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Type III effector diversification via both pathoadaptation and horizontal transfer in response to a coevolutionary
Wenbo Ma1, Frederick F T Dong, John Stavrinides
1Department of Cell and Systems Biology, University of Toronto, Toronto, Ontario, Canada.
The plant pathogen Pseudomonas syringae evolves defense-evading strategies through its HopZ proteins, driven by a coevolutionary arms race with host plants. This genetic diversity allows pathogens to maintain virulence while overcoming host immunity.
Area of Science:
- Evolutionary Biology
- Microbiology
- Plant Pathology
Background:
- The coevolutionary arms race between pathogens and hosts is crucial for understanding host-pathogen interactions.
- Type III secreted effector proteins play a key role in modulating host responses during infection.
Purpose of the Study:
- To investigate the molecular mechanisms and evolutionary progression of the HopZ effector protein family in Pseudomonas syringae.
- To understand how coevolutionary pressures shape the diversity and function of pathogen virulence factors.
Main Methods:
- Surveyed 96 P. syringae isolates to identify HopZ homologs.
- Sequenced and confirmed expression of HopZ alleles.
- Performed evolutionary analyses (PAML selection analysis) and functional assays.
Main Results:
- Identified three HopZ homologs (HopZ1, HopZ2, HopZ3) in 45% of strains.
- HopZ1 homologs are ancestral and diversified via mutation; HopZ2/HopZ3 were acquired through horizontal gene transfer.
- HopZ1 C-terminus is under positive selection, and all homologs possess cysteine-protease activity.
- Introduction of ancestral hopZ1 triggered host defense, unlike endogenous alleles, indicating functional divergence.
Conclusions:
- The P. syringae HopZ family diversifies through mutation and horizontal transfer, driven by host defense system selection.
- This genetic diversity enables pathogens to evade host immunity while retaining essential virulence functions.
- The evolution of HopZ impacts pathogen virulence and host range, highlighting the dynamic nature of host-pathogen coevolution.
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