Synergy between variant PRC1 complexes defines Polycomb-mediated gene repression (ChIP-Seq)
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ABSTRACT:
PROVIDER: PRJNA489754 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7798890_1.fastq.gz | Fastqsanger.gz | |||
| SRR7798890_2.fastq.gz | Fastqsanger.gz | |||
| SRR7798900_1.fastq.gz | Fastqsanger.gz | |||
| SRR7798900_2.fastq.gz | Fastqsanger.gz | |||
| SRR7798910_1.fastq.gz | Fastqsanger.gz |
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Project description:Synergy between variant PRC1 complexes defines Polycomb-mediated gene repression
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Project description:The Polycomb system modifies chromatin and plays an essential role in repressing gene expression to control normal mammalian development. However, the components and mechanisms that define how Polycomb protein complexes achieve this remain enigmatic. Here we use combinatorial genetic perturbation coupled with quantitative genomics to discover the central determinants of Polycomb-mediated gene repression in mouse embryonic stem cells. We demonstrate that canonical Polycomb repressive complex 1 (PRC1), which mediates higher order chromatin structures, contributes little to gene repression. Instead, we uncover an unexpectedly high degree of synergy between variant PRC1 complexes which is fundamental to gene repression. We further demonstrate that variant PRC1 complexes are responsible for distinct pools of H2A monoubiquitylation that are associated with repression of Polycomb target genes and silencing during X-chromosome inactivation. Together, these discoveries reveal a new variant PRC1-dependent logic for Polycomb-mediated gene repression.
2019-04-26 | GSE119618 | GEO
Project description:The Polycomb system modifies chromatin and plays an essential role in repressing gene expression to control normal mammalian development. However, the components and mechanisms that define how Polycomb protein complexes achieve this remain enigmatic. Here we use combinatorial genetic perturbation coupled with quantitative genomics to discover the central determinants of Polycomb-mediated gene repression in mouse embryonic stem cells. In contrast to prevailing views, we demonstrate that canonical Polycomb repressive complex 1 (PRC1), which mediates higher order chromatin structures, contributes little to gene repression. Instead, we uncover an unexpectedly high degree of synergy between variant PRC1 complexes which is fundamental to gene repression. We further demonstrate that variant PRC1 complexes are responsible for distinct pools of H2A monoubiquitylation that are associated with repression of Polycomb target genes and silencing during X-chromosome inactivation. Together, these discoveries reveal a new variant PRC1-dependent logic for Polycomb-mediated gene repression.
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Project description:Synergy between variant PRC1 complexes defines Polycomb-mediated gene repression (RNA-Seq)
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Project description:The Polycomb system modifies chromatin and plays an essential role in repressing gene expression to control normal mammalian development. However, the components and mechanisms that define how Polycomb protein complexes achieve this remain enigmatic. Here, we use combinatorial genetic perturbation coupled with quantitative genomics to discover the central determinants of Polycomb-mediated gene repression in mouse embryonic stem cells. We demonstrate that canonical Polycomb repressive complex 1 (PRC1), which mediates higher-order chromatin structures, contributes little to gene repression. Instead, we uncover an unexpectedly high degree of synergy between variant PRC1 complexes, which is fundamental to gene repression. We further demonstrate that variant PRC1 complexes are responsible for distinct pools of H2A monoubiquitylation that are associated with repression of Polycomb target genes and silencing during X chromosome inactivation. Together, these discoveries reveal a new variant PRC1-dependent logic for Polycomb-mediated gene repression.
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Project description:Polycomb Repressive Complexes (PRC), and their chromatin-modifying activities, are essential for the correct regulation of gene expression during cellular differentiation and development. Although their role in transcriptional repression is well described, a detailed molecular understanding of their complex assembly and enzymatic activity has been lacking. We therefore set out to characterize the relationship between PRC1 complex composition and its ability to catalyse H2AK119ub1 for one of the most abundant PRC1 complexes in embryonic stem cells, PCGF1-PRC1. Biochemical reconstitution of the PCGF1-PRC1 complex revealed that RYBP/YAF2 was essential for robust enzymatic activity of the complex. Using calibrated ChIP-seq for H2AK119ub1, we identify that RYBP-dependent PRC1 activity has a widespread role in shaping H2AK119ub1 levels genome-wide in mouse embryonic stem cells. Furthermore, these H2AK119ub1 levels stimulate PRC2 activity as part of an activity-based feedback loop, which we demonstrate is required for maintenance of transcriptional repression. Together, these observations uncover complex-based principles for PRC1 assembly and activity, and further our understanding of Polycomb domain function. This SuperSeries is composed of the SubSeries listed below.
