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  A phospho-dependent mechanism involving NCoR and KMT2D controls a permissive chromatin state at Notch target genes

Oswald, F., Rodriguez, P., Giaimo, B. D., Antonello, Z. A., Mira, L., Mittler, G., et al. (2016). A phospho-dependent mechanism involving NCoR and KMT2D controls a permissive chromatin state at Notch target genes. Nucleic Acids Research (London), 44, 4703-4720. doi:10.1093/nar/gkw105.

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Datensatz-Permalink: https://hdl.handle.net/11858/00-001M-0000-002C-B0C2-6 Versions-Permalink: https://hdl.handle.net/21.11116/0000-0008-A5EA-6
Genre: Zeitschriftenartikel

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https://academic.oup.com/nar/article/44/10/4703/2516070 (Verlagsversion)
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 Urheber:
Oswald, Franz1, Autor
Rodriguez, Patrick1, Autor
Giaimo, Benedetto Daniele1, Autor
Antonello, Zeus A.1, Autor
Mira, Laura1, Autor
Mittler, Gerhard2, Autor
Thiel, Verena N.1, Autor
Collins, Kelly J.1, Autor
Tabaja, Nassif1, Autor
Cizelsky, Wiebke1, Autor
Rothe, Melanie1, Autor
Kühl, Susanne J.1, Autor
Kühl, Michael1, Autor
Ferrante, Francesca1, Autor
Hein, Kerstin1, Autor
Kovall, Rhett A.1, Autor
Dominguez, Maria1, Autor
Borggrefe, Tilman1, Autor
Affiliations:
1External Organizations, ou_persistent22              
2Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, 79108 Freiburg, DE, ou_2243640              

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 Zusammenfassung: The transcriptional shift from repression to activation of target genes is crucial for the fidelity of Notch responses through incompletely understood mechanisms that likely involve chromatin-based control. To activate silenced genes, repressive chromatin marks are removed and active marks must be acquired. Histone H3 lysine-4 (H3K4) demethylases are key chromatin modifiers that establish the repressive chromatin state at Notch target genes. However, the counteracting histone methyltransferase required for the active chromatin state remained elusive. Here, we show that the RBP-J interacting factor SHARP is not only able to interact with the NCoR corepressor complex, but also with the H3K4 methyltransferase KMT2D coactivator complex. KMT2D and NCoR compete for the C-terminal SPOC-domain of SHARP. We reveal that the SPOC-domain exclusively binds to phosphorylated NCoR. The balance between NCoR and KMT2D binding is shifted upon mutating the phosphorylation sites of NCoR or upon inhibition of the NCoR kinase CK2β. Furthermore, we show that the homologs of SHARP and KMT2D in Drosophila also physically interact and control Notch-mediated functions in vivo. Together, our findings reveal how signaling can fine-tune a committed chromatin state by phosphorylation of a pivotal chromatin-modifier.

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Sprache(n): eng - English
 Datum: 2016
 Publikationsstatus: Erschienen
 Seiten: -
 Ort, Verlag, Ausgabe: -
 Inhaltsverzeichnis: -
 Art der Begutachtung: Expertenbegutachtung
 Identifikatoren: DOI: 10.1093/nar/gkw105
 Art des Abschluß: -

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Titel: Nucleic Acids Research (London)
  Andere : Nucleic Acids Res
Genre der Quelle: Zeitschrift
 Urheber:
Affiliations:
Ort, Verlag, Ausgabe: Oxford : Oxford University Press
Seiten: - Band / Heft: 44 Artikelnummer: - Start- / Endseite: 4703 - 4720 Identifikator: ISSN: 0305-1048
CoNE: https://pure.mpg.de/cone/journals/resource/110992357379342