Major effector loss reveals compensatory pathogenicity networks in a necrotrophic wheat pathogen
- 1Centre for Crop and Disease Management, School of Molecular and Life Sciences, Curtin University, Perth, Australia
Abstract
Necrotrophic effectors (NEs) are key determinants of virulence in the necrotrophic fungal pathogen Parastagonospora nodorum that causes septoria nodorum blotch of wheat. However, targeted removal of three important NEs SnToxA, SnTox1, and SnTox3 in the mutant{Delta} toxa13 previously revealed a redundancy mechanism is triggered, whereby pathogenicity on wheat is maintained. In this study, we investigated the gene regulatory profile underpinning this phenomenon and discover that virulence is not dependent on a fixed set of dominant effectors but instead arises from a flexible, epistatic compensatory network. Although host transcriptional responses to the P. nodorum wildtype SN15 and{Delta} toxa13 infection remained largely conserved, consistent with an overlapping disease-susceptibility pathway, a significant upregulation of candidate effector genes was observed in{Delta} toxa13. This included the recently characterised NE SnTox267, and several other candidate effectors able to induce necrosis in the non-host Nicotiana benthamiana, each carrying a predicted structural fold conserved across other pathogens. We therefore provide further direct evidence that virulence is maintained in P. nodorum lacking three NEs by an epistatic and compensatory effector network, underpinned by changes in pathogen gene expression. Targeting conserved effector-mediated virulence mechanisms rather than individual host-specific gene-for-gene interactions may provide a more tractable route to host resistance.
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BibTeX
@misc{morikawa2026major,
title = {{Major effector loss reveals compensatory pathogenicity networks in a necrotrophic wheat pathogen}},
author = {S. Morikawa and C. J. Verdonk and L. V. Lenzo and H. T. T. Phan and E. Furuki and K. Gagalova and J. W. Debler and C. J. Turo and C. Mousley and E. John and B. Henares and K.-C. Tan},
howpublished = {bioRxiv},
year = {2026},
month = sep,
doi = {10.64898/2026.09.14.751338},
url = {https://www.biorxiv.org/content/10.64898/2026.09.14.751338v1},
note = {CC BY-NC-ND},
}
RIS
TY - UNPB
TI - Major effector loss reveals compensatory pathogenicity networks in a necrotrophic wheat pathogen
AU - S. Morikawa
AU - C. J. Verdonk
AU - L. V. Lenzo
AU - H. T. T. Phan
AU - E. Furuki
AU - K. Gagalova
AU - J. W. Debler
AU - C. J. Turo
AU - C. Mousley
AU - E. John
AU - B. Henares
AU - K.-C. Tan
PY - 2026
DA - 2026/09/14
PB - bioRxiv
DO - 10.64898/2026.09.14.751338
UR - https://www.biorxiv.org/content/10.64898/2026.09.14.751338v1
AB - Necrotrophic effectors (NEs) are key determinants of virulence in the necrotrophic fungal pathogen Parastagonospora nodorum that causes septoria nodorum blotch of wheat. However, targeted removal of three important NEs SnToxA, SnTox1, and SnTox3 in the mutant{Delta} toxa13 previously revealed a redundancy mechanism is triggered, whereby pathogenicity on wheat is maintained. In this study, we investigated the gene regulatory profile underpinning this phenomenon and discover that virulence is not dependent on a fixed set of dominant effectors but instead arises from a flexible, epistatic compensatory network. Although host transcriptional responses to the P. nodorum wildtype SN15 and{Delta} toxa13 infection remained largely conserved, consistent with an overlapping disease-susceptibility pathway, a significant upregulation of candidate effector genes was observed in{Delta} toxa13. This included the recently characterised NE SnTox267, and several other candidate effectors able to induce necrosis in the non-host Nicotiana benthamiana, each carrying a predicted structural fold conserved across other pathogens. We therefore provide further direct evidence that virulence is maintained in P. nodorum lacking three NEs by an epistatic and compensatory effector network, underpinned by changes in pathogen gene expression. Targeting conserved effector-mediated virulence mechanisms rather than individual host-specific gene-for-gene interactions may provide a more tractable route to host resistance.
ER -