Metaeffector interactions modulate the type III effector-triggered immunity load of Pseudomonas syringae
Alexandre Martel1, Bradley Laflamme1, Clare Breit-McNally1
1Department of Cell and Systems Biology, University of Toronto, Toronto, Ontario, Canada.
Plos Pathogens
|May 16, 2022
Summary
Pseudomonas syringae bacteria use effector-effector interactions to suppress plant immunity (Effector-Triggered Immunity). This study reveals how these bacterial pathogens overcome host defenses by comparing effector repertoires and identifying specific suppression mechanisms.
Area of Science:
- Plant-microbe interactions
- Bacterial pathogenesis
- Plant immunity
Background:
- Pseudomonas syringae utilizes type III secreted effectors (T3SEs) for infection.
- Plant immunity involves Effector-Triggered Immunity (ETI) recognizing specific T3SEs.
- Pathogens must overcome ETI to cause disease, potentially through effector-effector interactions.
Purpose of the Study:
- To investigate how Pseudomonas syringae mitigates the load of ETI-eliciting T3SEs.
- To compare the ETI-elicitation profiles of divergent P. syringae strains (PtoDC3000 and PmaES4326).
- To identify metaeffector interactions that suppress ETI.
Main Methods:
- Screened 529 T3SE alleles from the P. syringae T3SE compendium (PsyTEC) on Arabidopsis thaliana Col-0.
- Compared ETI responses between P. syringae pv. tomato DC3000 and P. syringae pv. maculicola ES4326.
- Conducted ETI suppression screens to identify metaeffector roles.
Main Results:
- 69 T3SE alleles elicited ETI, with 19 differential responses between strains.
- Identified two novel ETI-eliciting families: AvrPto1 and HopT1.
- Discovered HopQ1a, HopG1c, and HopF1g suppress specific ETI responses, indicating metaeffector activity.
Conclusions:
- P. syringae strains possess distinct T3SE repertoires influencing ETI profiles.
- Metaeffector interactions play a crucial role in suppressing ETI, allowing pathogens to evade host defenses.
- Bacterial pathogens actively manage their effector load through suppression mechanisms to ensure successful infection.
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