20.2.2  Non-target site resistance mechanisms

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In addition to modifications of the target site, resistance can occur through restricted transport of herbicide to target sites. Plants with a herbicide-sensitive target enzyme can survive because the herbicide only reaches its target at sublethal concentrations. Non-target site resistance can be achieved by rapid metabolism of a herbicide to non-toxic products and, again, this is particularly prevalent in L. rigidum. Enhanced metabolism is most often catalysed by cytochrome P450-dependent microsomal oxidases acting on herbicides as sub-strates. This large family of enzymes also catalyses numerous reactions in plants in biosynthetic pathways for synthesis of lignins, gibberellins, carotenoids, steroids and cutin. Some examples of enhanced metabolism of herbicides providing resistance in L. rigidum are:

1. Elevated activity of cytochrome P450-dependent microsomal oxidases confers resistance to PSII-inhibiting herbicides (triazines) in some L. rigidum biotypes by accelerating de-alkylation of herbicide molecules at up to four times the rate in susceptible biotypes. The chemically unrelated, substituted-urea herbicide, chlorotoluron, is degraded by two enzymes. One enzyme produces a demethylated product and the other a ring-methyl-hydroxylated product. The demethylated product retains some activity against the chlorotoluron target site but the ring-methyl-hydroxylated product is entirely inactive as an inhibitor of PSII.

2. Resistant biotypes of L. rigidum metabolise certain ALS-inhibiting herbicides at twice the rate observed in susceptible biotypes through the action of cytochrome P450-dependent microsomal oxidase: only very low concentrations of the herbicide reach the active site. For example, chlorsulfuron is metabolised by hydroxylation of the phenyl ring, rendering the herbicide inactive (Figure 20.5).

3. Enhanced metabolism of ACCase-inhibiting herbicides occurs in many resistant populations of L. rigidum. In these populations, the ACCase-inhibiting herbicide diclofop is metabolised at about 1.5 times the rate observed in susceptible populations. In biotypes of Lolium and Avena spp. which are susceptible to diclofop, the herbicide can be directly conjugated to glucose. This reaction is believed to be reversible, hence providing a continuous pool of the active form of diclofop. Diclofop concurrently undergoes a slow aryl hydroxylation catalysed by a microsomal oxidase, followed by sugar conjugation. Resistant biotypes of L. rigidum have an enhanced ability to detoxify diclofop acid by accelerating the rate of aryl hydroxylation.


Figure 20.5 (a) Metabolism of chlorosulfuron in susceptible (Ο) and resistant (●) biotypes of L. rigidum. (b) Pathway of metabolism of chlorsulfuron in L. rigidum. The phenyl ring of shlorsulfuron is hydroxylated (top), giving a hydroxy-phenyl chlorsulfuron (centre) that is subsequently conjugated to glucose (bottom). This glucose conjugate is the major metabolite observed in both resistant and susceptible biotypes (Based on Christopher et al. 1991)