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Project description:R-loops are three-stranded nucleic acid structures that form naturally during transcription, especially over unmethylated CpG-rich promoters. In mESC, such promoters of developmental regulator genes are occupied by the Polycomb-repressor complexes PRC1 and PRC2. Here we have explored the possibility that R-loops form over Polycomb-repressed genes and play a role in their transcriptional silencing. Using single gene and genome-wide analyses, we show that R-loops form at a specific subset of PRC-target genes and contribute to Polycomb occupancy on chromatin. Removal of R-loops leads to an up-regulation of nascent and processed transcripts and the appearance of the elongating form of RNA polymerase II. In contrast, removal of PRC2 does not influence R-loop formation, transcriptional repression and PRC1 recruitment. We finally show that R-loops and PRC1 can repress Polycomb-target genes in the absence of PRC2. Our results uncover an unanticipated synergy between R-loops and PRC1 in Polycomb repression mechanisms.
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Project description:Polycomb Repressive Complexes (PRC), and their chromatin-modifying activities, are essential for the correct regulation of gene expression during cellular differentiation and development. Although their role in transcriptional repression is well described, a detailed molecular understanding of their complex assembly and enzymatic activity has been lacking. We therefore set out to characterize the relationship between PRC1 complex composition and its ability to catalyse H2AK119ub1 for one of the most abundant PRC1 complexes in embryonic stem cells, PCGF1-PRC1. Biochemical reconstitution of the PCGF1-PRC1 complex revealed that RYBP/YAF2 was essential for robust enzymatic activity of the complex. Using calibrated ChIP-seq for H2AK119ub1, we identify that RYBP-dependent PRC1 activity has a widespread role in shaping H2AK119ub1 levels genome-wide in mouse embryonic stem cells. Furthermore, these H2AK119ub1 levels stimulate PRC2 activity as part of an activity-based feedback loop, which we demonstrate is required for maintenance of transcriptional repression. Together, these observations uncover complex-based principles for PRC1 assembly and activity, and further our understanding of Polycomb domain function.
2016-10-05 | GSE83094 | GEO
Project description:Polycomb Repressive Complexes (PRC), and their chromatin-modifying activities, are essential for the correct regulation of gene expression during cellular differentiation and development. Although their role in transcriptional repression is well described, a detailed molecular understanding of their complex assembly and enzymatic activity has been lacking. We therefore set out to characterize the relationship between PRC1 complex composition and its ability to catalyse H2AK119ub1 for one of the most abundant PRC1 complexes in embryonic stem cells, PCGF1-PRC1. Biochemical reconstitution of the PCGF1-PRC1 complex revealed that RYBP/YAF2 was essential for robust enzymatic activity of the complex. Using calibrated ChIP-seq for H2AK119ub1, we identify that RYBP-dependent PRC1 activity has a widespread role in shaping H2AK119ub1 levels genome-wide in mouse embryonic stem cells. Furthermore, these H2AK119ub1 levels stimulate PRC2 activity as part of an activity-based feedback loop, which we demonstrate is required for maintenance of transcriptional repression. Together, these observations uncover complex-based principles for PRC1 assembly and activity, and further our understanding of Polycomb domain function.
2016-10-05 | GSE83134 | GEO
Project description:Polycomb Repressive Complexes (PRC), and their chromatin-modifying activities, are essential for the correct regulation of gene expression during cellular differentiation and development. Although their role in transcriptional repression is well described, a detailed molecular understanding of their complex assembly and enzymatic activity has been lacking. We therefore set out to characterize the relationship between PRC1 complex composition and its ability to catalyse H2AK119ub1 for one of the most abundant PRC1 complexes in embryonic stem cells, PCGF1-PRC1. Biochemical reconstitution of the PCGF1-PRC1 complex revealed that RYBP/YAF2 was essential for robust enzymatic activity of the complex. Using calibrated ChIP-seq for H2AK119ub1, we identify that RYBP-dependent PRC1 activity has a widespread role in shaping H2AK119ub1 levels genome-wide in mouse embryonic stem cells. Furthermore, these H2AK119ub1 levels stimulate PRC2 activity as part of an activity-based feedback loop, which we demonstrate is required for maintenance of transcriptional repression. Together, these observations uncover complex-based principles for PRC1 assembly and activity, and further our understanding of Polycomb domain function.
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