Purine catabolism is regarded as a housekeeping function that remobilizes
nitrogen for plant growth and development. However, emerging evidence suggests that certain
purine metabolites might contribute to stress protection of plants. Here, we show that in Arabidopsis, the intermediary metabolite
allantoin plays a role in abiotic stress tolerance via activation of
abscisic acid (ABA) metabolism. The aln loss-of-function of ALN, encoding
allantoinase, results in increased
allantoin accumulation, genome-wide up-regulation of stress-related genes and enhanced tolerance to drought-
shock and osmotic stress in aln mutant seedlings. This phenotype is not caused by a general response to
purine catabolism inhibition, but rather results from a specific effect of
allantoin.
Allantoin activates ABA production both through increased transcription of NCED3, encoding a key
enzyme in ABA biosynthesis, and through post-translational activation via high-molecular-weight complex formation of BG1, a β-
glucosidase hydrolysing
glucose-conjugated ABA. Exogenous application of
allantoin to wild-type plants also activates the two ABA-producing pathways that lead to ABA accumulation and stress-responsive gene expression, but this effect is abrogated in ABA-deficient and BG1-knockout mutants. We propose that
purine catabolism functions not only in
nitrogen metabolism, but also in stress tolerance by influencing ABA production, which is mediated by the possible regulatory action of
allantoin.