Lesson Media Objects
Auxin and Auxinic Herbicide Mechanism(s) of Action - Part 1 - Introduction
The auxinic herbicides (Figure 1) are structurally similar to the natural plant hormone, IAA (Figure 2). It has been proposed that receptors recognizing auxin and transducing that signal into a physiological response, are the auxin-binding proteins (ABP). Each receptor is thought to have a binding conformation that includes a naphthalene-binding platform, a carboxylic acid binding site and a hydrophobic transition zone located between the two binding elements (Figure 4).
Auxin influx and efflux carriers are a major mode of transport for auxin from cell to cell toward the base of the plant, also known as basipetal or polar transport. The H+/ IAA- influx carrier (Figure 6),
evenly distributed in the plasma membrane, recognizes the conjugate base of auxin, the anion IAA-, and two hydrogen ions (2 H+). This saturable carrier is able to actively transport IAA- against an electrochemical gradient across the plasma membrane by coupling to the transport of two H+ down their electrochemical gradient. Once inside the alkaline cytoplasm, the IAA- is recognized by a series of saturable efflux carriers (Figure 7) in the membrane on the lower side of each cell that carry IAA- to the cell wall region where it can diffuse to auxin influx carriers located on the cell below. Another contributor to basipetal or polar transport of auxin, is the simple diffusion of auxin across the plasma membrane in its lipophilic, undissociated acid form (IAAH) (Figure 8).
Because of its low pKa (link to pKa animation) of 4.7, the acid form of auxin (IAAH) predominates in the acidic cell wall region creating a large concentration gradient to drive diffusion of IAAH across the membrane into the cell. The Proton Motive Force of the cell is maintained by the hydrolysis of ATP by H+-ATPases located in the plasma membrane that pump out H+ into the cell wall space. Once in the alkaline cytoplasm, IAAH dissociates to the anion, IAA- and can accumulate as the anion because of its lower membrane permeability (Figure 9)
or efflux from the cell via the IAA- efflux carriers at the base of the cell.
These receptors are then thought to signal a cascade of events leading to physiological responses or plant death in the case of auxinic herbicides. The mechanism for the transduction of the signal may involve direct interaction of regulatory proteins with specific DNA sequences or secondary messengers. Protein kinases, Ca++-calmodulin, phosphoinositide metabolism, cyclic AMP, pH changes, redox reactions at the cell surface, membrane fatty acids and protein methylation have all been implicated in secondary messenger pathways in plants. For example, once auxin binds to a receptor, phospholipase C (PLC) is induced to hydrolyze the membrane lipid phosphatidylinositol (PIP2) which releases inositol-1,4,5-triphosphate (IP3) and diacylglycerol (DAG) (Figure 11a). The released (IP3) moves to the vacuole’s membrane, the tonoplast, and the IP3 binds to a receptor in that membrane (Figure 11b). The IP3 receptor then activates a Ca++ transporter that pumps Ca++ out if the vacuole into the cytosol. Increased Ca++ in the cytosol activates protein kinases and other enzymes that then activate other enzymes that catalyze the various reactions causing the metabolic changes associated with auxin or auxinic herbicide (Figure 11c). DAG can also activate protein kinases and other enzymes (Figure 11d).
A classic response to auxin or auxinic herbicides is cell elongation. Within 10 to 15 min of exposure to auxin, cell elongation is induced because of acid-induced cell wall loosening. The model best describing this process is the Acid Growth Hypothesis.
Cell walls become acidified by IAA turning on H+-ATPases via secondary messengers or by I1AA inducing, via changes in gene expression (Figures 12a, 12b, 12c, 12d), more H+-ATPase production for incorporation into the cell membrane (Figure 13).
The H+-ATPases pump H+ out of the cell, expending ATP to move H+ against its electrochemical gradient, further acidifying the cell wall region. Wall loosening during acidification involves rearrangements of the load-bearing bonds of the cell wall and probably is mediated through special proteins called expansins. Once the cell wall is loosened, the cell can expand by water moving into the cell, driven by the gradient of water potential. Water uptake into the cells creates an internal turgor pressure that pushes against the cell membrane and extends the cell wall. Cell elongation after 30 to 60 min does not involve acid-induced elongation, but is due to auxin turning on genes which help cells elongate by other mechanisms (i.e. synthesis of new cell wall material).
Ethylene synthesis begins with methionine and ATP combining to produce S-adenosyl-methionine (SAM) as catalyzed by SAM synthase. SAM is then converted to 1-aminocyclopropane-1-carboxylic acid (ACC) as catalyzed by ACC synthase. ACC synthase is induced by several stresses including flooding, wounding, IAA and auxinic herbicides (Figure 15).
The final step for ethylene production is catalyzed by ACC oxidase producing ethylene, hydrogen cyanide and carbon dioxide from ACC (Figure 14). Depending on the plant species, ethylene induced by auxin or auxinic herbicides may or may not play a role in subsequent plant death.
One example is the induction of H+-ATPase causing uncontrolled cell elongation (Figure 13). A second example is a multitude of gene products induced by auxins or auxinic herbicides which result in altered plant growth like epinasty through as yet unknown methods. Third, ethylene production is induced in broadleaf plant species when exposed to auxin or auxinic herbicides. Also, there are some grasses sensitive to auxinic herbicides and ethylene is induced in these species as well. However, ethylene is not always involved in plant death. In the case of quinclorac-sensitive grasses (i.e. barnyard grass), ethylene is induced after exposure to this auxinic herbicide; however, evidence suggests that these plants are relatively insensitive to ethylene itself and actually die from exposure to the high levels of hydrogen cyanide (HCN) released in the final step of ethylene biosynthesis (Figure 14). 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 itself 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 ABA and ABA mediates plant death via stomatal closure. 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.
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