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Crol contributes to PRE-mediated repression and Polycomb group proteins recruitment in Drosophila (RNA-seq)

ABSTRACT: Crol contributes to PRE-mediated repression and Polycomb group proteins recruitment in Drosophila (RNA-seq)

PROVIDER: PRJNA837457 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19176035.fastq.gz	Fastqsanger.gz
	SRR19176036.fastq.gz	Fastqsanger.gz
	SRR19176037.fastq.gz	Fastqsanger.gz
	SRR19176038.fastq.gz	Fastqsanger.gz
	SRR19176039.fastq.gz	Fastqsanger.gz

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Crol contributes to PRE-mediated repression and Polycomb group proteins recruitment in Drosophila

Project description:Crol contributes to PRE-mediated repression and Polycomb group proteins recruitment in Drosophila

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Crol contributes to PRE-mediated repression and Polycomb group proteins recruitment in Drosophila (ChIP-seq)

Project description:Crol contributes to PRE-mediated repression and Polycomb group proteins recruitment in Drosophila (ChIP-seq)

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Crol contributes to PRE-mediated repression and Polycomb group proteins recruitment in Drosophila (ChIP-seq)

Project description:The Polycomb group (PcG) proteins are fundamental epigenetic regulators that control the repressive state of target genes in multicellular organisms. One of the open questions is defining the mechanisms of PcG recruitment to chromatin. In Drosophila, the crucial role in PcG recruitment is thought to belong to DNA-binding proteins associated with Polycomb response elements (PREs). However, current data suggests that not all PRE-binding factors have been identified. Here, we report the identification of the transcription factor Crooked legs (Crol) as a novel PcG recruiter. Crol is a C2H2-type Zinc Finger protein that directly binds to poly(G)-rich DNA sequences. Mutation of Crol binding sites as well as crol CRISPR/Cas9 knockout diminish the repressive activity of PREs in transgenes. Like other PRE-DNA binding proteins, Crol co-localizes with PcG proteins inside and outside of H2K27me3 domains. Crol knockout impairs the recruitment of the PRC1 subunit Polyhomeotic and the PRE-binding protein Combgap at a subset of sites. The decreased binding of PcG proteins is accompanied by dysregulated transcription of target genes. Overall, our study identified Crol as a new important player in PcG recruitment and epigenetic regulation.

2023-04-19 | GSE202870 | GEO

Crol contributes to PRE-mediated repression and Polycomb group proteins recruitment in Drosophila (RNA-seq)

2023-04-19 | GSE202832 | GEO

Crol contributes to PRE-mediated repression and Polycomb group proteins recruitment in Drosophila.

Project description:The Polycomb group (PcG) proteins are fundamental epigenetic regulators that control the repressive state of target genes in multicellular organisms. One of the open questions is defining the mechanisms of PcG recruitment to chromatin. In Drosophila, the crucial role in PcG recruitment is thought to belong to DNA-binding proteins associated with Polycomb response elements (PREs). However, current data suggests that not all PRE-binding factors have been identified. Here, we report the identification of the transcription factor Crooked legs (Crol) as a novel PcG recruiter. Crol is a C2H2-type Zinc Finger protein that directly binds to poly(G)-rich DNA sequences. Mutation of Crol binding sites as well as crol CRISPR/Cas9 knockout diminish the repressive activity of PREs in transgenes. Like other PRE-DNA binding proteins, Crol co-localizes with PcG proteins inside and outside of H3K27me3 domains. Crol knockout impairs the recruitment of the PRC1 subunit Polyhomeotic and the PRE-binding protein Combgap at a subset of sites. The decreased binding of PcG proteins is accompanied by dysregulated transcription of target genes. Overall, our study identified Crol as a new important player in PcG recruitment and epigenetic regulation.

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Crol contributes to PRE-mediated repression and Polycomb group proteins recruitment in Drosophila

Project description:This SuperSeries is composed of the SubSeries listed below.

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Synergy between variant PRC1 complexes defines Polycomb-mediated gene repression (ChIP-Seq)

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

Polycomb dysfunctional transcriptional repression in muscle stem cells contributes to lamin dependent muscular dystrophy

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Synergy between variant PRC1 complexes defines Polycomb-mediated gene repression (RNA-Seq)

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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