Epigenetic regulation of transposon silencing

A large proportion of eukaryotic genomes consists of transposable elements (TE) and derived repetitive sequences. Through mobilization and transposition these sequences create genetic variation that is a threat to genome integrity. In recent years, it is however becoming increasingly clear that this genetic variation is an important source of functional variation upon which selection acts during evolution. All organisms have evolved mechanism that repress TE activity and transposition to protect genome integrity. However, in many organisms TE retain some residual activity at least during some developmental stages. This may be either because of inherent mechanistic limitations of the silencing process (silencing requires some transcription to occur in order to trigger the silencing machinery) or because of the potentially positive effects of TE activity. There is evidence that TE mobilization is induced under certain conditions such as strong environmental stress and hybridization. TE are also an invaluable tool to generate insertional mutants for research and breeding. For these reasons, it is of high importance to understand how TE are silenced and how this has been modified by natural variation. In this project we are interested in the underlying causes of the natural variation of TE silencing. This will help us to learn more about their regulation.

Recently, we have shown that one determinant of natural variation in TE silencing can be the genomic location of the TE through mapping and molecular analysis of the differential transcriptional activity of a MULE1 DNA transposon in two commonly used lab strains. Through bioinformatic analysis of over 200 sequenced accessions, we have described the overall polymorphisms of this transposon in the Arabidopsis thaliana lineage. Current areas of study involve the question how the host chromosomal environment influences TE silencing and other factors that determine natural variation of TE silencing.