Abstract
Phytopathogenic bacteria possess an arsenal of effector proteins that enable them to subvert host recognition and manipulate the host to promote pathogen fitness. The type III secretion system (T3SS) delivers type III-secreted effector proteins (T3SEs) from bacterial pathogens such as Pseudomonas syringae, Ralstonia solanacearum, and various Xanthomonas species. These T3SEs interact with and modify a range of intracellular host targets to alter their activity and thereby attenuate host immune signaling. Pathogens have evolved T3SEs with diverse biochemical activities, which can be difficult to predict in the absence of structural data. Interestingly, several T3SEs are activated following injection into the host cell. Here, we review T3SEs with documented enzymatic activities, as well as T3SEs that facilitate virulence-promoting processes either indirectly or through non-enzymatic mechanisms. We discuss the mechanisms by which T3SEs are activated in the cell, as well as how T3SEs modify host targets to promote virulence or trigger immunity. These mechanisms may suggest common enzymatic activities and convergent targets that could be manipulated to protect crop plants from infection.
Highlights
The outcome of plant–pathogen interactions is determined by a complex network of molecular events that involve proteins and other macromolecules from both the host and pathogen
pathogen-associated molecular patterns (PAMPs) recognition, pattern recognition receptors (PRRs) associate with additional transmembrane receptor-like kinase (RLK) such as BRI1ASSOCIATED RECEPTOR KINASE1 (BAK1) as well as receptor-like cytoplasmic kinases (RLCKs) to transduce an intracellular signal via mitogen-activated protein (MAP) kinase cascades for the activation of PAMP-triggered immunity (PTI) [4,5,6]
A large number of T3SEs are dedicated to the suppression of PTI by targeting PAMP perception and downstream kinase signaling cascades, cytoskeleton-mediated transport of defense-related cargo, phytohormone biosynthesis, and signaling pathways, as well as host gene expression
Summary
The outcome of plant–pathogen interactions is determined by a complex network of molecular events that involve proteins and other macromolecules from both the host and pathogen. PAMP recognition, PRRs associate with additional transmembrane RLKs such as BRI1ASSOCIATED RECEPTOR KINASE1 (BAK1) as well as receptor-like cytoplasmic kinases (RLCKs) to transduce an intracellular signal via mitogen-activated protein (MAP) kinase cascades for the activation of PAMP-triggered immunity (PTI) [4,5,6] This immune response involves transcriptional reprogramming, callose deposition in the cell wall, production of reactive oxygen species (ROS), and secretion of antimicrobial compounds, all of which serve to prevent an infection from becoming established. Faced with this defensive barrier, many phytopathogenic bacteria have evolved virulence effector proteins that are introduced into host cells via a needle-like structure known as a type III secretion system [7].
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