Biology subjects

Tom, C.

Publications and source records attributed to Tom, C..

4 recordsLinked to original sources

bioRxiv2026

Host-Botrytis co-transcriptomics reveals finely tuned interactions with closely related legumes

Generalist pathogens infect diverse plant hosts, yet how these interactions differ across hosts is poorly understood. Here, we conduct a molecular analysis of a generalist pathogen interacting with closely related hosts. A co-transcriptomic framework is used to dissect host-pathogen interactions between the generalist necrotroph Botrytis cinerea and two closely related legume hosts, common bean (Phaseolus vulgaris) and cowpea (Vigna unguiculata). Using a diverse set of 72 Botrytis isolates, we quantified lesion development alongside host and pathogen gene expression. Although lesion formation was driven primarily by pathogen genetic variation, transcriptomic responses in both host and pathogen exhibited significant host x isolate interactions. This indicated that extensive, fine-scale transcriptional plasticity created similar disease outcomes. Botrytis genes showing host-specific expression were enriched for cell wall-modifying enzymes and some specialized metabolic genes, indicating greater host responsiveness of these core virulence mechanisms than previously appreciated. Co-expression network analysis in both host and pathogen further showed that in both organisms, gene membership for individual networks are restructured in response to genetic diversity. For example in Botrytis, we identify different sets of genes host-dependently co-expressing with a non-ribosomal peptide synthetase (NRPS) gene cluster, suggesting divergent functional deployment of the same virulence machinery across closely related hosts. Both legume species exhibited extensive isolate-dependent transcriptional reprogramming, with approximately two-thirds of expressed host genes responding to pathogen diversity. While conserved defense pathways such as jasmonate/ethylene signaling and phenylpropanoid metabolism were upregulated in both hosts, the specific genes in the networks differed markedly, highlighting lineage-specific rewiring of defense strategies. These results suggest that generalist pathogen success is underpinned by pervasive gene expression plasticity in both host and pathogen, allowing similar phenotypic outcomes to emerge from highly divergent molecular states. SummaryO_LIGeneralist pathogens infect diverse plant hosts, yet how these interactions differ across hosts is poorly understood. This study investigates how a generalist pathogen achieves successful infection across closely related hosts, and how these hosts respond. C_LIO_LIA co-transcriptomic approach was applied to interactions between 72 genetically diverse isolates of the fungal necrotroph Botrytis cinerea and two legume hosts, common bean and cowpea. Lesion development and host and pathogen gene expression were quantified. C_LIO_LILesion formation was primarily driven by pathogen genetic variation, yet both host and pathogen transcriptomes showed strong host x isolate interactions. Both host and pathogen balance conserved responses with finely tuned, host-specific mechanisms. Further, host-dependent transcriptional responses involve network modulation around a common core of genes in both host and pathogen. C_LIO_LIGeneralist pathogen success is underpinned by pervasive gene expression plasticity in both host and pathogen, allowing similar phenotypic outcomes to emerge from highly divergent molecular states. C_LI

plant biology↗

bioRxiv2026

A multi-plant transcriptomic atlas reveals conserved and lineage specific defense architectures in response to Botrytis cinerea

Generalist pathogens pose a challenge to plant immunity by infecting diverse hosts while harboring extensive intraspecific genetic variation. Whether evolutionary distant plant lineages rely on a shared immune strategy or deploy distinct, lineage-specific defenses when confronted by these genetically variable members of the same pathogen species remains unresolved. Here, we employed a large-scale co-transcriptomic approach to map the immune landscape of ten diverse eudicot species infected with 72 genetically distinct Botrytis cinerea isolates. We identified a limited core of evolutionarily conserved defense orthologs, along with a vast landscape of lineage-specific transcriptional rewiring. While the broad physiological outcome such as metabolic reprogramming, cell wall modification, and suppression of growth-associated processes was shared across hosts, the regulatory pathways governing this were largely lineage-specific. Crucially, this immune landscape is dynamically shaped by pathogen diversity. Nearly three-quarters of host transcriptional responses were isolate-dependent, with the magnitude of defense activation defined by specific host-isolate combinations rather than a universal species-level response. Even host responses to shared virulence factors, including broadly expressed pathogens phytotoxins, were lineage specific. These findings show that plant immunity to generalist pathogens is built on conserved physiological outcomes executed through rapidly evolving, lineage-specific regulatory programs. This distinct regulatory architecture creates an immune landscape heavily modulated by specific host-isolate combinations, highlighting the necessity of integrating pathogen diversity into models of plant defense evolution and resistance breeding. Significance StatementAchieving durable, broad-spectrum crop protection remains difficult because plant immunity models often rely on limited species and overlook natural genetic diversity. Effective crop protection requires understanding how defense networks operate across diverse lineages. We tested this by measuring immune responses of ten phylogenetically diverse eudicots infected with 72 genetically distinct Botrytis cinerea isolates. We found that plants share conserved physiological defense outcomes achieved through highly divergent, lineage-specific regulatory networks. Host responses were strongly shaped by pathogen genetic diversity, with identical isolates eliciting different transcriptional responses in different hosts. This demonstrates that plant immunity quantitatively senses pathogen variation and disease outcomes emerge from specific host-isolate combinations. These findings explain the limits of resistance transfer and inform strategies for durable disease control.

