Regulation of abscisic acid metabolism: towards a metabolic basis for abscisic acid-cytokinin antagonism

The penultimate step in abscisic acid (ABA) biosynthesis involves oxidation of xanthoxal (XAN) catalysed by a molybdenum-cofactor (MoCo)-containing aldehyde oxidase (AO) and represents one potential site of regulation of ABA in plant tissues. In an attempt to understand the biochemical basis for cytokinin-abscisic acid (CK-ABA) antagonism the effect of several CKs, molybdate, tungstate and allopurinol (an inhibitor of xanthine oxidase activity and purine metabolism) on the formation of XAN, ABA and related catabolites in mesocarp of ripening avocado (Persea americana Mill. cv. Hass) was investigated. Treatment with either adenine (Ade), isopentenyladenine (2iP) or zeatin (Z) enhanced conversion of ABA to phaseic acid (PA) and caused a reduction in the amount of radioactivity incorporated from 3R-2-¹⁴C] mevalonolactone (MVL) into ABA by stimulating overall ABA metabolism. Ancymidol and N-(2-chloro-4-pyridyl)-N-phenylur ea (CPPU), while not affecting formation of PA and DPA, appeared to retard ABA biosynthesis which resulted in the accumulation of XAN. Tungstate caused accumulation of XAN at the expense of ABA and related acidic metabolites while molybdate and allopurinol accelerated ABA metabolism, i.e. formation of XAN, ABA, PA, and DPA. These findings are discussed in terms of the regulation of the ABA biosynthetic pathway in avocado fruit by CK-induced suppression of xanthine dehydrogenase (XDH) activity and a model illustrating the proposed metabolic interrelationship is presented.