Stress-Enhanced Metabolism of Abscisic Acid

Abstract

During water stress, abscisic acid (ABA) accumulates rapidly to high levels in leaves and roots, and various approaches have established that this increase is due to de novo synthesis rather than to liberation of ABA from a conjugate. Biosynthesis takes place via the indirect pathway in which ABA is derived from 9-cis xanthophylls, such as violaxanthin and neoxanthin. The first cleavage product is xanthoxin. Current evidence suggests that the rate-limiting step for ABA biosynthesis is the cleavage reaction. ¹⁸O from molecular oxygen is readily incorporated into the side chain of ABA and more slowly into the ring of the ABA molecule. The ¹⁸O labelling patterns of ABA from different sources vary due to differences in the size of the precursor pools (xanthophylls) and the turnover rates of intermediates which can result in exchange of ¹⁸O with the medium. Thus, although there are differences in the ¹⁸O labelling patterns of ABA from different materials, it is clear that in all systems investigated (stress or developmentally regulated) ABA is an oxidative cleavage product of larger precursor molecules, the xanthophylls. In Xanthium leaves, phaseic acid (PA) is the major catabolite of ABA, whereas the glucosyl ester of ABA (ABA-GE) accumulates slowly during prolonged stress. Upon rehydration of wilted leaves only PA is formed. Thus leaf water status is the determining factor for ABA metabolism since water deficits cause rapid ABA biosynthesis, and restoration of turgor results in rapid conversion of ABA to PA until the pre-stress ABA level is restored.