Figure 1.

Schematic representation of ABA biosynthesis, metabolism, and signal transduction pathways. (A) ABA biosynthesis mainly occurs through the carotenoid pathway, starting with carotenoid synthesis in plastids, particularly the cleavage of β-carotene. NCED is a key rate-limiting enzyme responsible for converting carotenoids into xanthoxin, which is then continuously oxidized in the cytoplasm to form ABA. ABA metabolism primarily follows two pathways: hydroxylation and glycosylation. In the hydroxylation pathway, CYP707A catalyzes the 8′-hydroxylation of ABA, ultimately producing the biologically inactive dihydrophaseic acid. In the glycosylation pathway, ABA can undergo conjugation with glucose, catalyzed by ABA-uridine diphosphate (UDP)glucosyltransferases (UGTs), to form ABA-glucosyl ester (ABA-GE), a biologically inactive storage or transport form of ABA. This inactive form can later be reactivated through enzymatic hydrolysis to release active ABA. (B) ABA signal transduction operates through a core module composed of PYL receptors, PP2C phosphatases, and SnRK2 protein kinases. When ABA levels increase, ABA binds to PYL receptors, inhibiting the activity of PP2C phosphatases and releasing the suppression of SnRK2s, thereby activating them. The activated SnRK2s phosphorylate downstream AREB/ABF transcription factors, which bind to ABRE cis-acting elements in DNA to activate the expression of target genes. Additionally, SnRK2s can activate certain ion channels, promoting stomatal closure.