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plant cells (White and Broadley
2003
). Rutschmann et al. (
2002
) observed the
apparent colocalization of the plasma membrane H
+
-ATPase and the tomato CDPK
in vivo, suggesting a potential role in the regulation of H
+
-ATPase pump activity by
Ca
2+
-induced CDPK.
Plasma membrane H
+
- ATPase has been reported to play important role in plant
innate immune responses. The early responses to the PAMP fl g22 treatment include
dynamic regulation of the plasma membrane H
+
- ATPases (Nuhse et al.
2007
;
Keinath et al.
2010
). Perception of fl g22 by the PRR FLS2 results in rapid membrane
depolarization and alkalinization of the apoplast, probably induced by inhibition of
H
+
- ATPases and activation of anion channels (Jeworutzki et al.
2010
). Calcium
infl ux at the plasma membrane occurs very rapidly after PAMP treatment and may
contribute to plasma membrane H
+
- ATPase regulation in plant cells during PAMP-
triggered immunity (Boller and Felix
2009
; Kim et al.
2010
). Stimulation of plasma
membrane ATPase activity induces the accumulation of salicylic acid (SA) and the
transcription of pathogenesis-related (PR) genes (Schaller and Oecking
1999
).
Stomatal closure is an immune response against bacterial pathogens. Bacterial
PAMPs induce stomatal closure, which is dependent on both SA- and abscisic acid
(ABA)-biosynthesis and associated signaling components (Melotto et al.
2006
;
Zhang et al.
2008
; Zeng and He
2010
). It has been reported that down-regulation of
plasma membrane H
+
- ATPase activity via ABA signaling system contributes to
PAMP-induced stomatal closure (Melotto et al.
2006
; Merlot et al.
2007
; Liu et al.
2009
; Elmore and Coaker
2011
).
4.7
Anion Channels in Ca
2+
Infl ux and Increase in [Ca
2+
]
cyt
Anion channels which mediate Cl
−
and NO
3
−
effl ux (Barbier-Brygoo et al.
2000
;
Vidhyasekaran
2007
) have been shown to be involved in defense signaling system.
Perception of fl g22 by the PRR FLS2 results in activation of anion channels
(Jeworutzki et al.
2010
). Activation of NO
3
−
effl ux has been shown to be dependent
on protein phosphorylation (Binet et al.
2001
; Wendehenne et al.
2002
). Protein
kinases act as positive regulators, while phosphatases negatively control the chain
of events leading to anion channel activity. Because of the outward-directed anion
gradients across the plasma membrane, the anion channels drive passive effl uxes
from the cytoplasm into the extracellular space (Wendehenne et al.
2002
). Anion
effl ux results in plasma membrane depolarization (Sanders et al.
2002
). Membrane
depolarization induces Ca
2+
infl ux across the plasma membrane (Thuleau et al.
1994
). It has also been shown that Ca
2+
infl ux may activate anion channels and
increases in cytoplasmic Ca
2+
activate anion channels (Ward et al.
1995
; Marten
et al.
2007
; Suh et al.
2007
). Cytoplasmic Ca
2+
elevation has been shown to result in
activation of S-type anion channels via phosphorylation (Schmidt et al.
1995
; Allen
et al.
1999
; Geiger et al.
2010
). The activated anion channels further intensify Ca
2+
infl ux which will pave the way for triggering Ca
2+
-mediated signaling system
(Fig.
4.3
).
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