ABA Signal Perception and ABA Receptors - Abscisic Acid: Metabolism, Transport and Signaling - page 94

Fig. 6.1 Proposed model for the functional mechanisms of ABAR. a A model in which ABAR
antagonizes WRKY40 transcription repressor to relieve ABA-responsive genes of inhibition
[modified from Shang et al. ( 2010 ) and Zhang et al. ( 2014 )]. WRKY40 negatively regulates ABA
signaling and inhibits expression of ABA-responsive genes, such as ABA-responsive transcrip-
tion factors (ABFs) including ABI4 and ABI5 . High level of ABA promotes ABAR-WRKY40
interaction and activates an unknown factor or signaling cascade to downregulate WRKY40
expression. Decrease of WRKY40 relieves ABI4 and ABI5 genes of inhibition. This ABAR-
WRKY40 coupled mechanism is inhibited by CPN20, which interacts with ABAR tightly at low
ABA level, competitively attenuating the interaction between ABAR and WRKY40. High level
of ABA inhibits the ABAR-CPN20 interaction, which in turn promotes the ABAR-WRKY40
interaction to trigger the downstream signaling to repress WRKY40 expression and finally
to induce physiological responses. b A model for the ABAR-mediated signaling network. In
addition to the ABAR/CPN20-WRKY40-ABI5-linked signaling as mentioned in the Figure a,
SOAR1 is involved in the ABAR-mediated signaling downstream of ABAR and upstream of
ABI5. See detailed explanation in the text. Arrows denote positive regulation or activation and
bars negative regulation or repression. The solid lines indicate direct effect, and dotted lines indi-
cate indirect effect or yet unknown mechanism. Question mark indicates unconfirmed link
regulator of ABA signaling (Mei et al. 2014 ). The intensity of the ABA overly
sensitive phenotypes of the two SOAR1 -knockdown mutants soar1 - 2 and soar1 -
3 is similar to, or stronger than, that of the well-characterized abi1 abi2 dou-
ble-knockout mutant. The intensity of the ABA-insensitive phenotypes of the
SOAR1 -overexpressing lines is much stronger than that of the abi1 - 1 dominant
mutant, abi4 , abi5 loss-of-function mutants and a strong ABI2 -overexpressing line
(Mei et al. 2014 ). Surprisingly, the seeds of the SOAR1 -overexpressors germinate
and their post-germination seedlings continue to grow in the medium containing
>200 ʼ M ()ABA (Mei et al. 2014 ). Previous studies reported that the seeds of
the srk2dei mutant, triple-knockout mutant of three SnRK2 members SnRK2.2,
SnRK2.3, and SnRK2.6, germinate and continue to grow in the presence of 50- or
100- ʼ M exogenous ABA, which is believed to completely impair ABA response
(Fujii and Zhu 2009 ; Nakashima et al. 2009 ; Umezawa et al. 2009 ). In this regard,