Agriculture Reference
In-Depth Information
The
Arabidopsis
cpk3
and
cpk6
show ABA-insensitive phenotypes in ABA-
induced stomatal closure, and the
cpk3 cpk6
double mutant shows stronger ABA-
insensitive stomatal phenotypes and Ca
2
+
-insensitive phenotypes in Ca
2
+
-induced
stomatal closure (Mori et al.
2006
). However,
cpk21
and
cpk23
single mutants do
not exhibit any stomatal phenotype in response to ABA (Geiger et al.
2010
,
2011
).
This suggests that AtCPK3 and AtCPK6 may play a more global role in regula-
tion of the ion fluxes involved in ABA-induced stomatal closure. At the whole-
plant level, overexpression of
AtCPK6
enhances salt- and drought stress tolerance,
whereas no altered stress tolerance is evident in the
cpk6
mutant line (Xu et al.
2010
), suggesting a functional redundancy among AtCPK6 and other CDPKs to
mediate stress signaling. Surprisingly,
cpk21
and
cpk23
mutants are drought toler-
ant, whereas overexpression of
AtCPK21
or
AtCPK23
results in plant oversensi-
tivity to drought or osmotic stress (Ma and Wu
2007
; Franz et al.
2011
), though
AtCPK21 and AtCPK23, functioning as ABA-induced, Ca
2
+
-dependent activa-
tors of SLAC-type anion currents as described above, should positively regulate
ABA-induced stomatal closure, and thus, one may expect that the
cpk21
and
cpk23
mutant decrease, but the
AtCPK21
- or
AtCPK23
overexpressors increase the ABA
sensitivity of stomatal movement and tolerance to drought. These opposite effects
in different levels (or between short-term response in the guard cells and long-term
response at the tissue or whole-plant level) suggest a high complexity of plant
stress signaling network where a sophisticated balance between positive and nega-
tive roles at the whole-plant level results in a final, physiological output.
CDPKs may also function to inhibit K
+
inward channels, such as KAT1, to
regulate ABA-induced stomatal closure. It has been reported that loss of function
of the
Arabidopsis CPK10
gene reduced ABA response in stomatal closure by
downregulating the ABA-induced inhibition of K
+
inward channels in guard cells,
suggesting that AtCPK10 may regulate KAT1 to mediate Ca
2
+
-dependent ABA
signaling in guard cells (Zou et al.
2010
). However, AtCPK4 and AtCPK11 are
important components of ABA signaling in guard cells, and the loss-of-function
mutants
cpk4
and
cpk11
display ABA-insensitive phenotypes in ABA-induced sto-
matal closure (Zhu et al.
2007
), but it remains unclear whether these two CDPKs
are involved in the Ca
2
+
-dependent activation of the ion channels in guard cells in
response to ABA, which merits further studies.
8.2.4 CDPKs and ABA Signaling: A Summary
CDPKs are versatile and evolutionarily conserved Ca
2
+
sensors that function as
central regulators of Ca
2
+
-mediated ABA and stress responses that are crucial for
plant survival. Recent advances have identified some key players in ABA sign-
aling, including AtCPK3, AtCPK4, AtCPK6, AtCPK10, AtCPK11, AtCPK12,
AtCPK21, AtCPK23, AtCPK32, OsCPK12, OsCPK21, and ZmCPK11, which
may function as crucial signaling nodes in ABA-signaling network. A broad range
of characteristics of CDPKs indicate complex and sophisticated Ca
2
+
-signaling
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