Role of the plasma membrane H + -ATPase in auxin-induced elongation growth: historical and new aspects

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Abstract
This article will cover historical and recent aspects of reactions and mechanisms involved in the auxin-induced signalling cascade that terminates in the dramatic elongation growth of cells and plant organs. Massive evidence has accumulated that the final target of auxin action is the plasma membrane H+-ATPase, which excretes H+ ions into the cell wall compartment and, in an antiport, takes up K+ ions through an inwardly rectifying K+ channel. The auxin-enhanced H+ pumping lowers the cell wall pH, activates pH-sensitive enzymes and proteins within the wall, and initiates cell-wall loosening and extension growth. These processes, induced by auxin or by the "super-auxin" fusicoccin, can be blocked instantly and specifically by a voltage inhibition of the H+-ATPase due to removal of K+ ions or the addition of K+-channel blockers. Vice versa, H+ pumping and growth are immediately switched on by addition of K+ ions. Furthermore, the treatment of segments either with auxin or with fusicoccin (which activates the H+-ATPase irreversibly) or with acid buffers (from outside) causes an identical transformation and degradation pattern of cell wall constituents during cell-wall loosening and growth. These and other results described below are in agreement with the acid-growth theory of elongation growth. However, objections to this theory are also discussed.