Transposable element (TE) activity results in genome instability in a wide variety of organisms, including humans. This instability has been associated with several diseases, including neurofibromatosis, hemophilia, and cancer. Epigenetic silencing is an efficient mechanism for the initiation and maintenance of TE repression on a genome-wide scale in both plants and animals. My overarching research goal is to understand the dynamic epigenetic nature of TE silencing.
In my research, I adopt a novel model system in which active DNA transposons can be silenced by de novo silencing triggers that are sources of small RNAs in maize (Slotkin and Lisch, 2005 and 2006; Wang, et al., 2020). This system provides us with unique advantages to induce and monitor the initiation and maintenance of silencing in various tissues and at various time points during maize development.
In a recent paper, we identified two independent “killer” alleles (Ack) that can induce the silencing of active maize Ac transposons (Wang et al. 2020). Ac killers represent the first case of TE silencing that can be attributable to self-initiated alternative transposition and demonstrate that Ac transposons silencing is initiated by small RNAs generated from the hairpin transcripts.
However, beyond this observation, the details of the silencing mechanism are not understood. Our working hypothesis is that Ack induces RNA-directed DNA methylation (RdDM) at all the small RNA targets genome-wide. We propose to perform next-generation sequencing experiments to identify the differentially methylated regions. Both the direct and indirect effects of Ack, both the initiation and maintenance of the silencing will be studied.
