Evolutionary Pathogenomics

Our research interest focusses on how antagonistic interactions shape rapid evolution of plant-pathogens and how species maintain their evolutionary potential in human-managed environments.

We employ a combination of genomics, phenomics and experimental evolution approaches to better understand the molecular basis of the plant-pathogen interactions. For this, we are working with the fungal wheat pathogen Zymoseptoria tritici causing the Septoria tritici blotch disease that damages wheat crops worldwide.

Rapid adaptation of a major wheat pathogen to dynamic host and fungicide environments during a single epidemic season

The critical ability to adapt to changing environments has shaped the evolution of all species, often through processes that enable the maintenance of genetic and phenotypic variation within populations. The time scale over which adaptative evolution occurs remains largely unknown for most species in most ecosystems. We use an extensive field experiment to provide a detailed assessment of the evolutionary processes affecting the local adaptation of a major wheat pathogen by combining population genomics and phenomics analyses of pathogen populations sampled at different time points during an epidemic season. We perform detailed mapping of complex phenotypes onto genotypes (i.e. genome-wide association studies, GWAS) to identify novel gene candidates underlying important traits. We also analyze composite phenotypes to seek evidence for trade-offs that may be involved in local adaptation to specific hosts and different classes of fungicides.

Effect of abiotic stress on genome architecture and evolution of the wheat pathogen Zymoseptoria tritici

One of the characteristics that makes Z. tritici particularly hard to control is the ability to rapidly adapt to various abiotic stresses. Z. tritici exhibit a general tendency for genome size variation, chromosome number variation and gene presence/absence variation which are thought to increase its adaptive potential. In fungi, genome stability is ensured by epigenetic regulation including histone modification, DNA methylations and repeat-induced point mutation (RIP). These mechanisms notably control for the proliferation of repeats by inducing mutation inducing mutations in duplicated sequences. In Z. tritici, presence of DNA methylation correlates with lowered TE activity and overall high mutation rates. However, mutations in genes or changes in expression regulation caused by transposable element (TEs) insertions have been linked to emerging fungicide resistance, rapid adaptation to environmental stresses and host resistance breakdown. Thereby, if decreased TE mobility is thought of as increasing genome stability, it might also lower evolutionary potential.
In this project, we explore the potential trade-off between genome stability and rapid adaptation potential of Z. tritici strains from natural populations and mutants with presence/absence of DNA methyltransferases. This project is in collaboration with Dr. Alice Feurtey.

 

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