Global population genomics and pangenome of the clubroot pathogen link clonal expansion and effector diversification to resistance breakdown in canola
Abstract
Clubroot disease, caused by the obligate biotrophic protist Plasmodiophora brassicae, threatens Brassica crops worldwide. Novel pathogen virulence frequently breaks resistance in agricultural crops, and yet explanations for isolate evolution remain unknown. We combined whole genome sequencing of 192 isolates from 24 countries with a pangenome analysis of 55 high-quality complete or nearly complete genome assemblies and performed functional effector analyses to investigate potential mechanisms of virulence emergence. Three major phylogenetic clusters were identified, including two highly clonal lineages with contrasting virulence profiles, and a genetically diverse population retaining signatures of recombination. Our findings support a model in which genome-wide purifying selection maintained core genome integrity, while effector genes evolved under less constraint. Despite a compact closed pangenome, we identified chromosome 17 as a major hotspot of single nucleotide and structural variations, transposable elements and expansion of ankyrin repeat effectors. Within the variable chromosome 17, PbAnk2 alleles from virulent and avirulent isolates encoded proteins with distinct predicted structures. PbAnk2 interacted with the Arabidopsis co-chaperone DJC31 in yeast two-hybrid and BiFC assays, whereas co-immunoprecipitation did not detect an interaction for the allele found in isolates that break CRa-mediated resistance, suggesting that allelic variation may alter PbAnk2's association with DJC31. These findings reveal the clonal expansion of virulent isolates and connect it to effector diversification that led to resistance breakdown and establish a genomic framework for pathogen surveillance and durable clubroot resistance.
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BibTeX
@misc{javed2026global,
title = {{Global population genomics and pangenome of the clubroot pathogen link clonal expansion and effector diversification to resistance breakdown in canola}},
author = {M. A. Javed and F. Sylvestre and S. M. Velasco Cuervo and S. Mukhopadhyay and R. Salih and A.-S. Brochu and E. I. Fantino and J. Wu and T. Marten Heick and A. Schwelm and Y. Aigu and L. Galindo-Gonzalez and S.-F. Hwang and P. Hellin and M. L. T. Rastas and N. Zamani-Noor and G. Cordsen Nielsen and R. Kiiker and L. Alden and A. Ficke and A. Mäe and D. Riquelme Toledo and A. T. Phan Lam and S.-i. Ito and C. A. dos Santos and M. Gorete Ferreira do Carmo and U. Miersch and G. Chongo and J. Jacobs and M. A. Campbell and P. Tobias and J. Downs and S. Choi and B. N. Kaiser and M. Prokchorchik and S. Strelkov and E. Perez-Lopez},
howpublished = {bioRxiv},
year = {2026},
month = oct,
doi = {10.64898/2026.10.14.759018},
url = {https://www.biorxiv.org/content/10.64898/2026.10.14.759018v1},
note = {CC BY-NC-ND},
}
RIS
TY - UNPB
TI - Global population genomics and pangenome of the clubroot pathogen link clonal expansion and effector diversification to resistance breakdown in canola
AU - M. A. Javed
AU - F. Sylvestre
AU - S. M. Velasco Cuervo
AU - S. Mukhopadhyay
AU - R. Salih
AU - A.-S. Brochu
AU - E. I. Fantino
AU - J. Wu
AU - T. Marten Heick
AU - A. Schwelm
AU - Y. Aigu
AU - L. Galindo-Gonzalez
AU - S.-F. Hwang
AU - P. Hellin
AU - M. L. T. Rastas
AU - N. Zamani-Noor
AU - G. Cordsen Nielsen
AU - R. Kiiker
AU - L. Alden
AU - A. Ficke
AU - A. Mäe
AU - D. Riquelme Toledo
AU - A. T. Phan Lam
AU - S.-i. Ito
AU - C. A. dos Santos
AU - M. Gorete Ferreira do Carmo
AU - U. Miersch
AU - G. Chongo
AU - J. Jacobs
AU - M. A. Campbell
AU - P. Tobias
AU - J. Downs
AU - S. Choi
AU - B. N. Kaiser
AU - M. Prokchorchik
AU - S. Strelkov
AU - E. Perez-Lopez
PY - 2026
DA - 2026/10/14
PB - bioRxiv
DO - 10.64898/2026.10.14.759018
UR - https://www.biorxiv.org/content/10.64898/2026.10.14.759018v1
AB - Clubroot disease, caused by the obligate biotrophic protist Plasmodiophora brassicae, threatens Brassica crops worldwide. Novel pathogen virulence frequently breaks resistance in agricultural crops, and yet explanations for isolate evolution remain unknown. We combined whole genome sequencing of 192 isolates from 24 countries with a pangenome analysis of 55 high-quality complete or nearly complete genome assemblies and performed functional effector analyses to investigate potential mechanisms of virulence emergence. Three major phylogenetic clusters were identified, including two highly clonal lineages with contrasting virulence profiles, and a genetically diverse population retaining signatures of recombination. Our findings support a model in which genome-wide purifying selection maintained core genome integrity, while effector genes evolved under less constraint. Despite a compact closed pangenome, we identified chromosome 17 as a major hotspot of single nucleotide and structural variations, transposable elements and expansion of ankyrin repeat effectors. Within the variable chromosome 17, PbAnk2 alleles from virulent and avirulent isolates encoded proteins with distinct predicted structures. PbAnk2 interacted with the Arabidopsis co-chaperone DJC31 in yeast two-hybrid and BiFC assays, whereas co-immunoprecipitation did not detect an interaction for the allele found in isolates that break CRa-mediated resistance, suggesting that allelic variation may alter PbAnk2's association with DJC31. These findings reveal the clonal expansion of virulent isolates and connect it to effector diversification that led to resistance breakdown and establish a genomic framework for pathogen surveillance and durable clubroot resistance.
ER -