GLISANDOS

The discovery and development of these compounds is recounted in detail by Kirby (1980), and represents one of the major agricultural advances of the twen-tieth century. They provided a means of selectively controlling broad-leaved

weeds in the world’s major food crops – cereals. Their selectivity in controlling broad-leaved weeds is marked and they can be effective at dose rates of less than 1 kg/ha.

Initial research during the late 1930s at the Jealotts Hill Research Sta-tion in Berkshire, England involved spraying mixtures of oat and the broad-leaved weed charlock (Sinapis arvensis) with the chemical rooting stimulant 1-naphthylacetic acid. The weeds were killed and the cereals remained unaffected.

The dose of around 10 kg/ha was uneconomic, but the results led to a search for other compounds effective at lower doses whilst retaining the selectivity. One of the compounds subsequently discovered was 4-chloro-2-methylphenoxyacetic acid (4-chloro-o-tolyloxyacetic acid) or MCPA, which was active at a rate of 1–1.5 kg/ha against many broad-leaved weeds in cereals.

The actual discovery of the growth regulatory properties of 1-naphthylacetic acid and other phenoxyacetic acids was made at the Boyce Thompson Institute in New York. Research there in the late 1930s showed that phenoxyacetic acids were particularly good growth regulators, with one of the most potent chemicals for producing seedless tomatoes being 2,4-dichlorophenoxyacetic acid (2,4-D). At the same time, workers at Rothamsted Experimental Station in Hertfordshire, England were working with derivatives of indolyl acetic acid (now of course known to be one of the principal endogenous plant growth regulatory substances) during studies into nodulation by Rhizobium. It quickly became clear that one of these, again 2,4-D, provided outstanding selective control of broad-leaved plants.

Little of the research carried out by both British and American workers was published at the time of their discovery because these molecules were consid-ered for use as biological war agents. Fortunately they were never used for this purpose during the Second World War, although sadly the hormone weedkiller 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) brought immense notoriety to the group, and herbicides in general, following its use as a defoliant during the Vietnam War. Ironically, it seemed that it was the selectivity of the chemicals – they would not kill cereals – that may have led to the decision not to use them during the Second World War.

In 1945 the first systemic hormone herbicide produced on a commercial scale – 2,4-D – was introduced in the USA, quickly followed in 1946 in the UK by the sodium salt of MCPA (Figure 2.3). These compounds were translocated and very small quantities were needed to kill plants. They affected broad-leaved plants systemically, causing stems to twist and bend, the roots to develop abnormal swellings and the leaves to turn yellow and die. In trials on turf and golf greens, broad-leaved weeds were killed without detriment to the grasses.

Wherever the new hormone-based weedkillers were used, the results were spectacular in terms of weed control. In the eastern counties of England, the

Cl

Herbicide Trade Name Dose rate (g/ha)

Picloram (1967) Tordon 960--2640 Fluroxypyr (1984) Starane 200 Triclopyr (1982) Garlon 960--1440

COOH OCH₃

Cl Cl

Dicamba

Herbicide Trade name Dose rate (g/ha) Dicamba (1961) In Condox 560

N

Quinmerac, introduced in 1997, is a constituent of Katamaran and applied at a dose rate of 250 g/ha

Quinclorac is marketed in Asia and North America as Facet

Figure 2.3 Auxin hormone herbicides.

red and yellow fields of wheat and barley, due to the high incidence of poppies (Papaver rhoeas– Figure 2.2) and charlock (Sinapis arvensis), became a thing of the past. The superb control of weeds with attendant increases in yield during a post-War era of food shortage led to further intensive research and development of hormone-based herbicides (Figure 2.3).

Further developments included MCPB, the butyric acid analogue of MCPA.

This compound can be used on a number of crops, not just monocotyledons, for weed control; allowing, for example, selective weed control in legume crops. In the 1950s, the 2-phenoxypropionic acid herbicides were developed with meco-prop – 2-(4-chloro-o-tolyoxy) meco-propionic acid, also known as CMPP – having good selective activity against cleavers (Galium aparine), which is poorly con-trolled by phenoxyacetic acids, and chickweed (Stellaria media) in cereals.

