Biology subjects

Delplace, F.

Publications and source records attributed to Delplace, F..

3 recordsLinked to original sources

bioRxiv2025

Co-optation of Transcription Factors Drives Evolution of Quantitative Disease Resistance Against a Necrotrophic Pathogen.

Wild relatives of crop species possess diverse levels of quantitative disease resistance (QDR) to biotic stresses, yet the genomic and regulatory mechanisms underlying these differences are poorly understood. In particular, how QDR against a generalist necrotrophic pathogen evolved and whether it is driven by conserved or species-specific regulatory networks remains unclear. Here, we examined the transcriptomic responses of five diverse wild tomato species that span a gradient of QDR. We initially hypothesised that conserved regulatory modules might control QDR. Instead, we use differential gene expression analysis and weighted gene co-expression network analysis (WGCNA) to find that species-specific regulatory features, encompassing both infection-induced and constitutively expressed genes, predominantly shape QDR levels. Although we identified an ethylene response factor among candidate genes for QDR-regulation, it did not fully account for the phenotypic variation. To further dissect the evolutionary basis of these regulatory patterns, we performed phylotranscriptomic analyses on gene regulatory networks. Notably, our findings reveal that the conserved NAC transcription factor 29 is pivotal in developing disease resistance only in S. pennellii. The differential regulation and altered downstream signalling pathways of NAC29 provide evidence for its co-option in the resistance mechanisms of S. pennellii. This finding highlights the species-specific rewiring of gene regulatory networks by repurposing a conserved regulatory element to enhance resistance against pathogens effectively. These results offer new insights into the evolutionary and regulatory complexity underlying QDR and emphasise the significance of species-specific gene regulation in shaping resistance against a cosmopolitan necrotrophic pathogen.

plant biology↗

bioRxiv2024

Diverse transcriptome reprogramming trajectories underlie quantitative disease resistance at the species level

Quantitative disease resistance (QDR) is an immune response limiting pathogen damage in plants. It involves transcriptomic reprogramming of numerous genes, each having a small contribution to plant immunity. Despite QDR broad-spectrum nature, the evolution of its underlying transcriptome reprogramming remains largely uncharacterized. Here, we analyzed global gene expression in response to the necrotrophic fungus Sclerotinia sclerotiorum in 23 Arabidopsis thaliana accessions of diverse origin and contrasted QDR phenotype. Over half of the species pan-transcriptome displayed local responses to S. sclerotiorum, with global reprogramming patterns incongruent with accessions phylogeny. Due to frequent small-amplitude variations, only [~]11% of responsive genes were common across all accessions, defining a core transcriptome enriched in highly-responsive genes. Co-expression and correlation analyses showed that QDR phenotypes result from the integration of numerous genes expression. Promoter sequence comparisons revealed that variation in DNA-binding sites within cis-regulatory regions contributing to gene expression rewiring. Finally, transcriptome-phenotype maps revealed abundant neutral networks connecting diverse QDR transcriptomes with no loss of resistance, hallmarks of robust and evolvable traits. This navigability associated with regulatory variation in core genes highlights their role in QDR evolvability. This work provides insights into the evolution of complex immune responses, informing models for plant disease dynamics. Classification: Biological Sciences, Plant Biology

plant biology↗

bioRxiv2024

The Arabidopsis leucine rich repeat receptor-like kinase MIK2 interacts with RKS1 and participates to the control of quantitative disease resistance to the bacterial pathogen Xanthomonas campestris

Molecular mechanisms underlying qualitative resistance have been intensively studied. In contrast, although quantitative disease resistance (QDR) is a common, durable and broad-spectrum form of immune responses in plants, only a few related functional analyses have been reported. In this context, the atypical kinase RKS1 is a major actor of QDR to the bacterial pathogen Xanthomonas campestris (Xcc) and is positioned in a robust protein-protein decentralized network. Among the putative interactors of RKS1 found by yeast two hybrid screening, we identified the receptor like kinase MDIS1-Interacting Receptor-like Kinase 2 (MIK2). Here, by multiple and complementary strategies including protein-protein interaction tests, mutant analysis and network reconstruction, we report that MIK2 is a component of RKS1 mediated QDR to Xcc. First, by co-localization experiment, co-immunoprecipitation (Co-IP) and Bimolecular Fluorescence Complementation (BiFC), we validated the physical interaction between RKS1 and MIK2 in the plasma membrane. Using mik2 mutants, we then showed that MIK2 is required for QDR at the same level as RKS1. Interestingly, a catalytic mutant of MIK2 was able to interact with RKS1 but unable to fully complement the mik2-1 mutant in response to Xcc. Finally, we investigated a potential role of the MIK2-RKS1 complex as a scaffolding component for coordination of perception events, by constructing a RKS1-MIK2 centered protein-protein network. Eight mutants corresponding to seven RLKs of this network showed a strong and significant alteration in QDR to Xcc. Our findings provide new insights into the molecular mechanisms underlying perception events involved in QDR to Xcc.

plant biology↗