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Fig. 4.1
Role of G protein-
ROS- Ca 2
+
-phosphorylation
in activation of Ca
2+
channels
PAMP
Activation
PRR
Activation
GTPase Rac
Phosphorylation
Phosphorylation
NADPH oxidase
Protein kinase
ROS
Ca
2+
permeable
channels
Feedback regulation
Opening of channels
Ca
2+
influx
Transient rise in cytosolic Ca
2+
4.2.3
Reactive Oxygen Species (ROS) Regulate Ca
2+
Infl ux
Reactive oxygen species (ROS) may regulate Ca
2+
infl ux through plasma membrane
transport proteins (Mori and Schroeder
2004
; Laohavisit et al.
2012
). Elicitor-
induced H
2
O
2
participates in [Ca
2+
]
cyt
increase, probably through the activation of
H
2
O
2
- sensitive Ca
2+
channels located in the plasma membrane (Lecourieux et al.
2002
). H
2
O
2
triggers calcium infl ux in tobacco (Takahashi et al.
1998
; Kawano and
Muto
2000
). An external stimulus, such as PAMP, increases activity of NADPH
oxidase which is involved in ROS production. Activation of the plasma membrane-
localized NADPH oxidase involves phosphorylation of two N-terminal Ser by a
calcium-dependent protein kinase as well as interaction with GTPase. NADPH
phosphorylation as well as binding to calcium synergizes NADPH activation
(Ogasawara et al.
2008
; Takeda et al.
2008
; Petry et al.
2010
). The increased activity
of NADPH oxidases induces ROS production. The ROS activates hyperpolariza-
tion- activated Ca
2+
infl ux current (Pei et al.
2000
; Foreman et al.
2003
). H
2
O
2
may
also be produced indirectly by producing more NADPH by means of Ca
2+
/
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