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Matthews, R.E.* ; Danac, J.M.C.* ; Naden, E.L.* ; Farleigh Smith, L.E.* ; Lestari, S.* ; Gungi, A.* ; Appert, A.* ; Buttress, T.* ; Verma, A.* ; Sinclair, O.* ; Chong, F. ; Suberu, J.* ; Antrobus, R.* ; Bonev, B. ; Dawson, M.A.* ; Reid, A.J.* ; Timms, R.T.* ; Ahringer, J.* ; Tchasovnikarova, I.A.*

CRAMP1 drives linker histone expression to enable Polycomb repression.

Mol. Cell 85, 2503-2516.e8 (2025)
Verlagsversion Forschungsdaten DOI PMC
Open Access Hybrid
Creative Commons Lizenzvertrag
In contrast to the well-understood role of core histones in DNA packaging, the function of the linker histone (H1) remains enigmatic. Challenging the prevailing view that linker histones are a general feature of heterochromatin, here we show a critical requirement for H1 in Polycomb repressive complex 2 (PRC2) function. A CRISPR-Cas9 genetic screen using a fluorescent PRC2 reporter identified an essential role for the poorly characterized gene CRAMP1 in PRC2-mediated repression. CRAMP1 localizes to the promoters of expressed H1 genes and positively regulates their transcription. CRAMP1 ablation simultaneously depletes all linker histones, which results in selective decompaction of H3K27me3-marked loci and derepression of PRC2 target genes without concomitant loss of PRC2 occupancy or enzymatic activity. Strikingly, we find that linker histones preferentially localize to genomic loci marked by H3K27me3 across diverse cell types and organisms. Altogether, these data demonstrate a prominent role for linker histones in epigenetic repression by PRC2.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter H1 ; Prc2 ; Polycomb ; Chromatin ; Epigenetic Silencing ; Epigenetics ; Heterochromatin ; Histone ; Linker Histone; H1 Variants; Methyltransferase Activity; Mouse Development; Chromatin-structure; Gene-expression; Drosophila; Proteins; Complex; Flash; Transcription
Sprache englisch
Veröffentlichungsjahr 2025
HGF-Berichtsjahr 2025
ISSN (print) / ISBN 1097-2765
e-ISSN 1097-4164
Zeitschrift Molecular Cell
Quellenangaben Band: 85, Heft: 13, Seiten: 2503-2516.e8 Artikelnummer: , Supplement: ,
Verlag Elsevier
Verlagsort 50 Hampshire St, Floor 5, Cambridge, Ma 02139 Usa
Begutachtungsstatus Peer reviewed
Institut(e) Helmholtz Pioneer Campus (HPC)
POF Topic(s) 30204 - Cell Programming and Repair
Forschungsfeld(er) Pioneer Campus
PSP-Element(e) G-510004-001
Förderungen Wellcome
Cancer Research UK
Cancer Research UK Cambridge Centre studentship
Gurdon Institute and Peterhouse
DOI 10.1016/j.molcel.2025.05.031
WOS ID 001530479400004
Scopus ID 105008031945
PubMed ID 40516528
Erfassungsdatum 2025-07-11
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