Projects

In eukaryotic genomes, the danger of transposon mobilization is controlled by the epigenetic pathways, which involve small interfering (si) RNA, DNA methylation and heterochromatin formation. However, it is still unknown how the host recognizes and differentiates transposons from normal genes in the first instance and initiates the epigenetic silencing. We previously found that transposon RNAs are weak in translation due to the suboptimal codon usage for ribosome association, which then leads to TE RNA localization to a specific cytoplasmic compartment, where siRNAs are produced. In fact, ribosome arrest is often associated with the cleavage of RNA and is usually followed by rapid RNA degradation, which raises an interesting question as to how TE RNA circumvents the RNA degradation pathway and enter the siRNA biogenesis pathway with greater preference. Therefore, the aim of this project is to dissect how the ribosome arrest-associated RNA control pathways interplay with the epigenetic silencing of transposons. This research will help unveil the long-lasting question of self and non-self recognition in biology and provide insights into the safeguarding of the host genome from foreign DNAs.

Funder: BBSRC

Led by: Benjamin Shone

Reference: Nature Plants, 2021; Plant Journal, 2021

In plants, it is well documented that transposon mobilization is strongly repressed by the epigenetic silencing pathways; however, its regulation at the post-transcriptional level remains relatively uninvestigated. We recently found that transposon RNA is marked by an epitranscriptomic mark, m6A RNA methylation, and thereby can be localized in the cytoplasmic compartments known as stress granules (SGs). Intriguingly, SG-localized AtALKBH9B selectively demethylates a heat-activated retroelement, Onsen, and subsequently releases it from spatial confinement, allowing for its mobilization. Moreover, m6A RNA methylation contributes to transpositional suppression by inhibiting virus-like particle assembly and extrachromosomal DNA production. Further to this discovery, we are keen to dissect the m6A-mediated transposon repression mechanisms by investigating the biochemical properties of m6A RNA demethylases and reader proteins. This project will provide the insights into the crosstalk and co-evolution of the host genome and transposons.

Funder: Durham University

Led by: Seunghui Mun

Reference: Genome Biology, 2022; Science Advances, 2023; Trends in Genetics, 2025