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depolarization of the membrane electrical potential (Huang et al.
1994
; White
2000
,
2004
). Membrane depolarization may be due to the activation of anion channels
(Sanders et al.
2002
; Jeworutzki et al.
2010
). Anion effl ux results in plasma
membrane depolarization, which in turn triggers the activation of voltage-depen-
dent Ca
2+
channels that mediate Ca
2+
infl ux (Ward et al.
1995
).
Application of the PAMPs fl g22 and elf18 induced rapid dose-dependent mem-
brane potential depolarizations and pronounced anion currents in
Arabidopsis thali-
ana
. The depolarization was superimposed by an increase in cytosolic calcium that
was indispensable for depolarization. The early immune signaling events induced
by the PAMPs fl g22 and elf18 were found to involve Ca
2+
-associated opening of
plasma membrane anion channels (Jeworutzki et al.
2010
). The elicitor-induced
Ca
2+
infl ux is inhibited by different anion-channel blockers (Ward et al.
1995
; Ebel
and Mithofer
1998
). It suggests that anion fl ux precedes and controls Ca
2+
infl ux.
The anion channels may initiate and amplify plasma membrane depolarization,
which in turn may activate Ca
2+
voltage-dependent channels.
It has also been reported that Ca
2+
infl ux is a prerequisite for the activation of
plasma membrane anion channels in several systems (Ward et al.
1995
; Jabs et al.
1997
; Wendehenne et al.
2002
). In cryptogein-treated tobacco cells, the major cal-
cium infl ux did not result from plasma membrane depolarization. Instead, the Ca
2+
infl ux occurred upstream and it triggered anion effl ux and plasma membrane depo-
larization, which in turn may mobilize some Ca
2+
voltage-dependent channels
(Pugin et al.
1997
; Wendehenne et al.
2002
). Collectively these results suggest that
initial Ca
2+
-infl ux may be through some voltage-dependent channels, independent
of anion effl ux and subsequent activation of Ca
2+
infl ux may be through the anion
effl ux-activated voltage-dependent channels.
The outward-rectifying K
+
channels found in the plasma membrane of plant cells
are also Ca
2+
-permeable depolarization-activated channels. These Ca
2+
-permeable
outward rectifying K
+
channels activate signifi cantly at voltages more positive than
about −50 mV under most physiological conditions and catalyze a large K
+
effl ux
simultaneously with a small Ca
2+
infl ux (White and Broadley
2003
). These channels
may play a role in the initial Ca
2+
infl ux into the cytosol.
The rice two-pore channel1 (OsTPC1) is a putative voltage-gated Ca
2+
-permeable
channel (Kurusu et al.
2005
; Hamada et al.
2012
). Overexpression of
OsTPC1
induced several defense-related signaling systems, resulting in induction of oxida-
tive burst and activation of a mitogen-activated protein kinase and hypersensitive
cell death. Retrotransposon-insertional mutagenesis of
OsTPC1
resulted in suppres-
sion of activation of the MAP kinase and hypersensitive-related cell death (Kurusu
et al.
2005
). The OsTPC1 has been shown to play a critical role in hypersensitive
cell death induced by a fungal xylanase protein (TvX) elicitor in suspension-cultured
rice cells (Hamada et al.
2012
). TvX induced a prolonged increase in cytosolic Ca
2+
,
mainly due to a Ca
2+
infl ux through the plasma membrane. TvX induced production
of major diterpenoid phytoalexins and the expression of diterpene cyclase genes
involved in phytoalexin biosynthesis (Hamada et al.
2012
). These results suggest
that the Ca
2+
-permeable voltage-gated channels may act as key regulators of defense
signaling system.
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