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

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.