Effect of hydroxylated carotenoid deficiency on ABA accumulation in Arabidopsis

Abstract

Abscisic acid (ABA) is a sesquiterpene compound (C15) derived from C40 carotenoids. The immediate carotenoid precursors for ABA biosynthesis, 9‐cis‐violaxanthin and 9′‐cis‐neoxanthin, are produced from β‐carotene by a series of hydroxylation, epoxidation, and isomerization reactions. Carotenoid hydroxylase deficient mutants contain severely reduced levels of violaxanthin and neoxanthin ( < 20% of wild type level) and provide a unique system to correlate carotenoid substrate availability and ABA production in photosynthetic tissues under non‐stressed conditions. Quantitative measurements indicated that ABA levels in the carotenoid hydroxylase mutants are reduced nearly 50% compared to the wild type plants under non‐stressed conditions. When drought‐stressed, wild type plants showed up to a 17‐fold increase in ABA levels, while ABA levels in the carotenoid hydroxylase mutants were only increased 6‐ to 7‐fold (25% of wild type drought‐stressed ABA levels). Expression of AtNCED3 (Arabidopsis thaliana nine‐cis‐epoxycarotenoid dioxygenase 3, the rate‐limiting activity for ABA biosynthesis) was induced in the carotenoid hydroxylase mutants, but to a lesser extent than the 40‐fold increase in wild type plants. Therefore, the reduced ABA accumulation in response to drought‐stress is at least partially due to the attenuated increase in AtNCED3 gene expression in the carotenoid hydroxylase mutants. The remaining violaxanthin and neoxanthin in the carotenoid hydroxylase mutants can not be converted into ABA, indicating that there is probably a separate pool of violaxanthin and neoxanthin that is not accessible to the cleavage enzymes, because it is sequestered in the light‐harvesting complexes.