genomics↗

bioRxiv2025

Combined generalist and host-specific transcriptional strategies enable host generalism in the fungal pathogen Botrytis cinerea

How generalist pathogens infect phylogenetically diverse hosts remains a central question in plant-pathogen biology. In particular, the extent to which broad host range is enabled by genetic variation versus transcriptional plasticity is unclear. To investigate how variation and plasticity contribute to generalism, we studied the generalist necrotrophic fungus Botrytis cinerea that infects more than 1,500 plant species. Using a cross-infection matrix of 72 B. cinerea isolates infected on 57 plant genotypes distributed across 15 eudicot species, we identified general and host-dependent fungal components of lesion formation. Transcriptome profiling at 48 hours post-inoculation revealed two distinct pathogen gene modules: (1) a set of general lesion-associated genes enriched in primary metabolism, showing similar expression across hosts but varied among isolates; and (2) a set of high-entropy, host specific-inducible genes, organized into distinct co-regulated modules that respond dynamically to specific host cues. Both gene sets were genomically dispersed, lacking structural clustering, and were under different levels of selective constraints. Our results demonstrate that B. cinerea employs a modular transcriptional strategy that integrates a core metabolic program along with a plastic, host-responsive regulatory network to achieve broad host colonization. This study presents the most comprehensive cross-species co-transcriptomic dataset to date for any fungal phytopathogen, highlighting transcriptional plasticity as a key mechanism underlying generalism in plant-fungal interactions. Moreover, the identification of conserved fungal gene targets across diverse hosts offers a foundation for developing broad-spectrum resistance strategies in multiple crops.

genomics↗

bioRxiv2023

A pangenomic atlas reveals that eco-evolutionary dynamics shape plant pathogen type VI secretion systems

Soil-borne Ralstonia solanacearum species complex (RSSC) bacteria disrupt rhizosphere and endophytic microbial communities as they invade roots and fatally wilt plants. RSSC pathogens secrete antimicrobial toxins using a type VI secretion system (T6SS). To investigate how evolution and ecology have shaped pathogen T6SS biology, we analyzed the T6SS gene content and architecture across the RSSC pangenome and their evolutionarily relatives. Our analysis reveals that two ecologically similar Burkholderiaceae taxa, xylem pathogenic RSSC bacteria and Acidovorax, have convergently evolved to wield large arsenals of T6SS toxins. To understand the mechanisms underlying genomic enrichment of T6SS toxins, we compiled an atlas of 1,069 auxiliary ("aux") T6SS toxin clusters across 99 high-quality RSSC genomes. We classified 25 types of aux clusters with toxins that predominantly target lipids, nucleic acids, or unknown cellular substrates. The aux clusters were in diverse genetic neighborhoods and had complex phylogenetic distributions, suggesting frequent horizontal gene flow. Phages and other mobile genetic elements account for most of the aux cluster acquisition on the chromosome but very little on the megaplasmid. Nevertheless, RSSC genomes were more enriched in aux clusters on the megaplasmid. Secondary replicons like megaplasmids often evolve more rapidly than the more evolutionarily stable chromosome. Although the single ancestral T6SS was broadly conserved in the RSSC, the T6SS was convergently lost in atypical lineages with vectored transmission. Overall, our data suggest dynamic interplay between the lifestyle of soil-transmitted RSSC lineages and the evolution of T6SSs with robust arsenals of toxins. This pangenomic atlas poises the RSSC as an emerging, tractable model to understand the role of the T6SS in shaping pathogen populations.

evolutionary biology↗