Transposons, or “jumping genes”, are mobile DNA elements that can move around within a genome. When they excise from one location in the genome and re-insert into another location, transposons can potentially disrupt genes. To mitigate this potential for disruption, genomes have evolved mechanisms to silence transposons and stop them from excising. 

Frédéric Berger, Senior group leader at the GMI, has shown that in the plant Arabidopsis thaliana, transposons are silenced by modifying the chromatin environment – the complex of DNA and proteins within the nucleus. In Arabidopsis, a protein called DDM1 is recruited to transposons, where it deposits a specific variant of the histone H2A, a protein involved in DNA packaging. This modification keeps the transposons quiet and prevents them from jumping to new locations in the genome. However, an important question remains: How is DDM1 alerted to the presence of a transposon in the genome, and what guides it to silence the element?

To address this question, the Berger lab seeks to find members of a putative DDM1 complex that recruit DDM1 to transposons. In the new project funded by the FWF, the researchers will employ two complementary experimental approaches: a forward genetic screen and a biochemical method that combines proximity labelling and mass spectrometry to identify proteins interacting with DDM1. The team also aims to understand the specific roles of various domains within the DDM1 protein. The potential implications of this work extend beyond Arabidopsis. In crop plants, selective modulation of gene silencing across an entire genome remains a significant challenge. By uncovering new mechanisms of targeted gene silencing, this research has the potential to expand the toolkit for synthetic genome manipulation, offering novel ways to control gene expression in plants.

“We are very grateful for the support by the FWF, it allows us to dive deeper into the mechanisms of chromatin remodeling and transposon silencing”, says Frédéric Berger. “By uncovering how proteins like DDM1 are recruited to transposon, we hope to broaden our understanding of transposon silencing and provide new tools for targeting epigenetic silencing.”