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PAMP-triggered immunity (PTI) requires a signal transduction from receptors
to downstream components via the MAPK cascade and many of the known
PAMPs were shown to activate MAP kinases (Pitzschke et al.
2009a
,
b
). MAPK
signaling is activated by fl agellin in
Arabidopsis
(Wu et al.
2011
). The MAPK
module MEKK1-MKK4/MKK5-MPK3/MPK6 has been proposed to be respon-
sible for fl g22 signal transmission (Asai et al.
2002
). The involvement of MEKK1
in fl g22-induced MKK4/MKK5-MPK3/MPK6 signaling is unlikely, since
mekk1
mutant plants are compromised in fl g22-triggered activation of MPK4, but show
normal activation of MPK3 and MPK6 (Suarez-Rodriguez et al.
2007
). The
PAMP-induced FLS2 activation leads to activation of the MAP kinase pathways
MEKK4/5 and MPK3/6 and MEKK1-MKK1/2-MPK4, leading to transcription of
defense-related genes through the WRKY transcription factors WRKY22/29 and
WRKY25/33 (Nicaise et al.
2009
).
The fl agellin derived peptide fl g22 triggers a rapid and strong activation of
MPK3, MPK4 and MPK6 (Droillard et al. 2004). MPK3, MPK6, MKK4, and
MKK5 form a cascade that positively regulates plant defenses (Pitzschke et al.
2009a
). Flg22 activates the expression of
MPK3
in
Arabidopsis
(Denoux et al.
2008
). MPK3 has been shown to be required for camalexin accumulation upon
Botrytis cinerea
infection (Ren et al. 2008). MPK3 phosphorylates a plant VirE2-
interacting protein 1 (VIP1), a bZIP transcription factor (Liu et al.
2010
; Zhang and
Zhou
2010
). VIP1 is a direct target of the PAMP-induced MPK3. Upon phosphory-
lation by MPK3, VIP1 relocalizes from the cytoplasm to the nucleus and regulates
the expression of the
PR1
pathogenesis-related gene (Djamei et al.
2007
). The
MPK3 pathway is also involved in JA/ET signaling system (Takahashi et al.
2007
).
Inactivation of MPK3 and MPK6 by the
Pseudomonas syringae
effector HopA/1
and inactivation of MKKs by the
P
.
syringae
effector HopF2 severely impair PAMP-
induced defenses and render plants highly susceptible to nonpathogenic
P
.
syringae
bacteria (Zhang et al.
2007a
; Wang et al.
2010c
). The results suggest that activation
of MPK3 and MPK6 by the PAMP is an important component in plant immune
responses. A recent study has shown that fl g22 treatment increases expression of
another
MPK
gene,
MPK11
in
Arabidopsis
(Bethke et al.
2012
).
Flg22 induces the MAP kinase gene
MPK4
(Suarez-Rodriguez et al.
2007
;
Denoux et al.
2008
). The MPK4 suppresses SA accumulation but induces the JA
pathway (Brodersen et al. 2006). MPK4 interacts with its substrate MKS1; the latter
interacts with WRKY transcription factors WRKY25 and WRKY33 (Andreasson
et al.
2005
). MPK4, MKS1, and WRKY33 form a complex in the nucleus, and the
fl g22-induced MPK4 activation releases WRKY33 from the complex. This enables
WRKY33 to directly activate transcription of PAD3, which encodes a cytochrome
P450 involved in the phytoalexin camalexin biosynthesis (Qiu et al.
2008b
). MPK4,
its upstream MAP kinase kinases MKK1 and MKK2, and the MAP kinase kinase
kinase MEKK1 form a cascade that negatively regulates defenses in
Arabidopsis
because loss-of-function mutations in this cascade result in constitutive activation
of defenses (M
száros et al.
2006
; Suarez-Rodriguez et al.
2007
; Gao et al.
2008a
;
Qiu et al.
2008a
; Pitzschke et al.
2009b
).
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