The Molecular Basis of ABA-Mediated Plant Response to Drought - Abiotic Stress: Plant Responses and Applications in Agriculture - page 106

The ability of ABA to move long distances allows it to serve as a critical stress messenger.
ABA transport was long assumed to be a diffusive process, mainly due to the ability of ABA
to diffuse passively across biological membranes when it is in a protonated state [50]. The
last step of ABA biosynthesis occurs in the cytosol where pH is estimated to be 7.2-7.4. In the
apoplastic space, where ABA is meant to be transported before reaching the target cell, the
pH is estimated to be around 5.0-6.0. Although ABA can be passively transported from a
low pH to a higher one with a pH gradient, there is a need for the transporter to allow ABA
to get into the target cell and to be exported from the cell to the apoplast. During stress re‐
sponse, the strong alkalization of apoplastic pH would slow ABA diffusive transport from
the apoplastic space to the target cells. Because of the predominance of a non-protonated
ABA state, there is a need for the existence of ABA transporters. The identification of ABA
transporters in target cell membranes, such as the cell membranes of guard cells, has re‐
solved the problem of how ABA gets into the cells when passive transport is decreased un‐
der stress conditions. One of the identified ABA importers is ABCG40 (ARABIDOPSIS
THALIANA ATP-BINDING CASSETTE G40) described by Kang et al [51]. The expression
of ABCG40 is not tissue specific and its product localizes in cell membranes [51]. Kuromori
et al [52] identified another ABA importer - ABCG22 (ARABIDOPSIS THALIANA ATP-
BINDING CASSETTE G22). The gene encoding this transporter is mainly expressed in
guard cells. Also, the expulsion of ABA into the intercellular space is mediated by transport‐
ers such as ABCG25 (ARABIDOPSIS THALIANA ATP-BINDING CASSETTE G25). ABCG25
is expressed mainly in vacuolar tissue, where ABA is synthesized [53].
A breakthrough in understanding ABA signaling occurred recently when several groups
identified key ABA receptors. Chemical genetics emerged as the solution for the problem of
the identification of receptor. Pyrabactin (4-bromo-N-[pyridine-2-yl methyl]naphthalene-1-
sulfonamide) is a synthetic compound that partially mimics the inhibitory effect of ABA
during seed germination and seedling development. Using a series of pyrabactin-resistant
mutants and the map-based cloning approach, several genes encoding ABA-binding pro‐
teins, among them PYR1 (PYRABACTIN-RESISTANCE 1) have been identified [3]. PYR1 is
one of the 14 homologs (PYL - PYRABACTIN RESISTANCE LIKE) present in the Arabidop‐
sis genome [1-4]. After receiving ABA from ABC transporters, the PYR/PYL/RCAR-ABA
(PYRABACTIN-RESISTANCE 1/ PYRABACTIN RESISTANCE LIKE/ REGULATORY COM‐
PONENT OF ABA RECEPTOR) complex perceives ABA intracellularly and forms ternary
complexes inhibiting clade A of PP2Cs (PROTEIN PHOSPHATASE 2C), the negative regu‐
lators of ABA signaling, such as ABI1 (ABA INSENSITIVE 1), ABI2 (ABA INSENSITIVE 2),
HAB1 (HYPERSENSITIVE TO ABA1) [1-2; Table 1].
This allows the activation of down-stream targets of PP2Cs - the Sucrose nonfermenting 1-
related subfamily 2 protein kinases (SnRK2), such as SnRK2.2/D, SnRK2.3/E and SnRK2.6/
OST1/E which are the key players in the regulation of ABA signaling [54-57; Figure 1].
The last enzyme, OST1 (OPEN STOMATA1), displays dominant kinase activity during
drought stress response when the ABA signal is relayed to the guard cells. Mutants in OST1
showed a wilty phenotype under water deficit conditions [58]. Mutants for the other two
ABA-activated kinases, SnRK2.2 and SnRK2.3 , did not show a drought-sensitive phenotype