ABA and the Floral Transition - Abscisic Acid: Metabolism, Transport and Signaling - page 364

control of flowering time (Kurup et al. 2001 ; Rohde et al. 2000a ). abi3 mutants
are early flowering under both SDs and LDs while ABI3 overexpression results in
an increased vegetative phase under LDs (Kurup et al. 2001 ; Rohde et al. 2000a ;
Zhang et al. 2009 ). The question arises as to how ABI3 affects the floral transi-
tion. The role of ABI3 in transcriptional reprogramming is complex (M￶nke et al.
2012 ; Suzuki et al. 2009 ). Following spray with ABA, abi3 mutants display high
levels of TSF , suggesting a repressive role for ABI3 on TSF expression (Suzuki
et al. 2003 ). In germinating seeds, expression of another florigen gene ( MFT ) is
downregulated by ABI3. MFT is then involved in a negative feedback regulation of
ABA signalling by directly repressing ABI5 (Xi et al. 2010 ). It is unclear whether
this model can be extended to the regulation of the vegetative phase. However,
these data could provide a molecular framework for how florigen-like proteins,
ABI3 and ABA related bZIPs interact. Second they point to a model where ABI3
acts as a negative regulator of flowering through downregulation of florigen-like
genes. Intriguingly, the physical interaction between ABI3 and CO might explain
the ABI3-mediated regulation of the florigen genes. ABI3 binds to the CO CCT
(CO, CO-like, TOC1) domain (Kurup et al. 2001 ). The CCT domain appears to be
involved in the recruitment of the CO protein to the promoter of FT (Tiwari et al.
2010 ). Thus, binding of ABI3 may interfere with CO (and perhaps other CCT-
domain containing proteins) binding to chromatin. A more precise understanding
of ABI3-action warrants further investigation and could provide valuable clues as
to how ABA and photoperiod interact to affect flowering.
Combined genetic and expression data suggest a model where ABI3 acts
upstream of ABI5 . First the abi3 germination defects can be rescued by the ectopic
expression of ABI5 . Conversely the ectopic expression of ABI3 cannot rescue the
germination defect of abi5 mutants. Second elevated ABI3 levels trigger ABI5
protein expression in the presence of ABA (Lopez-Molina et al. 2002 ). ABI3 also
interacts with ABI5, suggesting a mode of cross talk between ABI3 and ABI5
(Nakamura et al. 2001 ). Thus, besides negatively regulating florigen-like genes,
ABI3 may also delay flowering indirectly, through upregulation of ABI5 .
ABI3 activity is regulated through ubiquitination and subsequent proteasome-
dependent degradation (Zhang et al. 2009 ). An ABI3-interacting protein (AIP2)
can polyubiquitinate ABI3 and affect ABI3 levels in vivo. A model has emerged
where increasing ABA levels trigger AIP2 transcriptional activation. AIP2 in turn
negatively regulates ABA signalling by targeting ABI3 for destruction. These data
argue against the idea that the flowering repressive role of ABA is dependent on
ABI3, because ABA would promote its degradation.
Other transcription factors play a role in ABA signalling and have been
reported to alter the floral transition. ABA modulates the nuclear import and activ-
ity of a set of transcription factor to regulate gene expression. ABA can positively
regulate the transcription of SOC1 through the action of the OXIDATIVE STRESS
2 ( OXS2 ) zinc-finger transcription factor family. These proteins are able bind in an
ABA-dependent manner the promoter of SOC1 and multiple mutants in the OXS2
family are late flowering, consistent with the proposed OXS2 role as activators of
flowering (Blanvillain et al. 2011 ).