Cross Talk Between Light and ABA Signaling - Abscisic Acid: Metabolism, Transport and Signaling - page 253

cell wall loosening, cell division, and hormone pathways to initiate seed germi-
nation (Shi et al. 2013 ). Hence, HFR1 defines a new positive regulator of phyB-
dependent seed germination.
Recently, Lim et al. ( 2013 ) demonstrated that ABI3, ABI5, and DELLAs form
a complex on the SOM promoter to activate SOM expression in imbibed seeds in
response to high temperature. ABI5 is a bZIP transcription factor that plays impor-
tant role in ABA signaling and ABA responses (Finkelstein and Lynch 2000 ). Two
previous researches identified two types of transcription factors that directly regu-
late ABI5 expression (Chen et al. 2008 ; Tang et al. 2013 ). A ChIP study indicates
that HY5 directly binds to the promoter region of ABI5 , and the binding ability
was significantly enhanced by exogenous ABA treatment. Consistent with this
observation, HY5 is required for the expression of ABA-inducible genes, such as
ABI3 , RAB18 , AtEM1 , and AtEM6 , in seeds and during seed germination (Chen
et al. 2008 ). Consequently, hy5 mutant seeds are less sensitive to the inhibition of
ABA and glucose on germination (Chen et al. 2008 ).
FHY3 is another type of transcription factor that directly binds to the promoter
of ABI5 and activates its expression (Tang et al. 2013 ). Disruption of FHY3 and/or
its homology gene, FAR1, reduces sensitivity to ABA-mediated inhibition of seed
germination. Germination of the fhy3 mutant seeds is also less sensitive to salt and
osmotic stress than that of the wild type (Tang et al. 2013 ). Strikingly, constitutive
expression of ABI5 restores the seed germination response of fhy3 . Furthermore,
the expression of several ABA-responsive genes (e.g., ABI1 , ABI2 , ABF3 , RAB18 ,
KIN2 , COR47 , DREB2A , and RD22 ) is decreased in the fhy3 and/or far1 mutants
during seed imbibition (Tang et al. 2013 ).
Although both phyA and phyB photoreceptors are essential for seed germina-
tion, the mechanism underlying their distinct roles has long been a mystery. Using
a seed coat bedding assay system where dissected embryos are cultured on a layer
of dissected seed coats, Lee and coauthors ( 2012 ) demonstrated that phyA and
phyB spatially control seed germination in embryo and endosperm, respectively, in
response to far-red light irradiation. The endosperm mediates far-red repression of
phyB-dependent germination, whereas FR stimulation of phyA-dependent germina-
tion occurs only in the embryo. These responses specifically involve the light sign-
aling genes PIL5 and RGL2 in the endosperm and PIL5, SOM, GAI, and RGA in
the embryo, where they regulate the expression of GA and ABA biosynthetic genes
in each tissue (Lee et al. 2012 ). Therefore, early upon seed imbibition, far-red light
inactivation of phyB leads to ABA biosynthesis and releases from the endosperm
to prevent phyA-dependent promotion of germination in the embryo. This involves
an extended regulatory network where ABA overrides phyA signaling by interfer-
ing with the expression of light signaling genes and GA and ABA metabolic genes.
Over time, a weakening of ABA-dependent responses takes place, thus allowing
phyA-dependent germination after a later light treatment. This results in a phyA-
dependent “explosive” germination unlike phyB-dependent germination (Lee et al.
2012 ). Furthermore, far-red light repression of germination involves stabilized
DELLA proteins GAI, RGA, and RGL2 that stimulate endogenous ABA biosynthe-
sis, which in turn blocks germination through ABI3 (Piskurewicz et al. 2009 ).