DYNAMET

Interplay of plant one-carbon metabolism and redox homeostasis in the context of dynamic DNA methylation (DYNAMET)

DNA methylation is faithfully maintained during replication to stably silence transposable elements and thereby ensure genome integrity. However, environmental impact, such as pathogens, heat, and drought, can cause DNA methylation changes. Moreover, such epigenetic changes may serve as memory to confer resistance against recurring stress - physiological responses known as acclimation or priming. Accordingly, epigenetic variation in plants is influenced by environmental factors and may even contribute to natural selection. It is therefore of great interest, if we can use epigenetic variation to grow plants that are more resistant to pathogens or can better cope with climate change. To this end, it is crucial to know more about the dynamics of DNA methylation. Our aim is to further elucidate the molecular mechanisms that control DNA methylation changes and their effects on plant fitness under environmental stress.

 

In DYNAMET, we address this aim by studying the interaction of one-carbon (C1) metabolism, redox homeostasis, and epigenetic regulation. C1 metabolism provides the methyl donor S-adenosylmethionine required for DNA methylation. Accordingly, perturbations in C1 metabolism can drastically affect genome-wide DNA methylation patterns and transcriptional gene silencing. We are investigating how stress-induced redox changes are linked to alterations in C1 metabolism and epigenetic regulation in the model plant Arabidopsis thaliana and in barley. For this we use interdisciplinary approaches, which combine cutting-edge phenotyping, genomics, metabolite profiling, and functional analyses. By discovering new regulatory mechanisms involved in plant acclimation we want to contribute to new solutions for sustainable crop production and food security for future generations.

The DNA methylation-sensitive reporter SDCpro-GFP. Left: In wild-type, DNA methylation leads to silencing of GFP. Right: Loss of DNA methylation leads to GFP expression.