How treated plants die

It is not clearly understood how treated plants die following ALS inhibition. The diminution of the branched-chain amino acid pool will contribute to a cessation of protein synthesis, but although nanomolar concentrations of herbicide can inhibit ALS within minutes in vitro, it may take up to two months for the death of intact weeds in the field. Addition of the three branched-chain amino acids to culture media alleviates symptoms of ALS-)nhibiting herbicides (Ray, 1984; Shaner and Reider, 1986; Usui et al., 1991; Shimizu et al., 1994; Yamashita et al., 1994). Several physiological and metabolic alterations have been proposed to contribute to weed death. For example, LaRossa and colleagues (cited by Ray, 1989) have found that ALS inhibition results in an accumulation of its substrate, 2-ketobutyrate, which is toxic to S. typhimurium. 2 - Aminobutyrate has been shown to accumulate in plants treated with ALS inhibitors, but symptoms of ALS inhibition do not appear to be due to 2-aminobutyrate toxicity. Treatment with ALS inhibitors results in a drop in the concentration of valine and isoleucine and a rise in the concentrations of threonine, alanine and norvaline as well as 2-aminobutyrate. The accumulation of abnormal amino acids (e.g. norvaline) due to increased 2-ketobutyrate concentrations cannot, therefore, be discounted as a possible cause of herbicide-related phytotoxicity.

Accumulation of singlet oxygen has also been observed after treatment with ALS inhibitors, possibly as a result of an oxygen-consuming side-reaction exhibited by ALS when its main enzymic process is inhibited (Durner et al., 1994). However, whole plant symptoms differ markedly from other herbicides, the mode of action of which is the production of active oxygen species, suggesting this is not the primary cause of plant death with ALS inhibitors.

One common observation following treatment with ALS inhibitors is a very rapid and potent inhibition of cell division, with the result that an inhibition of elongation of young roots and leaves is evident within 3 h after application. Rost (1984) found that chlorsulfuron blocked the progression of the cell cycle in dividing root cells from peas within 24h, from G2 to mitosis (M) and reduced movement from G1 to DNA synthesis (S). This is a rapid effect on the cell cycle with no direct effect on the mitotic apparatus, which can be overcome by inclusion of isoleucine and valine in the incubation medium. Separate reports that ALS inhibitors may indirectly inhibit DNA synthesis may explain these observations. Furthermore, the involvement of polyamines have been implicated in sulphony-lurea action, since the discovery by Giardini and Carosi (1990) that chlorsulfuron causes a reduction in spermidine concentration in Zea root tips which could be responsible for this effect in the cell cycle. These findings have created a new interest in cell-cycle research since they imply a possible regulatory role of branched-chain amino acids in the control of plant cell division.

Growth is therefore retarded or inhibited within hours of foliar treatment, but physical symptoms may take days to develop, first appearing as chlorosis and necrosis in young meristematic regions of both shoots and roots. Young leaves appear wilted, and these effects spread to the rest of the plant. Leaf veins typically develop increased anthocyanin formation (reddening), and leaf abscission is commonly observed, both symptoms being typical responses to stress ethylene production. Under optimum growth conditions plant death may follow within ten days, although up to two months may elapse when weed growth is slow. When ALS inhibitors are applied before the crop is planted or has emerged, susceptible weeds will germinate and grow, presumably utilising stored seed reserves. However, further growth of broadleaf weeds stops at the cotyledon stage, and before the two-leaf stage in grasses.

9.5.2 Selectivity

A striking feature of the ALS inhibitors is their highly selective action at low dosage. Indeed, some cereals have been reported to tolerate up to 4000 times more chlorsulfuron than some susceptible broadleaf species. Various studies have shown that this extreme species sensitivity is not due to herbicide uptake, movement or sensitivity to ALS, but is correlated to very rapid rates of metabolism in the tolerant crop. In the tolerant crop soybean the degradation half-life of triazolopyrimidines has been shown to be 49 hours compared to 165.3 hours in the susceptible species pitted morning glory (Swisher et al., 1991). Several sites on the sulphonylurea molecule are locations for enzyme attack and more than one enzyme system has been demonstrated to be active in their detoxification, as summarised in Figure 9.8 (Beyer et al., 1987).

This extreme species sensitivity may have dramatic consequences to a following crop in the same land. For example, since wheat is more than 1000 times more tolerant to chlorsulfuron than the extremely sensitive sugar beet, which may be inhibited by as little as 0.1 part herbicide per billion parts of soil, then low sulphonylurea residues are crucial to the success of this rotational crop. Chlorsulfuron detoxification in the soil is principally due to microbial action which may degrade the herbicide within one to two months under

Wheat Chlorsulfuron metsulfuron-methyl (aryl hydroxylation followed by glucosylation)

Soybean

Chlorimuron-ethyl (rapid chlorine displacement and conjugation with glutathione)

Barley

Chlorsulfuron metsulfuron-methyl (bond cleavage by amidase activity)

Rice

Bensulfuron-methyl (6-methoxy oxidation to a hydroxyl derivative and subsequent glucosylation)

Figure 9.8 Sulphonylurea metabolism in various crops (from Beyer et al., 1987).

optimum conditions. However, when conditions of low temperature, high rainfall, and high soil pH arise, microbial breakdown is greatly reduced and, if prolonged, sufficient residues of chlorsulfuron may remain to cause major damage in succeeding crops for up to a year after the original treatment. The most sensitive crops to chlorsulfuron residues appear to be lentils, sugar beet and onions, but flax, maize, sunflower, mustard, oilseed rape, potatoes and lucerne are also sensitive (Beyer et al., 1987; Blair and Martin 1988). Similar sensitivity to imidazolinone and triazolopyrimidine residues have not yet been reported.

Rapid differential metabolism also provides an explanation for the selectivity of the imidazolinones. Thus, de-esterification of imazamethabenz to phytotoxic acids is observed in susceptible species such as wild oat, and ring methyl hydroxylation followed by glucosylation inactivates the molecule in tolerant maize and wheat (Figure 9.9) .

A further aspect of imidazolinone action is noteworthy and remains to be explained. Namely, about 1000 times more imidazolinone is needed to inhibit ALS in vitro than an equivalent sulphonylurea, but only five times more herbicide is needed to kill the weed.

Since the sulphonylureas and imidazolinones are such potent inhibitors of ALS and may retain residual activity in soils under certain conditions, it may be predicted that resistant plants will eventually evolve. However, resistance has developed in a surprisingly short time and at present resistance cases to ALS inhibitors are more prevalent than cases to other herbicides that have been used for many more years (Heap, 2007). The use of chlorsulfuron and metsulfuron-methyl in minimum tillage winter wheat monoculture for four to five consecutive years has resulted in resistant biotypes of prickly lettuce (Lactuca serriola), Kochia (Kochia scoparia), Russian thistle (Salsola iberica) and chickweed (Stellaria media). Although the degree of resistance varies with both biotype and herbicide, it is clear that cross-resistance to the imidazolinones is evident, and a modified, less sensitive ALS is thought to be present in resistant biotypes (Reed et al., 1989). Furthermore, resistant biotypes of L. serriola have been crossed with domestic lettuce (L. sativa) by

(inactive)

Glu (inactive)

Figure 9.9 Differences in the metabolism of imidazolinones between wheat (tolerant) and wild oats (susceptible).

(inactive)

Glu (inactive)

Figure 9.9 Differences in the metabolism of imidazolinones between wheat (tolerant) and wild oats (susceptible).

Mallory-Smith and colleagues (1990), with the result that inherited resistance is controlled by a single gene with incomplete dominance.

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