Further research in the 1960s and 1970s led to the introduction of benzoic acids such as dicamba, pyridine derivatives including clopyralid and triclopyr, the extremely persistent compound picloram, and fluroxypyr, which was used very extensively for weed control in cereals in the UK during the 1980s and 1990s. In the late 1980s a new generation of hormone herbicides, the quinoline carboxylic acids, was developed, including quinmerac and quinclorac (Grossman, 1998), the former being widely used for weed control in broad-leaved crops such as oilseed rape. Uniquely among auxin herbicides, the quinoline carboxylic acids have the capacity to control some grass weeds in cereal crops.

The morphological changes (Figure 2.4) that occur in susceptible species following application of these herbicides are characteristic of an overdose of auxins. Under normal conditions, the synthesis of auxin and its role in plant growth and development is under strict control. Applications of hormone herbi-cides may result in the uptake of around 100μg of synthetic hormone per plant – about 1000 times more auxin than is already present in the plant. Control systems within the plant cannot cope with such a massive auxin overdose, and death effectively occurs due to uncontrolled growth (Cobb, 1991).

Alterations in the permeability of membranes, particularly to cations, occur within a few minutes of application of these herbicides to susceptible plants.

Ethylene is released and this results in pronounced epinastic effects charac-terised by severe twisting of petioles and leaves. This growth distortion can occur within a few hours of application (Figure 2.4). Stomatal function is also affected and carbohydrate reserves may be mobilised. Cambial activity may be stimulated and, as a consequence, in the week following application stems generally thicken and elongate with the formation of adventitious roots. Leaf chlorosis, root disintegration and plant death soon follow.

Despite their extensive use for over half a century, the molecular basis of action of auxin hormone herbicides is still not clear, largely due to the lack of understanding of the precise mode of action of natural auxins. The activity of natural auxins may follow their binding to an auxin-binding prot-ein on the plant cell membrane: changes in plasma membrane potential may then quickly follow. Expression of certain genes is stimulated, leading to syn-thesis of key regulatory enzymes such as 1-aminocyclopropane-1-carboxylic

⇒

Shortly after application (12 h), twisting and distortion of the dicotyledon--pea--is evident

⇒

Seven days after treatment, chlorosis, severe distortion, stunting, and the beginning of necrosis are apparent

⇒

Fourteen days after treatment, the peas are dead, but the cereals remain unaffected

Figure 2.4 Selectivity of the hormone herbicide MCPA.

acid (ACC) synthase. ACC synthase is involved in the production of ethylene, and stress metabolites such as abscisic acid. Large doses of auxins may lead to massive changes in membrane permeability and over-expression of ACC synthase leading ultimately to the gross morphological changes noted above.

In terms of acute toxicity, hormone weedkillers only affect plant tissues.

Receptors for these synthetic auxins may be present only on the plasma mem-brane of susceptible plant species, and not in other organisms. Further selec-tivity for individual plant groups such as MCPB in legume crops is due to

metabolism. Oxidation of the molecule to MCPA occurs in broad-leaved species other than legumes, the latter thus remaining unaffected. However, the reasons why most of the hormone-based herbicides affect dicotyledonous rather than monocotyledonous plant species are, as with the mode of action, not yet clear.

Selectivity has been linked to the morphological nature of the leaf surface in the two groups, with monocotyledons retaining far less herbicide in their upright, narrow leaves than broad-leaved dicotyledonous plants. Differences in uptake of hormone herbicides have been reported between species but these differences are not sufficient to explain selectivity. It is possible that selectivity may be due to a difference in sensitivity or structure of auxin receptors in dicotyledons and monocotyledons, but confirmation of this hypothesis requires the full character-isation of auxin-binding proteins from plant cell membranes. The situation has been further complicated by the development of the quinoline carboxylic acids such as quinclorac, which is able to control some monocotyledonous weeds in rice: whether this specificity is due to slight differences in the receptors of plant species or metabolism/detoxification of quinclorac in rice remains to be resolved.