ABA Regulation of the Cold Stress Response in Plants - Abscisic Acid: Metabolism, Transport and Signaling - page 332

Xiong et al. 2002b ). Cold acclimation was shown to be impaired in an aba1
mutant, which has also reduced expression of specific COR genes (Mantyla et al.
1995 ). The expression of none of the ABA biosynthesis genes is affected by cold
treatment in Arabidopsis (Lee et al. 2005 ). Therefore, ABA biosynthesis is not an
early event in response to cold stress. Consistent with this, foliar application of
ABA to a wide range of plant species does not induce cold hardness or freezing
tolerance (Gusta et al. 2005 ). A recent study showed that cold stress specifically
activate the expression of ABA biosynthesis genes in reproductive organs, such as
the inflorescence meristem, with only slightly increased expression in the leaves
and vegetable organs (Baron et al. 2012 ). This finding supports the notion of ABA
function in stimulating and hastening plant harvests under adverse environmental
conditions. Taken together, ABA may function late in the development of cold-
induced metabolic changes and is required for determining the maximum levels of
cold tolerance in plants.
ABA activates a wide array of genes associated with stress response,
seed dormancy, and stomatal movement through the ABA signalling pathway
(Yamaguchi-Shinozaki and Shinozaki 2006 ). The PYR/PYL/RCAR family
of proteins are ABA receptors that can inhibit the activity of the type-2C pro-
tein phosphatase PP2C in the presence of ABA, relieving the repression of the
SnRK2 kinases activity, which in turn phosphorylates other downstream regu-
lators (Furihata et al. 2006 ; Ma et al. 2009 ; Park et al. 2009 ). Overexpression
of TaSnRK2.3 in Arabidopsis results in enhanced root-system architecture and
significantly enhances the tolerance of this species to drought, salt, and freez-
ing stresses (Tian et al. 2013 ), whereas downregulation of PP2CA proteins
increases ABA sensitivity and accelerates cold acclimation in transgenic plants
(Tahtiharju and Palva 2001 ). Promoter analysis found that some DRE/CRT
motif-containing COR genes are induced by cold and dehydration and impaired
in ABA-deficient mutants (Thomashow 1999 ; Shinozaki and Yamaguchi-
Shinozaki 2000 ). As mentioned earlier, CBFs/DREB1s and their homolog,
CBF4, were shown to bind to CRT/DRE motifs in vivo. CBF4 expression is
induced by drought and ABA, but not by cold, which is quite distinctive from
CBF1 - CBF3 . Overexpression of CBF4 results in increased freezing and
drought tolerance (Haake et al. 2002 ). It appears that at least three separate
regulatory signalling pathways exist that are mediated by the binding of tran-
scription factors to CRT/DRE motifs. Among these, cold-induced CBF1-CBF3
and drought-induced DREB2 are the primary transcription factors that control
gene expression through the ABA-independent pathway, whereas CBF4 acts as
a regulator of the ABA response (Thomashow 1999 ; Shinozaki and Yamaguchi-
Shinozaki 2000 ). In addition to the CRT/DRE motif, many cold-response gene
promoters harbour ABRE cis -elements that can be activated in vivo by ABA
through direct binding of bZIP transcription-factor proteins (AREBs/ABFs,
ABRE-binding proteins/factors) (Uno et al. 2000 ). This evidence explains that
expression of the COR genes is regulated by both ABA-dependent and ABA-
independent pathways (Fig. 17.1 ).