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Stress‐induced abscisic acid transients and stimulus‐response‐coupling
Author(s) -
Cowan A. K.,
Richardson G. R.,
Maurel J. C. G.
Publication year - 1997
Publication title -
physiologia plantarum
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.351
H-Index - 146
eISSN - 1399-3054
pISSN - 0031-9317
DOI - 10.1111/j.1399-3054.1997.tb03053.x
Subject(s) - abscisic acid , microbiology and biotechnology , stimulus (psychology) , receptor , biology , gene expression , intracellular , biophysics , chemistry , biochemistry , gene , psychology , psychotherapist
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.