Embedded Files
Experimental dissection and genomic characterization of bacterial plant pathogen emergence
Experimental dissection and genomic characterization of bacterial plant pathogen emergence
How do bacterial plant pathogens evolve to evade immune detection and infect (formerly) resistant hosts?
How do bacterial plant pathogens evolve to evade immune detection and infect (formerly) resistant hosts?
Supervised by Professor Marcus Dillon at the University of Toronto Department of Ecology and Evolutionary Biology, I sought to understand how bacterial plant pathogens evolve on resistant hosts to evade immune detection and thereby improve their in planta fitness.
Infected leaves from 8 different plants from an evolved lineage. Chlorosis (yellowing of leaves) is a disease symptom of P. syringae. Leaves are quite yellow, indicating high virulence of this lineage.
To approach this problem, I conducted an in planta evolution experiment by serially passaging the globally significant bacterial plant pathogen Pseudomonas syringae pv. maculicola str. YM7930 through the model plant host Arabidopsis thaliana, which is able to resist it, and I monitored phenotypic changes through time. I observed rapid evolution: within just 5 infections, the average P. syringae emerged as a strong pathogen.
But how did it evolve so quickly? What was driving such rapid host adaptation? I dove into the genomics of the ancestral strain to find out.
In planta concentration, as a measure of virulence, over evolutionary time. Grey lines represent independently evolved lineages, red line indicates the average across all lineages at each timepoint with standard error in dashed red. Dashed black line indicates our “strong pathogen” cutoff, based on data we collected from highly virulent P. syringae strains. Within just 5 weeks, we see the average lineage emerges as a strong pathogen.
How does the genomic context of virulence factors influence pathogen evolution?
How does the genomic context of virulence factors influence pathogen evolution?
Genomic context refers to the content around a gene within the genome. This can be RNA loci, noncoding sequences, or protein-coding genes, as well as nucleotide content (e.g. GC %). Genomic context of virulence factors is critical to understanding their evolution, as virulence factor loss and acquisition are some of the most important mechanisms of host adaptation for pathogens. Genomic context can inform the rate of genomic flux (i.e. how readily a region of the genome is gained or lost). For instance, genomic islands (regions of the genome that can be readily excised from the genome, circularized and maintained as a pseudo-plasmid, then lost or re-integrated back into the genome) are common mechanisms of horizontal transfer of virulence factors. In this case, virulence factors can be rapidly gained or lost, which facilitates rapid host adaptation.
In P. syringae, there’s an important virulence factor called hopAR1 that limits the pathogenicity of some P. syringae strains on A. thaliana because HopAR1 is recognized by the A. thaliana resistance gene RPS5. In some P. syringae lineages, HopAR1 is present in a genomic island. I identified a putative prophage island in the ancestral strain of my evolution experiment that bears HopAR1. However, surprisingly, I found that the prophage island was not lost through evolutionary time. Instead, there were several other SNPs that seem to contribute to host adaptation. Check out my publication, Newfeld et al. (2025) Mol. Plant Pathol. for more info.
P. syringae core genome phylogeny with coloured bars indicating hopAR1a allele. Some distributions match the core genome phylogeny (e.g. hopAR1c in green) while others are distributed across the phylogeny (e.g. hopAR1b in yellow).
Google Sites
Report abuse