E2F6 initiates stable epigenetic silencing of germline genes during embryonic development

In mouse development, long-term silencing by CpG island DNA methylation is specifically targeted to germline genes; however, the molecular mechanisms of this specificity remain unclear. Here, we demonstrate that the transcription factor E2F6, a member of the polycomb repressive complex 1.6 (PRC1.6),...

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Detalles Bibliográficos
Autores: Dahlet, Thomas, Truss, Matthias, Frede, Ute, Al Adhami, Hala, Bardet, Anaïs F., Dumas, Michael, Vallet, Judith, Chicher, Johana, Hammann, Philippe, Kottnik, Sarah, Hansen, Peter, Luz, Uschi, Alvarez, Gonzalo, Auclair, Ghislain, Hecht, Jochen, Robinson, Peter N., Hagemeier, Christian, Weber, Michael
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2021
País:España
Institución:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)
Repositorio:Recercat. Dipósit de la Recerca de Catalunya
OAI Identifier:oai:recercat.cat:10230/53178
Acceso en línea:http://hdl.handle.net/10230/53178
http://dx.doi.org/10.1038/s41467-021-23596-w
Access Level:acceso abierto
Palabra clave:Epigenètica
Embriologia
ADN -- Metilació
Cèl·lules mare embrionàries
Descripción
Sumario:In mouse development, long-term silencing by CpG island DNA methylation is specifically targeted to germline genes; however, the molecular mechanisms of this specificity remain unclear. Here, we demonstrate that the transcription factor E2F6, a member of the polycomb repressive complex 1.6 (PRC1.6), is critical to target and initiate epigenetic silencing at germline genes in early embryogenesis. Genome-wide, E2F6 binds preferentially to CpG islands in embryonic cells. E2F6 cooperates with MGA to silence a subgroup of germline genes in mouse embryonic stem cells and in embryos, a function that critically depends on the E2F6 marked box domain. Inactivation of E2f6 leads to a failure to deposit CpG island DNA methylation at these genes during implantation. Furthermore, E2F6 is required to initiate epigenetic silencing in early embryonic cells but becomes dispensable for the maintenance in differentiated cells. Our findings elucidate the mechanisms of epigenetic targeting of germline genes and provide a paradigm for how transient repression signals by DNA-binding factors in early embryonic cells are translated into long-term epigenetic silencing during mouse development.