Journal
GENES & DEVELOPMENT
Volume 24, Issue 6, Pages 590-601Publisher
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.563210
Keywords
Histone demethylase; RBP-J; Notch target gene repression; T cells; Drosophila; tumorigenesis
Categories
Funding
- DFG, Collaborative Research Center [BO-1639, SFB592/C3, SFB518/A18, SFB497/B9]
- Max-Planck Society
- Ministerio de Ciencia e Innovacion [BFU2006-05150, CSD2007-00023]
- Asociacion Espanola Contra el Cancer (AECC) [2008/134]
- Foundation Marcelino Botin
- European Union [UE-HEALH-F2-2008-201666]
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Timely acquisition of cell fates and the elaborate control of growth in numerous organs depend on Notch signaling. Upon ligand binding, the core transcription factor RBP-J activates transcription of Notch target genes. In the absence of signaling, RBP-J switches off target gene expression, assuring the tight spatiotemporal control of the response by a mechanism incompletely understood. Here we show that the histone demethylase KDM5A is an integral, conserved component of Notch/RBP-J gene silencing. Methylation of histone H3 Lys 4 is dynamically erased and re-established at RBP-J sites upon inhibition and reactivation of Notch signaling. KDM5A interacts physically with RBP-J; this interaction is conserved in Drosophila and is crucial for Notch-induced growth and tumorigenesis responses.
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