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Balan, T.* ; Petitalot, A.* ; Albert, J.R.* ; Abbou, L.* ; Chevreux, G.* ; Al-Sady, B.* ; Aygenli, B.Ö. ; Bartke, T. ; Margueron, R.* ; Duharcourt, S.*

A H3K27me3 reader complex couples H3K27me3 accumulation to nascent transcription of transposable elements in Paramecium.

Genome Biol., DOI: 10.1186/s13059-026-04045-7 (2026)
Article in press DOI PMC
Creative Commons Lizenzvertrag
Open Access Gold möglich sobald Verlagsversion bei der ZB eingereicht worden ist.
BACKGROUND: The ability to deposit histone H3K27-trimethyl (me3) marks is essential for transcriptional repression by Polycomb Repressive Complex 2 (PRC2). This is largely attributed to Polycomb repressive complex 1 (PRC1), whose recruitment is H3K27me3-dependent. Yet it is unclear how H3K27me3 contributes to transcription regulation independently of PRC1. RESULTS: To address this question, we identified H3K27me3-binding proteins in the unicellular eukaryote Paramecium where PRC2 targets transposable elements (TEs) and PRC1 is absent. We show that the chromodomain protein Firefly is a H3K27me3 reader in vitro and accumulates onto TEs in a H3K27me3-dependent manner. We also identify Firefly interactors: Sleepy, a coiled-coil containing protein and TfIIs4, a transcription elongation factor. We show that Firefly, Sleepy and TfIIs4 are jointly required in vivo for correct H3K27me3 accumulation and nascent transcription at TEs. CONCLUSIONS: This positive feedback loop to enrich H3K27me3 at TEs is analogous to self-reinforcing loops leading to H3K9 methylation at repeats in fungi, plants and animals. Our work reveals a unique association between H3K27me3 readers and active transcription.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Chromodomain ; Ciliates ; Histone Modifications ; Nascent Transcription ; Polycomb Repressive Complex ; Programmed Dna Elimination ; Transposable Elements
ISSN (print) / ISBN 1474-760X
e-ISSN 1465-6906
Zeitschrift Genome Biology
Verlag Springer
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Functional Epigenetics (IFE)