MODIFICATION

Polycomb complexes play crucial developmental roles by controlling cell type-specific transcription programs that determine cell identity in both animals and plants. Transcriptional repression associated with Polycomb repressive complex 2 (PRC2) is ensured by Polycomb repressive complex 1 (PRC1), which binds to H3K27me3, the modification catalyzed by PRC2. However, in the absence of PRC1, transcriptional repression is still maintained by PRC2. The mechanism by which H3K27me3 contributes to transcriptional repression independently of PRC1 remains unclear. We will address this important question using the DNA elimination paradigm in ciliates. In the unicellular ciliate Paramecium, PRC2-catalyzed histone modifications are deposited on transposable elements, triggering their elimination from the somatic genome. However, how the deposition of repressive histone modifications at transposable elements leads to their elimination is currently unknown. Notably, PRC1 is absent in the ciliate Paramecium, providing a unique opportunity to identify the proteins that act downstream H3K27me3 independently of PRC1. In this proposal, we aim to uncover how H3K27me3 triggers DNA elimination. Our preliminary data have identified new factors required for this process. We will use multidisciplinary, cutting-edge approaches that combine functional genomics, biochemistry and proteomics, to decipher the mechanisms of action of these factors.