PAMP Signaling in Plant Innate Immunity - PAMP Signals in Plant Innate Immunity: Signal Perception and Transduction - page 107

Pathogen effectors recognized by NB-LRR proteins activate defense responses
similar to those activated by PAMPs. However, ETI generally activates them in a
more prolonged and robust fashion than PTI and usually includes the hypersensitive
response (HR) (Tsuda and Katagiri 2010 ). The PAMP- and effector- activated
signaling pathways include Ca 2+ fl uxes, MAP kinase cascade, ROS production, hor-
mone signaling network, and transcriptional reprogramming. The triggered plant
immune responses include accumulation of pathogenesis-related proteins, deposi-
tion of lignin and callose in the cell wall, and production of anti-microbial com-
pounds (Tsuda and Katagiri 2010 ; Gimenez-Ibanez and Rathjen 2010 ).

2.31 Effectors May Suppress PAMP-Triggered Immunity

2.31.1 Inhibition of PAMP-Triggered Immunity

Several pathogens are capable of delivering effector proteins into the host cell to
enhance virulence and these effectors often inhibit PAMP-triggered immunity (PTI)
(Göhre and Robatzek 2008 ; Song and Yang 2010 ; Szczesny et al. 2010 ; Zhang et al.
2010b ; Akimoto-Tomiyama et al. 2012 ). Some effectors may also suppress the
immune response induced by another effector produced by the same pathogen
(Szczesny et al. 2010 ). Some pathogens have acquired effectors to collectively over-
come PTI and ETI in their host plants (Zhang et al. 2010b ; Block and Alfano 2011 ).
The bacterial pathogen Pseudomonas syringae suppresses both PTI and ETI by the
injection of type III effector (T3E) proteins into host cells (Block and Alfano 2011 ).
Pathogens secrete several effectors (virulence factors, toxins) into the host cell and
suppress or disable PAMPs-induced signaling pathways. This results in effector-
triggered susceptibility (ETS) (Hauck and Thilmony 2003 ; Li et al. 2005a ; He et al.
2006 ; Jones and Dangl 2006 ; Nomura et al. 2006 ; Zhang et al. 2007a ; Göhre et al.
2008 ; Cui et al. 2009 ; Hogenhout et al. 2009 ; Wu et al. 2011 ).

2.31.2 Effectors May Degrade PRRs

Major function of effectors is to suppress PAMP-triggered defense responses. Some
effectors have been shown to degrade the PRRs and inhibit PAMP-triggered immunity.
Flagellin (fl g22) is the PAMP recognized in several bacterial pathogens including
Pseudomonas syringae pv. tomato . The PAMP fl g22 is perceived by the PRR FLS2
in Arabidopsis . AvrPtoB is the effector secreted by the bacterial pathogen. The
AvrPtoB associates with FLS2 through its N terminus and the interaction is enhanced
by the PAMP fl g22 activation. The effector AvrPtoB promotes degradation of the
PRR FLS2. The AvrPtoB has been recognized as an E3 ubiquitin ligase and it
structurally and functionally mimics E3 ubiquitin ligase (Janjusevic et al. 2006;
Abramovitch et al. 2006 ). The C-terminal region (residues 400-550) of AvrPtoB