Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA248724 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Gene silencing triggers Polycomb Repressive Complex 2 recruitment to CpG islands genome-wide [ChIP-seq_Input]
| PRJNA248723 | ENA
Project description:Gene silencing triggers Polycomb Repressive Complex 2 recruitment to CpG islands genome-wide [ChIP-seq_drugs]
| PRJNA248725 | ENA
Project description:Gene silencing triggers Polycomb Repressive Complex 2 recruitment to CpG islands genome-wide
| PRJNA248718 | ENA
Project description:Gene silencing triggers Polycomb Repressive Complex 2 recruitment to CpG islands genome-wide [iTC-seq_drugs]
| PRJNA248719 | ENA
Project description:Gene silencing triggers Polycomb Repressive Complex 2 recruitment to CpG islands genome-wide [RNA-seq_differentiation]
| PRJNA248720 | ENA
Project description:Gene silencing triggers Polycomb Repressive Complex 2 recruitment to CpG islands genome-wide [RNA-seq_PcG-KO]
| PRJNA248721 | ENA
Project description:CpG island elements are associated with most mammalian gene promoters, yet how they contribute to gene regulation remains poorly understood. Recently it has become clear that a subset of CpG islands in embryonic stem cells can act as polycomb response elements and are recognized by the polycomb silencing systems to regulate the expression of genes involved in pluripotency and early developmental transcription programs. How CpG islands function mechanistically as nucleation sites for polycomb repressive complexes remains unknown. Here we discover that the KDM2B protein, by virtue of its ZF-CxxC DNA binding domain, specifically recognizes non-methylated DNA in CpG islands elements genome-wide. Through a physical interaction with the polycomb repressive complex 1 (PRC1), KDM2B targets PRC1 to CpG islands where it contributes to H2AK119ub1 and gene repression at a subset of polycomb targets. Unexpectedly, we also find that CpG islands are occupied by low levels of PRC1 throughout the genome, suggesting that the KDM2B-PRC1 complex may sample CpG island associated genes for susceptibility to polycomb mediated silencing. These observations demonstrate an unexpected and direct link between recognition of CpG islands by KDM2B and targeting of the polycomb repressive system. This provides the basis for a new model describing the functionality of CpG islands as mammalian PREs. ChIP-Seq to compare KDM2A vs. KDM2B genome-wide binding profiles and to understand the contribution of KDM2B to RING1B nucleation. Binding of Kdm2a and Kdm2b to the genome was examined in wildtype mESC, and Kdm2b and Ring1b in mESC where Kdm2b has been stably knocked down by shRNA.
2012-12-26 | E-GEOD-40860 | biostudies-arrayexpress
Project description:CpG island elements are associated with most mammalian gene promoters, yet how they contribute to gene regulation remains poorly understood. Recently it has become clear that a subset of CpG islands in embryonic stem cells can act as polycomb response elements and are recognized by the polycomb silencing systems to regulate the expression of genes involved in pluripotency and early developmental transcription programs. How CpG islands function mechanistically as nucleation sites for polycomb repressive complexes remains unknown. Here we discover that the KDM2B protein, by virtue of its ZF-CxxC DNA binding domain, specifically recognizes non-methylated DNA in CpG islands elements genome-wide. Through a physical interaction with the polycomb repressive complex 1 (PRC1), KDM2B targets PRC1 to CpG islands where it contributes to H2AK119ub1 and gene repression at a subset of polycomb targets. Unexpectedly, we also find that CpG islands are occupied by low levels of PRC1 throughout the genome, suggesting that the KDM2B-PRC1 complex may sample CpG island associated genes for susceptibility to polycomb mediated silencing. These observations demonstrate an unexpected and direct link between recognition of CpG islands by KDM2B and targeting of the polycomb repressive system. This provides the basis for a new model describing the functionality of CpG islands as mammalian PREs.
2012-12-26 | GSE40860 | GEO
Project description: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 vivo, 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 mammalian development.
2021-04-22 | PXD023974 | Pride
Project description:Polycomb repressive complex 1 (PRC1) catalyzes H2A monoubiquitination (uH2A) and regulates pluripotency in embryonic stem cells (ESCs). However the mechanisms controlling PRC1 recruitment and activity are largely unknown. Here we show that Fbxl10 interacts with Ring1B and Nspc1, forming a non-canonical PRC1. We demonstrate that Fbxl10-PRC1 is essential for H2A ubiquitination in mouse ESCs. Genome-wide analyses reveal that Fbxl10 preferentially binds to CpG islands and co-localizes with Ring1B on Polycomb target genes. Notably, Fbxl10 depletion causes modest dissociation of Ring1B but a major loss of uH2A on target genes. Furthermore rescue experiments for Fbxl10 reveal that its DNA binding capability and integration into PRC1 are required for proper H2A ubiquitination. ES cells lacking Fbxl10, like previously characterized Polycomb mutants, show a severely compromised capacity for successful differentiation. Our results shed light on a novel mechanism how CpG islands regulate chromatin function by affecting polycomb recruitment and activity. All ChIP-seq reactions were performed in either untransfected cells, cells expressing scrambled shRNA or Fbxl10 shRNA, Ring1b-/- or Suz12-/- mouse ES cells
2012-12-31 | E-GEOD-37930 | biostudies-arrayexpress