Cross Talk of Signaling Pathways Between ABA and Other Phytohormones - Abscisic Acid: Metabolism, Transport and Signaling - page 241

(loss of GAI, RGA, RGL1, and RGL2) is relatively resistant to the growth-inhib-
itory effects of ABA (Achard et al. 2006 ). Therefore, while during seed germina-
tion, ABA seems to act downstream of DELLA, it affects Arabidopsis growth via
DELLA. It is thus possible that distinct mechanisms of interaction between GA
and ABA are utilized for different developmental decisions.
Further, the fine-tuning of the cross talk between GA and ABA was recently
demonstrated in Arabidopsis . Both ABA and GA can induce the expression of
microRNA159 (miR159), which targets the MYB33 mRNA. Interestingly, MYB33
promotes ABA responses in seeds and GA responses in flowers. Thus, the two
antagonistic hormones exert their actions through a common mediator, MYB33,
and desensitize their signaling through the same homeostatic mechanism, miR159,
at different developmental stages (Achard et al. 2004 ; Reyes and Chua 2007 ).
Recently, Golldack et al. ( 2013 ) uncovered novel antagonizing roles of GA and
ABA in integrating growth and development in plants with environmental signal-
ing. GRAS transcription factors of the DELLA and SCARECROW-LIKE (SCL)
types play a key role as major growth regulators and have pivotal functions in
modulating GA signaling (Golldack et al. 2013 ). In contrast to a pivotal role of
GRAS family transcriptional factors in plant growth regulation, recent work has
suggested that the DELLA and SCL proteins integrate generic GA responses into
ABA-controlled abiotic stress tolerance (Golldack et al. 2013 ).
ABA and GA are the primary factors that antagonistically regulate the transi-
tion from dormancy to germination. High ABA and low GA content in seeds
promote seed dormancy. However, the underlying molecular mechanism involv-
ing cross talk between ABA and GA in this process remains to be elucidated. Shu
et al. ( 2013 ) recently found that ABI4, the key transcription factor in the ABA-
signaling pathway, indeed controls primary seed dormancy. This result contradicts
the previous conclusion that ABI4 is not involved in the control of seed dormancy.
Several lines of evidence support this conclusion. For example, detailed physi-
ological analysis of the germination of abi4 seeds that were harvested immedi-
ately and stored for various periods of time and subjected to various treatments
showed that ABI4 negatively regulates primary seed dormancy (Shu et al. 2013 ).
The molecular mechanism responsible for this control is that ABI4 directly or
indirectly regulates the key genes of the ABA and GA biogenesis pathways,
which then regulates the ABA and GA contents in seeds (Shu et al. 2013 ). Taken
together, this study suggests that ABI4 is a key factor that regulates primary seed
dormancy by mediating the regulation of GA biogenesis (Shu et al. 2013 ).
12.5 Cross Talk Between ABA and Ethylene
The plant hormones ethylene and ABA have antagonistic functions in the control
of plant growth and development, including seed germination and early seedling
development. Ethylene and ABA may control the biosynthesis, catabolism, or
signaling of the other to enhance their antagonistic effects on seed germination