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

Abstract：

: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.

journal_name

Nucleic Acids Res

journal_title

Nucleic acids research

authors

Oswald F,Rodriguez P,Giaimo BD,Antonello ZA,Mira L,Mittler G,Thiel VN,Collins KJ,Tabaja N,Cizelsky W,Rothe M,Kühl SJ,Kühl M,Ferrante F,Hein K,Kovall RA,Dominguez M,Borggrefe T

doi

10.1093/nar/gkw105

subject

Has Abstract

pub_date

2016-06-02 00:00:00

pages

4703-20

issue

10

eissn

0305-1048

issn

1362-4962

pii

gkw105

journal_volume

44

pub_type

杂志文章

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