Plant targets for Pseudomonas syringae type III effectors: virulence targets or guarded decoys?

Abstract

The phytopathogenic bacterium Pseudomonas syringae can suppress both pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) and effector-triggered immunity (ETI) by the injection of type III effector (T3E) proteins into host cells. T3Es achieve immune suppression using a variety of strategies including interference with immune receptor signaling, blocking RNA pathways and vesicle trafficking, and altering organelle function. T3Es can be recognized directly or indirectly by resistance proteins monitoring specific T3E targets resulting in ETI. It is presently unclear whether the monitored targets represent bona fide virulence targets or guarded decoys. Extensive overlap between PTI and ETI signaling suggests that T3Es may suppress both pathways through common targets and by possessing multiple activities.

Effector Biology of Plant-Associated Organisms: Concepts and Perspectives

“…Bacterial plant pathogens need to combat plant immunity elicited by conserved patterns such as flagellin and the elongation factor thermo unstable (EF-Tu). Therefore, many of the bacterial type-III effectors suppress plant immunity, particularly the signaling pathways triggered by flagellin and EF-Tu (Block and Alfano 2011). Similarly, fungal plant pathogens have evolved effectors that disable the immune pathway triggered by the cell wall molecule chitin (de Jonge et al 2011).…”

The Pseudomonas syringae Type III Effector AvrRpt2 Promotes Pathogen Virulence via Stimulating Arabidopsis Auxin/Indole Acetic Acid Protein Turnover

“…Sequencing and genetic studies have identified many key pathogenicity and virulence determinants in P. syringae, including global virulence regulators, the type III secretion system, phytotoxins, and exopolysaccharides (Buell et al, 2003). The type III secretion system mediates the delivery of a plethora of effector proteins into host cells, where they sabotage host immune responses and physiology to favor pathogen survival and multiplication in susceptible plants and trigger defense responses in resistant plants (Mudgett, 2005;Göhre and Robatzek, 2008;Büttner and He, 2009;Block and Alfano, 2011;Feng and Zhou, 2012;Lindeberg et al, 2012). Much progress has been made toward understanding the virulence functions of individual effectors in promoting pathogenicity.…”

“…Much progress has been made toward understanding the virulence functions of individual effectors in promoting pathogenicity. In particular, many type III effectors are able to interfere with or suppress host immunity by directly hijacking key components in PTI signaling (Mudgett, 2005;Göhre and Robatzek, 2008;Büttner and He, 2009;Block and Alfano, 2011;Feng and Zhou, 2012;Lindeberg et al, 2012). However, it is much less understood how these effectors modulate host physiology to favor infection.…”

Pseudomonas syringae naturally lacking the canonical type III secretion system are ubiquitous in nonagricultural habitats, are phylogenetically diverse and can be pathogenic

“…By delivering effectors that suppress the defense mechanisms of hosts (Hueck, 1998;Cornelis and Van Gijsegem, 2000;Block and Alfano, 2011), it contributes to creating more favorable conditions for bacterial multiplication in the host. The functions and evolutionary origins of this secretion system have been intensively explored because of its critical role in pathogenicity (Troisfontaines and Cornelis, 2005).…”