During germination, Arabidopsis hypocotyl elongation is regulated by auxin. Recent work has suggested that abscisic acid (ABA) also plays a role in this process. Here, Lucia Strader and colleagues identify an Arabidopsis mutant that is resistant to auxin-induced repression of hypocotyl growth in dark conditions. In light conditions, where application of auxin promotes hypocotyl growth, the mutant shoots elongate less than their wild-type counterparts. The authors show that a mutation in ABSCISIC ALDEHYDE OXIDASE3 (AAO3) confers this resistance to auxin. The AAO3 enzyme catalyses the last step in the ABA biosynthesis pathway, and the authors confirm that mutations in other ABA biosynthesis enzymes can also produce auxin resistance. Auxin treatment also leads to higher ABA levels in the shoot. By contrast, ABA biosynthesis mutants are not resistant to auxin’s effects on root elongation, suggesting that root and shoot elongation are regulated by distinct pathways. Indeed, RNA sequencing reveals little overlap between shoot and root transcripts following auxin exposure, whereas ABA biosynthesis mutant shoots exhibit clear differences from wild-type shoots in terms of the genes that are downregulated by auxin exposure. Overall, this work suggests that auxin promotes ABA biosynthesis that, in turn, supports auxin-mediated downregulation of target genes to appropriately regulate hypocotyl elongation.
