Poster abstracts

Poster number 42 submitted by Andrea McCue

The initiation of epigenetic silencing of active transposable elements is triggered by RDR6

Andrea D. McCue (Molecular Genetics, The Ohio State University), Saivageethi Nuthikattu (Molecular Genetics, The Ohio State University), Kaushik Panda (Molecular Genetics, The Ohio State University), Dalen Fultz (MCDB, The Ohio State University), Christopher DeFraia (Molecular Genetics, The Ohio State University), Erica N. Thomas (Molecular Genetics, The Ohio State University)

Abstract:
Transposable elements (TEs) are mobile fragments of DNA that are repressed in both plant and animal genomes through the epigenetic inheritance of repressed chromatin and expression states. The epigenetic silencing of TEs in plants is mediated by a process of RNA-directed DNA methylation (RdDM). Two pathways of RdDM have been identified: Pol IV-RdDM, which has been shown to be responsible for the de novo initiation, corrective reestablishment, and epigenetic maintenance of TE and/or transgene silencing, and RDR6-RdDM, which was recently identified as necessary for maintaining the repression for a few TEs. We have further characterized RDR6-RdDM using a genome-wide search to identify TEs that generate RDR6-dependent small interfering RNAs (siRNAs). We have determined that TEs only produce RDR6-dependent siRNAs when transcriptionally active, and we have experimentally identified two TE sub-families as direct targets of RDR6-RdDM. We used these TEs to test the function of RDR6-RdDM in assays for the de novo initiation, corrective reestablishment and maintenance of TE silencing. We found that RDR6-RdDM plays no role in maintaining TE silencing. Rather, we find that RDR6 and Pol IV are two independent entry points into RdDM and epigenetic silencing which perform distinct functions in the silencing of TEs: Pol IV-RdDM functions to maintain TE silencing and to initiate silencing in a Pol II expression-independent manner, while RDR6-RdDM functions to recognize active TE Pol II-derived transcripts to both trigger and correctively reestablish TE methylation and epigenetic silencing.

Keywords: transposable elements, epigenetics, small RNAs