Project description:Quantitative disease resistance (QDR) is an almost universal and often broad-spectrum process in plants, serving to limit the damage caused by pathogen infections. It represents the primary form of plant immunity that reduces disease symptoms induced by numerous pathogens actively killing host cells during infection, including the necrotrophic pathogen Sclerotinia sclerotiorum. Investigating the evolutionary origins of QDR against necrotrophic fungi is crucial for comprehending how plant resistance evolves. To explore the diversity of local responses to S. sclerotiorum within a plant species level, we conducted a comprehensive analysis of the entire transcriptomes from 23 accessions of Arabidopsis thaliana, mainly distributed across Europe. More than half on the pan-transcriptome displayed local responses toS. sclerotiorum, including similar transcriptome patterns. Notably, core S. sclerotiorum-responsive genes exhibited a clear gene age pattern, dominated by older genes forming protein-protein networks that continuously acquiring new hubs. Comparative transcriptome analyses revealed QDR is associated with quantitative expression variations specific to accession subsets. By comparison of promoter sequences, we have shown evidence that accession subsets independently evolved and acquired specific cis-regulatory elements, confering Sclerotinia resistance. This scenario suggests multiple exaptation trajectories of novel QDR genes through species-level cis-regulation. This study sheds light on the regulation of QDR-associated genes within a species, contributing to our understanding of the molecular mechanisms of plant fungal resistance.
Project description:The host range of parasites is an important factor in assessing the dynamics of disease epidemics. The evolution of pathogens to accommodate new hosts may lead to host range expansion, a process the molecular bases of which are largely enigmatic. The fungus Sclerotinia sclerotiorum parasitizes more than 400 plant species from diverse eudicot families while its close relative, S. trifoliorum, is restricted to plants from the Fabaceae family. We analyzed S. sclerotiorum global transcriptome reprogramming on hosts from six botanical families and reveal a flexible, host-specific transcriptional program driven by core and host-response co-expression (SPREx) gene clusters. We generated a chromosome-level genome assembly for S. trifoliorum and found near-complete gene space conservation in broad and narrow host range Sclerotinia species. However, S. trifoliorum showed increased sensitivity to the Brassicaceae defense compound camalexin. Inter-specific transcriptome analyses revealed a lack of transcriptional response to camalexin in S. trifoliorum and provide evidence that cis-regulatory variation associates with the genetic accommodation of Brassicaceae in the Sclerotinia host range. Our work demonstrates adaptive plasticity of a broad host range pathogen with specific responses to different host plants and demonstrates the co-existence of signatures for generalist and polyspecialist life styles in the genome of a plant pathogen. We reason that this mechanism enables the emergence of new disease with no or limited gene flow between strains and species, and could underlie the emergence of new epidemics originating from wild plants in agricultural settings.
Project description:Sclerotinia sclerotiorum, the causal agent of white mould, is a necrotrophic fungal pathogen responsible for extensive crop loss. Current control options rely heavily on the application of chemical fungicides that are becoming less effective and may lead to the development of fungal resistance. In the current study, we used a foliar spray application of boron to protect Brassica napus (canola) from S. sclerotiorum infection using whole plant infection assays. Application of boron to aerial surfaces of the canola plant reduced the number of S. sclerotiorum forming lesions by 87% compared to an untreated control. We used dual RNA sequencing to profile the effect of boron on both the host plant and fungal pathogen during the infection process. Differential gene expression analysis and gene ontology term enrichment further revealed the mode of action of a foliar boron spray at the mRNA level. A single foliar application of boron primed the plant defense response through the induction of genes associated with systemic acquired resistance while an application of boron followed by S. sclerotiorum infection induced genes associated with defense-response-related cellular signalling cascades. Additionally, in S. sclerotiorum inoculated on boron-treated B. napus, we uncovered gene activity in response to salicylic acid breakdown, consistent with salicylic-acid-dependent systemic acquired resistance induction within the host plant. Taken together, this study demonstrates that a foliar application of boron results in priming of the B. napus plant defense response, likely through systemic acquired resistance, thereby contributing to increased tolerance to S. sclerotiorum infection.
Project description:To understand the plant-pathogen interaction comprehensively, it is valuable to monitor the gene expression profiles of both interacting organisms simultaneously in the same infected plant tissue. Using RNA-Seq, we analyzed the mixed transcriptome of rice and blast fungus in infected leaves at 24 hours post-inoculation. We demonstrated that our method detected the gene expression of both the host plant and pathogen simultaneously in the same infected leaf blades in natural infection conditions without any artificial treatments. Using compatible (Ina86-137) and incompatible (P91-15B) fungal strains as pathogens, we revealed the differential expression profiles of the compatible and incompatible interactions and observed that the responsive gene expression was more drastic in the incompatible interaction. Our mixed transcriptome analysis is useful for the simultaneous elucidation of the tactics of host plant defense and pathogen attack.