Transcriptional Plasticity of Trichoderma atroviride in Response to Different Plant Pathogens
- 1Univ Angers, INRAE, Institut Agro, UMR 1345 IRHS, SFR 4207 QUASAV, Angers, France
Abstract
Fungal mycoparasitism is commonly viewed as a broadly conserved lifestyle relying on the secretion of cell wall-degrading enzymes and specialized metabolites. However, whether Trichoderma deploys a universal antagonistic program or dynamically adapts its molecular arsenal according to prey identity remains largely unknown. Here, we investigated the phenotypic and transcriptomic responses of four highly antagonistic Trichoderma atroviride strains confronted with damping-off pathogens from three phylogenetically distinct lineages: the ascomycete Alternaria brassicicola, the basidiomycete Rhizoctonia solani, and the oomycete Globisporangium ultimum. In vitro confrontation assays were performed between the four T. atroviride strains and nine pathogen strains (three strains per species). Despite notable intraspecific variation in pathogen sensitivity, all four T. atroviride strains remained highly effective against all tested pathogens. Comparative RNA-seq analyses during direct confrontation with one representative strain per pathogen species revealed strong prey-dependent transcriptional plasticity. Interactions with the two fungal pathogens elicited a robust induction of classical mycoparasitic machinery, including glycoside hydrolases, secreted peptidases, and effector-like proteins, whereas these responses were markedly attenuated in interaction with G. ultimum. Specialized metabolite biosynthetic genes were broadly induced across all interactions, but with largely distinct gene sets depending on the pathogen, with the strongest divergence observed for confrontation with G. ultimum. Beyond this shared response, each fungal pathogen also triggered a distinct host-specific program. In response to A. brassicicola and R. solani, T. atroviride induced distinct sets of genes associated with cell wall organization, while the response to R. solani specifically involved the activation of peroxisomal functions and aromatic amino acid biosynthesis pathways. Receptors potentially involved in pathogen perception also showed pathogen-dependent expression patterns, with distinct GPCRs (G protein-coupled receptors) overexpressed depending on the pathogen encountered. NLRs (NOD-like receptors) displayed a similar pattern, although overexpression was detected only in response to A. brassicicola and G. ultimum. Together, these results demonstrate that T. atroviride does not rely on a fixed mycoparasitic program but instead dynamically remodels its transcriptome according to prey identity, revealing a high degree of transcriptional plasticity underlying broad-spectrum antagonism.
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BibTeX
@misc{bremand2026transcriptional,
title = {{Transcriptional Plasticity of Trichoderma atroviride in Response to Different Plant Pathogens}},
author = {E. Bremand and F. Bastide and J. Colou and N. Denance and T. Guillemette},
howpublished = {bioRxiv},
year = {2026},
month = sep,
doi = {10.64898/2026.09.15.751736},
url = {https://www.biorxiv.org/content/10.64898/2026.09.15.751736v1},
note = {CC BY-NC},
}
RIS
TY - UNPB
TI - Transcriptional Plasticity of Trichoderma atroviride in Response to Different Plant Pathogens
AU - E. Bremand
AU - F. Bastide
AU - J. Colou
AU - N. Denance
AU - T. Guillemette
PY - 2026
DA - 2026/09/15
PB - bioRxiv
DO - 10.64898/2026.09.15.751736
UR - https://www.biorxiv.org/content/10.64898/2026.09.15.751736v1
AB - Fungal mycoparasitism is commonly viewed as a broadly conserved lifestyle relying on the secretion of cell wall-degrading enzymes and specialized metabolites. However, whether Trichoderma deploys a universal antagonistic program or dynamically adapts its molecular arsenal according to prey identity remains largely unknown. Here, we investigated the phenotypic and transcriptomic responses of four highly antagonistic Trichoderma atroviride strains confronted with damping-off pathogens from three phylogenetically distinct lineages: the ascomycete Alternaria brassicicola, the basidiomycete Rhizoctonia solani, and the oomycete Globisporangium ultimum. In vitro confrontation assays were performed between the four T. atroviride strains and nine pathogen strains (three strains per species). Despite notable intraspecific variation in pathogen sensitivity, all four T. atroviride strains remained highly effective against all tested pathogens. Comparative RNA-seq analyses during direct confrontation with one representative strain per pathogen species revealed strong prey-dependent transcriptional plasticity. Interactions with the two fungal pathogens elicited a robust induction of classical mycoparasitic machinery, including glycoside hydrolases, secreted peptidases, and effector-like proteins, whereas these responses were markedly attenuated in interaction with G. ultimum. Specialized metabolite biosynthetic genes were broadly induced across all interactions, but with largely distinct gene sets depending on the pathogen, with the strongest divergence observed for confrontation with G. ultimum. Beyond this shared response, each fungal pathogen also triggered a distinct host-specific program. In response to A. brassicicola and R. solani, T. atroviride induced distinct sets of genes associated with cell wall organization, while the response to R. solani specifically involved the activation of peroxisomal functions and aromatic amino acid biosynthesis pathways. Receptors potentially involved in pathogen perception also showed pathogen-dependent expression patterns, with distinct GPCRs (G protein-coupled receptors) overexpressed depending on the pathogen encountered. NLRs (NOD-like receptors) displayed a similar pattern, although overexpression was detected only in response to A. brassicicola and G. ultimum. Together, these results demonstrate that T. atroviride does not rely on a fixed mycoparasitic program but instead dynamically remodels its transcriptome according to prey identity, revealing a high degree of transcriptional plasticity underlying broad-spectrum antagonism.
ER -