Protein Kinases and Phosphatases Involved in ABA Signaling - Abscisic Acid: Metabolism, Transport and Signaling - page 144

Arabidopsis identified SnRK2.2 and SnRK2.3, two SnRK members most closely
related to SnRK2.6 (Hrabak et al. 2003 ), as key positive regulators of ABA signal-
ing: The snrk2.2 and 2.3 single mutants show weak, while the snrk2.2 / 2.3 double
mutant exhibits strong ABA-insensitive phenotypes in terms of seed germination
and seedling growth (Fujii et al. 2007 ). Thus, SnRK2.2 and SnRK2.3 function
redundantly in ABA-induced inhibition of seed germination and postgermination
growth (Fujii et al. 2007 ). These results led to a hypothesis of functional segre-
gation between SnRK2.6 and SnRK2.2/2.3, i.e., SnRK2.6 functions in guard
cells, whereas SnRK2.2 and SnRK2.3 specialize in seed germination and seed-
ling growth regulation (Fujii et al. 2007 ). However, further investigations found
that, in the snrk2.2 / 3 / 6 triple mutant, nearly all major ABA responses are blocked
(Fujii and Zhu 2009 ; Nakashima et al. 2009 ; Fujita et al. 2009 ), demonstrating that
these functionally segregated kinases SnRK2.2, SnRK2.3, and SnRK2.6 still work
redundantly in ABA regulation of guard cells, seed germination, and seedling
growth, acting together as a core signaling point in ABA-signaling pathways. The
expression profile of the three SnRK genes supports their redundant, cooperative
roles in the major ABA responses: SnRK2.6 is expressed not only in guard cells,
but also in several other tissues, and SnRK2.2 and SnRK2.3 are expressed in all tis-
sues (Fujii et al. 2007 , 2011 ).
Other members of the Arabidopsis SnRK2 subfamily are likely to play roles
in ABA and/or stress signaling. Loss-of-function mutations in two other closet
homologous SnRK genes, SnRK2.7 and SnRK2.8 , affect expression of ABA-
and drought-responsive genes, suggesting their potential roles in ABA signal-
ing, though the snrk2.7/2.8 double mutant shows wild-type phenotypes probably
because of functional redundancy (Mizoguchi et al. 2010 ). Fujii et al. ( 2011 ) gen-
erated an Arabidopsis decuple mutant carrying mutations in all 10 members of the
SnRK2 subfamily, snrk2.1/2/3/4/5/6/7/8/9/10 and observed that this mutant grows
poorly under hyperosmotic stress conditions but is similar to the wild type in the
absence of osmotic stress, revealing critical functions of the SnRK2s in osmotic
stress signaling and tolerance.
8.3.3.3 Downstream Targets and Functional Mechanism of
Arabidopsis SnRK2S
The Arabidopsis SnRK2s, like PKABA1 and AAPK (as mentioned earlier) as
well as SnRK1s, phosphorylate downstream targets to mediate ABA signal-
ing (Zhang et al. 2008 , and also see test above). SnRK2s have been shown
to phosphorylate and activate ABA-responsive bZIP transcription factor
ABFs(ABF1-ABF4 and ABI5)and regulate ABA-responsive genes to medi-
ate ABA signaling(Boudsocq et al. 2004 ; Kobayashi et al. 2004 ; Furihata et al.
2006 ; Yoshida et al. 2006b ; Fujii et al. 2007 ; Fujii and Zhu 2009 ; Fujii et al.
2009 ). In addition to the ABFs, guard cell anion channel SLAC1 was identi-
fied as a substrate of the SnRK2.6/OST1, and the inward K + channel is also
likely to be a substrate of SnRK2.6 (Lee et al. 2009 , 2013 ; Geiger et al. 2009 ,