Project description:Anthropogenic nutrient inputs alter soil biodiversity; however, it remains largely unknown whether changes in soil microeukaryotes (fungi and protists) are primarily driven by direct effects, such as modifications in soil properties, or by indirect effects, such as plant diversity loss. To disentangle these mechanisms, we investigated the long-term effects (11 years) of fertilization and manipulated plant diversity (1, 2, or 4 plant species) on soil microeukaryote communities in a temperate grassland experiment using long-amplicon rRNA sequencing. Our results indicate that fertilization generally had a stronger influence on microeukaryote communities than plant species richness. Fertilization altered the community composition of fungi and protists, increased OTU richness by 20.8% and 52.7%, respectively, and shifted community dominance from fungi to protists. Regarding plant diversity, we observed an effect exclusively on the protist community. Changes were primarily explained by increased plant biomass (driven by both fertilization and plant diversity) and by higher soil phosphorus and lower soil pH levels (driven exclusively by fertilization). Regarding life strategies, we observed synergistic treatment effects: fertilization primarily enhanced fungal saprophytes (only richness), fungal animal pathogens, and protist consumers, whereas plant diversity affected phototrophic protists (reduction) and protist animal pathogens (enhancement). Notably, fertilization and plant diversity decline together led to a cumulative increase in fungal plant pathogens. In conclusion, we highlight that fertilisation alone has a significant effect on soil microeukaryotes, while the additional decline in plant diversity affects different soil groups that are not directly affected by fertilisation. This synergistic pattern indicates that fertilization can influence the entire microeukaryote community through direct and indirect mechanisms, with a cumulative enhancement on certain groups, such as plant pathogens.
Project description:Fungal antagonism shapes microbial community structure and provides an ecological basis for biological control. Although mycoviruses have been implicated in fungal antagonism, their effects are generally attributed to indirect modulation of resident host physiology.
Project description:Candida albicans is the most common human fungal pathogen, causing diseases ranging from local to life-threating systemic infections. Tyrosine kinase 2 (TYK2), a crucial mediator in several cytokine signaling pathways, has been associated with protective functions in various microbial infections. However, its specific contribution in the immune response to fungal infections has remained elusive. In this study, we show that mice lacking TYK2 or its enzymatic activity exhibit enhanced resistance to C. albicans skin infections, limiting fungal spread and accelerating wound healing. Impaired TYK2-signaling prompted the formation of a distinctive layer of necrotic neutrophils around the fungal pathogens. Transcriptomic analysis revealed TYK2's pivotal role in regulating interferon-inducible genes in neutrophils, thereby impacting their antifungal capacity during infection. Furthermore, we show that TYK2-dependent interferon-gamma (IFNg) production contributes to fungal dissemination from the skin to the kidneys. Our study uncovers a hitherto unrecognized detrimental role of TYK2 in cutaneous C. albicans infections.