Detoxification herbicide resistance

Stalker, D.M., McBride, K.E., and MalyJ, L.D. Herbicide resistance in transgenic plants expressing a bacterial detoxification gene. Science (Washington, DC), 242(4877) 419-423, 1988. 

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 general, herbicide resistance can be achieved through four primary strategies detoxification of the herbicide to a non-phytotoxic metabolite expression of an herbicide insensitive target overexpression of the herbicide target and cellular sequestration of the herbicide away from the target. Of these, only the first two strategies have been successfully used to develop commercial products to date. Readers are referred to other reviews on herbicide resistance [3, 4]. 

Herbicide Detoxification Herbicide Selectivity in Crops and Herbicide Resistance in Weeds... 

As indicated in Figure 1, a number of different enzymes participate in the detoxification of herbicides in plants. Some herbicides are acted on by only a single enzyme, whereas for others several modifications occur in sequence. Not surprisingly, the same enzymes that are responsible for selectivity of herbicides in crops are also responsible for herbicide resistance in weeds. 

Herbicide resistance has evolved in a number of weed species to many herbicides as a result of more rapid CYP-dependent detoxification. Some examples are provided in Table I. Evidence for increased CYP activity in these populations has come from the use of specific CYP inhibitors as synergists and from identification of the hydroxylated products of herbicide detoxification. 

Table I. Herbicide Resistance in Weeds as a Result of Increased CYP-dependent Detoxification...

It is tempting to conclude that the same members of the GST and CYP superfamilies are responsible for crop selectivity and herbicide resistance in weeds. However, this is probably unlikely to be the case. It is likely that any member of either of these superfamilies able to detoxify a herbicide could be recruited in the selection process leading to resistance. Indeed in the cases of resistance in L. rigidum and A, myosuroides where increased herbicide detoxification is implicated, the weeds also become resistant to herbicides that will control cereals like wheat (72,57). 

These experiments demonstrate that the pathways for inducing CYPs involved in herbicide detoxification in wheat and L, rigidum can be different. In addition, a different pattern of induction occurs in herbicide-resistant L rigidum plants compared to susceptible plants. 

Figure 6. Effect of inducers on detoxification of herbicides in wheat (M), herbicide susceptible L rigidum ( ) and herbicide-resistant L rigidum (M), Bars are the mean amount ( SE) of herbicide remaining 24 h after treatment The CYP inducers naphthalic anhydride (NA, I mM), 2,4-D (500 juM), phenobarbital (PB, 1 mM) and ethanol (EtOH, 3%) were applied in hydroponic culture 24 h prior to the addition of herbicides (Preston, C. unpublished data).

Some populations of herbicide-resistant weeds are resistant as a result of increased herbicide detoxification mechanisms. Where this has occurred, the same detoxification processes are involved as in crops. However, as the major detoxifying enzymes occur in large superfamilies in plants, the enzymes recruited for resistance in weeds are not necessarily the same as those responsible for herbicide detoxification in crops. This means that patterns of resistance in weeds do not necessarily follow the patterns of selectivity in crops and that regulation of the detoxification process may be different. 

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. 

In crop protection as well, understanding plant metabolism is of paramount importance to increase selectivity and to address resistance of chemical compounds. Moreover, dissipation of a compound in the aquatic ecosystem is very similar to the excretion phenomena of the bodies. An extensive amount of evidence has been accumulated to support the involvement of CYPs in the metabolism and detoxification of herbicides, fungicides and insecticides. The understanding of their biotransformations at the molecular level may be extremely helpful for herbicide- or insecticide-synergistic development. 

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. 

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. 

Christopher, J.T., S.B. Powles, J.A.M. Holtum, and D.R. Liljegren (1991). Cross-resistance to herbicides in annual ryegrass (Lolium rigi-dum) II Chlorsulfuron resistance involves a wheat-like detoxification system. Plant Physiol., 100 1036-1043. 

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. 

Phytoalexins are an Important component of the plant disease defense reaction called the hypersensitive response. Successful pathogens have evolved methods for dealing with plant phytoalexins. Including suppressors of their production, detoxification of the phytoalexins and In some cases avoiding elaboration of substances, called elicitors, that would otherwise Initiate the defense reaction. Elicitors obtained from pathogens are of considerable utility for study of various aspects of plant biology because of their interaction with the products of plant disease resistance genes. Substantial information has been obtained on how elicitors are perceived by plant cells and how they function, but much remains to be done. Finally, elicitors may prove of value for the economic production of exotic plant secondary metabolites and as specific herbicides. 

The use of herbicide rotation to avoid resistance will not be successful in cases where resistance is conferred by non-specific detoxification mechanisms that act on herbicides with different modes of action. In this case, selection for weeds resistant to members of two or more mode-of-action groups can and does occur [9]. Therefore, alternating or rotating amongst herbicides from different mode-of-action groups does necessarily delay resistance development. Clearly, there is no simple herbicide rotation solution to resistance avoidance. The tremendous genetic diversity in some seed populations allows the evolution of resistance, with the resistance mechanism simply reflecting the nature of the selection pressure that was applied. 

In certain situations it is possible to overcome herbicide metabolism-based resistance by adding an ingredient that will block detoxification of the herbicide in the resistant weed. One example is with propanil-resistant Echinochloa colona in rice in Latin America. The addition of piperophos, an organophosphate insecticide that inhibits the aryl acylamidase activity that confers resistance on the weed biotype [11]. This combination, based on an undo standing of the resistance mechanism, has beat approved for use on resistant... 

A direct relationship has been observed between the ability of some plant species to form 0-glucosldes of herbicides and resistance of those species to the herbicides however. In most cases a phase I reaction proceeds glucose conjugation and It Is not known whether the phase I reaction or conjugation results In herbicide detoxification. Chlorpropham is metabolized in plants by ring-hydroxylation and subsequent conjugation with glucose (Equation 3). In vitro, the... 

The broad-spectrum, moderate, cross-resistance of black-grass is quite unlike the almost complete immunity to a single herbicide or specific group of herbicides which can arise as a result of structural modifications to sites of action, as is observed in cases of triazine and simazine resistance ( 2 Rather, it indicates a deficiency of herbicide arriving at the site of action. This could be due to restricted uptake and/or inhibited translocation to the site of action, or rapid degradation and detoxification of the herbicide within the resistant plant. 

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