Evolvability of an organism – the ability to adapt rapidly – requires genetic variability. However, the generation of new variants is ultimately constrained by deleterious effects resulting in a trade-off between evolvability and stability. In eukaryotes, genetic variation caused by single mutations or structural variants, including transposable elements (TEs), can be deleterious, neutral, or beneficial. This project aims to unravel the evolvability potential and constraints of a major pathogen in response to environmental stress and investigate the prevalence of adaptative single mutations and TE variants during stress adaptation. DNA methyltransferases are thought to be involved in TE silencing in an emerging evolutionary and fungal biology model: the wheat pathogen Zymoseptoria tritici. The recent inactivation of DNA methyltransferases has occurred in Z. tritici natural populations. Strains with active DNA methyltransferases have an increased mutation rate and a decrease in TE mobility. In contrast, strains with inactive DNA methyltransferases have a reduced mutation rate and increased TE mobility. We combine molecular genetics and evolution experiments with genomics, epigenomics, and phenomics to unravel how the dynamics between TE mobility and host-genome regulatory mechanisms affect the evolvability of a major wheat pathogen.

This project aims at investigating: i) if DNA methyltransferases can be considered as mutator genes - for which defect directly or indirectly promotes an increase in genetic variability, ii) how variation in transposition rates compared to mutation rates impact evolvability, and iii) how and if parallel adaptation can emerge from mutational and transpositional hotspots.