JMJD3 intrinsically disordered region links the 3D-genome structure to TGFβ-dependent transcription activation

Enhancers are key regulatory elements that govern gene expression programs in response to developmental signals. However, how multiple enhancers arrange in the 3D-space to control the activation of a specific promoter remains unclear. To address this question, we exploited our previously characteriz...

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Detalles Bibliográficos
Autores: Vicioso Mantis, Marta, Fueyo, Raquel, Navarro, Claudia, Cruz-Molina, Sara, Ijcken, Wilfred F. J.van, Rebollo, Elena, Rada-Iglesias, Álvaro, Martínez-Balbás, Marian
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2022
País:España
Institución:Consejo Superior de Investigaciones Científicas (CSIC)
Repositorio:DIGITAL.CSIC. Repositorio Institucional del CSIC
OAI Identifier:oai:digital.csic.es:10261/281181
Acceso en línea:http://hdl.handle.net/10261/281181
Access Level:acceso abierto
Palabra clave:Chromatin structure
Transcriptional regulatory elements
Descripción
Sumario:Enhancers are key regulatory elements that govern gene expression programs in response to developmental signals. However, how multiple enhancers arrange in the 3D-space to control the activation of a specific promoter remains unclear. To address this question, we exploited our previously characterized TGFβ-response model, the neural stem cells, focusing on a ~374 kb locus where enhancers abound. Our 4C-seq experiments reveal that the TGFβ pathway drives the assembly of an enhancer-cluster and precise gene activation. We discover that the TGFβ pathway coactivator JMJD3 is essential to maintain these structures. Using live-cell imaging techniques, we demonstrate that an intrinsically disordered region contained in JMJD3 is involved in the formation of phase-separated biomolecular condensates, which are found in the enhancer-cluster. Overall, in this work we uncover novel functions for the coactivator JMJD3, and we shed light on the relationships between the 3D-conformation of the chromatin and the TGFβ-driven response during mammalian neurogenesis.