Overall Mechanism(s) of Auxin Effects

When an auxinic herbicide is applied to a plant, receptors recognize it and a signal-transduction cascade leading to plant death is initiated (Figures 14a, 14b, 14c, 14d).

Fig. 14a: Signal-transduction pathways begin after auxin binds to the receptor (Image credit: Tracy Sterling, Deana Namuth, Jeremy Steele, and Smitha Kasinadhuni)

Fig. 14b: Secondary messengers turn on transcription of a gene; H+-ATPase in this example (Image credit: Tracy Sterling, Deana Namuth, Jeremy Steele, and Smitha Kasinadhuni)

Fig. 14c: RNA from the induced gene product is translated (Image credit: Tracy Sterling, Deana Namuth, Jeremy Steele, and Smitha Kasinadhuni)

Fig. 14d: The induced gene product is H+-ATPase; this will be incorporated into the membrane and cause acid-induced cell elongation (Image credit: Tracy Sterling, Deana Namuth, Jeremy Steele, and Smitha Kasinadhuni)

Fig. 15: Auxinic herbicides induce production of several possible gene products (Image credit: Tracy Sterling, Deana Namuth, Jeremy Steele, and Smitha Kasinadhuni)

It is not known if only one of these pathways cause plant death or if several are involved. More than likely, several signal-transduction pathways are initiated. Therefore, there are probably several phytotoxic scenarios possible because several gene products may be induced (Figure 15). Examples of three major gene products induced by auxins and their involvement in plant death are shown in the animation ‘Overall Picture of Auxinic Herbicide Action’.

One example is the induction of H+-ATPase causing uncontrolled cell elongation (Figure 11). Second, ethylene production is induced in broadleaf plant species when exposed to auxin or auxinic herbicides (Figure 12). Also, there are some grasses sensitive to auxinic herbicides and ethylene is induced in these species as well

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However, ethylene is not always involved in plant death. In the case of quinclorac-sensitive grasses (i.e. barnyardgrass), ethylene is induced after exposure to this auxinic herbicide; however, evidence suggests that these plants are relatively insensitive to ethylene itself and may die from exposure to the high levels of hydrogen cyanide (HCN) released in the final step of ethylene biosynthesis (Figure 12) or from inhibition of cell wall formation in their roots as described in the next section (Figure 16).

In the case of broadleaf species, it appears the role of ethylene in plant death is species dependent. Although ethylene is induced in most broadleaf species after exposure to auxinic herbicides, some broadleaf species (i.e. Chrysanthemum, chickweed, tobacco, yellow starthistle) are tolerant to exogenous ethylene and phytotoxic symptoms induced by the herbicide are unaltered in the presence of ethylene biosynthesis inhibitors, suggesting ethylene plays no role in plant death. There are other broadleaf species (i.e. tomato) where auxin-induced ethylene induces the production of abscisic acid (ABA) and ABA mediates plant death via stomatal closure. Stomatal closure reduces the ability of the plant to cool itself through transpiration and also leads to reduced photosynthesis because carbon dioxide can no longer enter the leaf. Although the exact role of ethylene evolution in the mode of action of auxinic herbicides is unknown, experimental evidence suggests it is a secondary response. However, ethylene may be a critical messenger responsible for rapid transmission of the auxin or auxinic herbicide effect throughout the entire plant. A third example of gene products induced by auxins or auxinic herbicides includes those which alter plant growth through as yet unknown mechanisms.