Figure 2.

Abscisic acid biosynthesis, catabolism, deconjugation, transport, and signaling. ABA biosynthesis (A) is mainly induced by upregulating NCED3, ZEP, and AAO genes. At the same time as the biosynthesis of ABA is induced, the catabolism (B) that is performed by CYP707A1-4 is inhibited. The balance between active and inactive ABA in the cell is achieved not only by the regulation of biosynthesis and catabolism but also by ABA conjugation and deconjugation. The most widespread conjugate is the ABA glucosyl ester (ABA-GE), which is catalyzed by ABA glucosyltransferase (C). ABA delivery to the guard cells via ABCG transporters such as AGCG22 (D) promotes a cascade of reactions. The core of early ABA signaling involves ABA receptors – PYR/PYL/RCAR proteins, PP2Cs, and SnRKs (E). After binding ABA to the receptor, the negative regulatory action of PP2Cs is inhibited and SnRKs are able to phosphorylate and activate downstream targets in order to transduce the ABA signal.