Biology subjects

Thon, M.

Publications and source records attributed to Thon, M..

3 recordsLinked to original sources

bioRxiv2026

Adaptive genomic compartments shaped by giant mobile elements underpin the ancient emergence of fungal pathogenicity

The emergence of new fungal pathogens often depends on the acquisition of complex adaptive traits, yet the mechanisms by which such traits arise remain poorly understood. Here we show that a biosynthetic gene cluster required for pathogenicity in the lupin pathogenic fungus Colletotrichum lupini was acquired within a genomic region derived from a giant Starship transposable element. Comparative and population genomic analyses reveal that the C. lupini genome contains multiple regions derived from ancestrally active Starship elements, enriched in lineage-specific genes and strongly induced during plant infection. One such region harbours a hybrid polyketide synthase-nonribosomal peptide synthetase (PKS-NRPS) gene cluster that is conserved in pathogenic isolates but absent from closely related non-pathogenic species and from a non-pathogenic strain. Phylogenetic analyses of the PKS-NRPS backbone gene reveal incongruence with species relationships and a distribution across deeply divergent fungal lineages, consistent with horizontal acquisition. Disruption of the PKS-NRPS backbone gene abolishes pathogenicity, demonstrating that this cluster is required for host infection. Phylogenomic analyses further indicate that lupin pathogenicity emerged once within the C. lupini lineage prior to its diversification. Together, these findings identify a Starship-associated virulence determinant and support a model in which giant cargo-mobilizing mobile elements generate genomic novelty by facilitating the acquisition, assembly and integration of adaptive traits during the emergence of fungal pathogenicity.

genetics↗

bioRxiv2025

Gene duplication drove functional divergence of two effectors in the maize anthracnose pathogen

Colletotrichum species rank among the most important fungal pathogens, threatening food security by infecting nearly all major crops worldwide. Colletotrichum graminicola, the causal agent of maize anthracnose, secretes effector proteins to manipulate host defences and promote colonization. Building on previous work characterizing the nuclear effector CgEP1, we characterized its paralog CgEP4, which is highly conserved across strains of C. graminicola. Phylogenetic analysis of the two genes and their homologs in other species revealed that they originated from a gene duplication event approximately 28 to 18 million years ago, predating the diversification of the Graminicola species complex. This timing aligns with the ecological expansion of C4 grasses, suggesting that the functional divergence of these effectors was an adaptive response to facilitate the colonization of emerging monocot hosts. Functional characterization using gene deletion mutants demonstrated that CgEP4 has a critical role in pathogenicity, characterized by a significant reduction in virulence, delayed penetration, enhanced papilla formation, and decreased fungal biomass. This virulence defect is associated with compromised host colonization and a failure to suppress basal host defences. In the absence of CgEP4, the pathogen also showed defects in general fungal physiology and stress tolerance. Overall, our findings establish CgEP4 as a new, essential nuclear-localized effector that promotes fungal entry and colonization by manipulating host responses. Our findings demonstrate that evolutionary analysis is a valuable tool for discovering new genes important for host adaptation and pathogen evolution.

plant biology↗

bioRxiv2025

A Sacrificial 3D Printed Vessel-on-Chip Demonstrates a Versatile Approach to Model Connective Tissue Pathology

For in vitro organ models, perfused vasculature is crucial to overcome nutrient diffusion limits and to generate immunocompetent models by allowing trans-endothelial migration of immune cells in and out of the tissue. However, vasculature is often disregarded due to its complexity to generate and the necessity to integrate flow. The aim here was to overcome these limitations by combining 3D printing and multi-organ-chip technology to generate a vascularized, fibroblast-populated connective tissue matrix on-chip. A 3D printed, sacrificial, water-dissolvable structure was incorporated into a multi-organ-chip to generate hollow channels within a collagen/fibrin hydrogel. Subsequently, the channels were populated with endothelial cells. Different hydrogel concentrations of fibrin were used to mimic healthy and early granulation tissue. The vessels were perfused, and stable metabolic/viability conditions (lactate dehydrogenase, glucose, lactate) acquired after 3 days for 7 days total. In high fibrin gels, angiogenic sprouting and increased secretion of angiogenic cytokines was observed. Perfusion with monocytes revealed differentiation into macrophages and migration across the endothelium into the tissue. In conclusion, the versatile, easy method to pattern hydrogels in multi-organ-chips can serve as the basis to build the next generation of vascularized, immunocompetent human organ models, and opens new possibilities to study health and disease.

bioengineering↗