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[59]. The triple mutant snrk2.2/d snrk2.3/I snrk2.6/e displayed an extremely sensitive pheno‐
type under water deficit conditions. Transcriptomic studies of the triple mutant showed a
down-regulation of genes encoding PP2Cs, which suggested a feedback loop in the tran‐
scription regulation of PP2Cs by SnRKs [54].
Figure 1. ABA synthesis, catabolism, conjugation and response in a scheme.
One of the earliest plant responses to water deficit condition, and one regulated mainly in
an ABA-dependent manner, is the closure of stomata. The closing or opening of the pore is a
result of the osmotic shrinking or swelling, of the two surrounding stoma guard cells. ABA
acts directly on the guard cells and induces stomata closure via an efflux of potassium and
anions from the guard cells [60]. ABA regulation of the membrane ion channels is mediated
by increased cytosolic Ca 2+ resulting from the release of Ca 2+ from intracellular stores and a
Ca 2+ influx from the extracellular space. It is worth noting that a number of mutations that
affect ABA signaling in regards to stomatal action during drought have been characterized.
Dominant mutations have been described in genes that encode type-2C phosphatases - ABI1
(ABA INSENSITIVE 1) and ABI2 (ABA INSENSITIVE 2) [61-62], whereas recessive muta‐
tions that lead to supersensitivity to ABA in regards to stomata closure are found in genes
that encode farnesyltransferase β-subunit - ERA1 (ENHANCED RESPONSIVE TO ABA1)
[63-64], a larger subunit of cap binding complex CBP80 (CAP BINDING PROTEIN 80) [65]
and the Sm-like snRNP protein SAD1 (SUPERSENSITIVE TO ABA AND DROUGHT 1) [66].
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