Extreme drought can deactivate ABA biosynthesis in embolism-resistant species

The phytohormone abscisic acid (ABA) is synthesised by plants during drought to close stomata and regulate desiccation tolerance pathways. Conifers and some angiosperms with embolism-resistant xylem show a peaking-type (p-type) response in ABA levels, in which ABA levels increase early in drought then decrease as drought progresses, declining to pre-stressed levels. The mechanism behind this dynamic remains unknown. Here, we sought to characterise the mechanism driving p-type ABA dynamics in the conifer Callitris rhomboidea and the highly drought-resistant angiosperm Umbellularia californica. We measured leaf water potentials (psi l), stomatal conductance, ABA, conjugates and phaseic acid (PA) levels in potted plants during a prolonged but non-fatal drought. Both species displayed a p-type ABA dynamic during prolonged drought. In branches collected before and after the peak in endogenous ABA levels in planta, that were rehydrated overnight and then bench dried, ABA biosynthesis was deactivated beyond leaf turgor loss point. Considerable conversion of ABA to conjugates was found to occur during drought, but not catabolism to PA. The mechanism driving the decline in ABA levels in p-type species may be conserved across embolism-resistant seed plants and is mediated by sustained conjugation of ABA and the deactivation of ABA accumulation as psi l becomes more negative than turgor loss. We find that abscisic acid biosynthesis is deactivated after leaf turgor loss point during extreme drought, but that the conjugation of ABA to inactive forms remains constant, leading to a decline in ABA levels in embolism-resistant species.