Mitogen-Activated Protein Kinase Cascades in Plant Innate Immunity - PAMP Signals in Plant Innate Immunity: Signal Perception and Transduction - page 361

Zhang et al. 2007c , 2012c ; Shen et al. 2010 ; Jammes et al. 2011 ; Schikora et al.
2011 ; Hettenhausen et al. 2012 ), fungal (Wang et al. 2009 ; Shi et al. 2010 , 2011 ),
and oomycete (Zhang et al. 2007c ) diseases.
Pathogens secrete effectors to suppress the immune responses activated by PAMP
elicitors. The bacterial effectors AvrPto and AvrPtoB act as suppressors of early-
defense gene transcription and MAPK signaling. These effectors intercept multiple
PAMP-mediated signaling upstream of MAPKKK at the plasma membrane linked to
the receptor (He et al. 2006 ). The Pseudomonas syringae effector HopF2 shows
mono-ADP- ribosyltransferase activity and it inhibits the MAPKK MKK5 preventing
the phosphorylation of MPK3 and MPK6 in response to PAMP treatment (Wang et al.
2010 ). HopPtoD2 is the effector secreted by Pseudomonas syringae pv. tomato DC3000
and it possessed tyrosine phosphatase activity (Espinosa et al. 2003 ). A constitutively
active MAPK kinase, NtMEK2, is involved in triggering hypersensitive responses.
The effector HopPtoD2 suppressed the action of NtMEK2 in eliciting defense
responses. It has been suggested that inactivation of MAPK pathways is a virulence
strategy by the bacterial pathogen (Bretz et al. 2003 ; Espinosa et al. 2003 ).
HopF2 has been found to be a potent suppressor of early immune gene transcrip-
tion and mitogen-activated protein kinase signaling activated by multiple PAMPs,
including bacterial fl agellin, ef-Tu, peptidoglycan, lipopolysaccharide and HrpZ1
harpin, and fungal chitin (Wu et al. 2011 ). The conserved surface-exposed residues
of HopF2 may be essential for its PAMP suppression activity. HopF2 is targeted to
the plant plasma membrane through a putative myristoylation site, and the mem-
brane association appears to be required for its PAMP-suppression function (Wu
et al. 2011 ). These results suggest that HopF2 likely intercepts PAMP signaling
at the plasma membrane immediately of signal perception. Expression of HopF2
in transgenic plants compromised plant nonhost immunity to bacterial pathogen
P . syringae pv. phaseolicola and plant immunity to the fungal pathogen Botrytis
cinerea (Wu et al. 2011 ). HopF2 severely impairs PAMP-induced defenses and
render plants highly susceptible to nonpathogenic P . syringae bacteria (Wang et al.
2010 ). These results suggest that HopF2 plays important role in suppression of
function of multiple PAMP signaling.
A Pseudomonas syringae effector HopAI1 inactivates the MAPKs MPK3 and
MPK6 to suppress PAMP-induced immunity in plants (Zhang et al. 2007b ). HopAI1
inactivates MAPKs by removing the phosphate group from phosphothreonine
through phosphothreonine lyase activity. The inhibition of MAPKs by HopI1 sup-
presses transcriptional activation of PAMP response genes (Zhang et al. 2012c ). The
HopAI1 has been shown to inhibit MPK4, a negative regulator of defense responses.
The MEKK1-MKK1/MKK2-MPK4 cascade negatively regulates plant immune
responses (Kong et al. 2012 ). However, when the MAPK cascade is targeted by
HopAI1, it positively regulates the basal immunity, probably due to inhibition of
MPK4 by the effector (Zhang et al. 2012c ). P . syringae effector AvrB interacts with
and stimulates the activity of MPK4, a negative regulator of plant defense responses,
thereby perturbing hormone signaling and enhancing plant susceptibility (Cui et al.
2010 ). Collectively, these studies suggest that pathogens secrete effectors, which
suppress the action of MAPKs in triggering plant immune responses.