Stress-induced abscisic acid transients and stimulus-response-coupling

Loss of cell turgor and distortion of the plasma membrane occur as a result of dehydration and precede the stress-induced bulk increase in concentration of tissue abscisic acid. The latter has been correlated with induction of stress-related gene expression. However, several different stresses may trigger the same coupling mechanism. Thus, at least three signalling pathways have been proposed: abscisic acid-requiring, abscisic acid-responsive, and mechanosensory. In this paper, the role and contribution of stress-induced abscisic acid transients is examined in an attempt to explain apparent abscisic acid-dependent and -independent stimulus-response-coupling. Early, intermediate, and late response stages are defined within the stress-induced abscisic acid transient and at least four signalling mechanisms are identified. These include, early and late intracellular modulation of gene expression through depression and/or negative regulation, rapid membrane-initiated calcium release and ion channel activation, and late (slow) hormone-receptor induction of gene expression. An assessment of these proposed ABA signalling mechanisms in terms of AABA-dependent and -independent stimulus-response-coupling strongly suggests that rapid responses may not be a prerequisite for slow responses and that the receptor proteins involved have different steric requirements, i.e., they are tissue- and/or cell-specific.