295-348. In Roe, R.M. J.D. Burton, and R.J. Kuhr, eds., Herbicide Activity Toxicology, Biochemistry and Molecular Biology. Amsterdam, The Netherlands I. O. S. Press, Inc. 

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). 

Diebold et al. (2003) concluded that multiple resistance in a Powell amaranth biotype in Ontario was due to the presence of altered target sites for triazine and imidazolinone herbicides. 

Hall et al. (1998) reported that an ALS-resistant biotype of false cleavers was cross-resistant to a broad range of ALS inhibitors, as well as to an auxin-type herbicide, quinclorac, which had never before been applied to these fields. A similar case of quinclorac multiple resistance in smooth crabgrass has been reported in California when plants were previously treated with ACCase herbicides. Data suggest a target site-based mechanism of resistance involving the accumulation of cyanide derived from stimulated ACC synthesis, which is a precursor of ethylene (Abdallah et al., 2004). 

In relation with resistance of weeds to herbicides, Duke et al. (2000) mentioned that new mechanisms of action for herbicides are highly desirable to fight evolution of resistance in weeds, to create or exploit unique market niches, and to cope with new regulatory legislation. Comparison of the known molecular target sites of synthetic herbicides and natural phytotoxins reveals that there is little redundancy. Comparatively little effort has been expended on determination of the sites of action of phytotoxins from natural sources, suggesting that intensive study of these molecules will reveal many more novel mechanisms of action. These authors gave some examples of natural products that inhibit unexploited steps in the amino acid, nucleic acid, and other biosynthetic pathways AAL-toxin, hydantocidin, and various plant-derived terpenoids. 

Table 1. Summary of confirmed cases of herbicide resistance in weeds, arranged by herbicide class and target site. From [1].

Herbicide class Target site Number of confirmed resistant biotypes... 

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. 

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