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Stag2 regulates hematopoietic differentiation and self-renewal through alterations in gene expression and topological control

ABSTRACT: Stag2 regulates hematopoietic differentiation and self-renewal through alterations in gene expression and topological control

PROVIDER: PRJNA488956 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7777920_1.fastq.gz	Fastqsanger.gz
	SRR7777920_2.fastq.gz	Fastqsanger.gz
	SRR7777921_1.fastq.gz	Fastqsanger.gz
	SRR7777921_2.fastq.gz	Fastqsanger.gz
	SRR7777922_1.fastq.gz	Fastqsanger.gz

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Stag2 regulates hematopoietic differentiation and self-renewal through alterations in gene expression and topological control

Project description:We performed HiC analyzed on wildtype and Stag2 knock-out hematopoietic progeitor cells and integrated with Stag2 ChIP-seq and RNAseq data to identy genes whose expression and tological structures are regulated by Stag2 during hematopoietic differentiation and self-renewal.

2019-09-02 | GSE119366 | GEO

Cohesin Members Stag1 and Stag2 Display Distinct Roles in Chromatin Accessibility and Topological Control of HSC Self-Renewal and Differentiation [RNA_LinNegBM]

Project description:Transcriptional regulators, including the cohesin complex member STAG2, are recurrently mutated in cancer. The role of STAG2 in gene regulation, hematopoiesis, and tumor suppression remains unresolved. We show that Stag2 deletion in hematopoietic stem and progenitor cells (HSPCs) results in altered hematopoietic function, increased self-renewal, and impaired differentiation. Chromatin immunoprecipitation (ChIP) sequencing revealed that, although Stag2 and Stag1 bind a shared set of genomic loci, a component of Stag2 binding sites is unoccupied by Stag1, even in Stag2-deficient HSPCs. Although concurrent loss of Stag2 and Stag1 abrogated hematopoiesis, Stag2 loss alone decreased chromatin accessibility and transcription of lineage-specification genes, including Ebf1 and Pax5, leading to increased self-renewal and reduced HSPC commitment to the B cell lineage. Our data illustrate a role for Stag2 in transformation and transcriptional dysregulation distinct from its shared role with Stag1 in chromosomal segregation.

2019-09-26 | GSE138007 | GEO

Cohesin Members Stag1 and Stag2 Display Distinct Roles in Chromatin Accessibility and Topological Control of HSC Self-Renewal and Differentiation [ATAC_LSK_GMP_CFUE_Stag2KOWT]

2019-09-26 | GSE138003 | GEO

Cohesin Members Stag1 and Stag2 Display Distinct Roles in Chromatin Accessibility and Topological Control of HSC Self-Renewal and Differentiation [RNA_3populations_LSK_GMP_CFUE]

2019-09-26 | GSE138006 | GEO

Cohesin Members Stag1 and Stag2 Display Distinct Roles in Chromatin Accessibility and Topological Control of HSC Self-Renewal and Differentiation [ChIP_LinNeg_Stag1Stag2CTCF]

2019-09-26 | GSE138005 | GEO

Cohesin Members Stag1 and Stag2 Display Distinct Roles in Chromatin Accessibility and Topological Control of HSC Self-Renewal and Differentiation [ATAC_LinNegBM]

2019-09-26 | GSE138004 | GEO

Stag1 and Stag2 regulate cell fate decisions in hematopoiesis through non-redundant topological control [I]

Project description:Transcriptional regulators, including the cohesin complex member STAG2, are recurrently mutated in cancer. The role of STAG2 in gene regulation, hematopoiesis, and tumor suppression remains unresolved. We show Stag2 deletion in hematopoietic stem/progenitor cells (HSPC) results in altered hematopoietic function, increased self-renewal, and impaired differentiation. ChIP-sequencing revealed that while Stag2 and Stag1 bind a shared set of genomic loci, a component of Stag2 binding sites are unoccupied by Stag1 even in Stag2-deficient HSPCs. While concurrent loss of Stag2 and Stag1 abrogated hematopoiesis, Stag2 loss alone decreased chromatin accessibility and transcription of lineage-specification genes, including Ebf1 and Pax5, leading to increased self-renewal and reduced HSPC commitment to the B-cell lineage. Our data illustrate a role for Stag2 in transformation and transcriptional dysregulation distinct from its shared role with Stag1 in chromosomal segregation.

2019-09-23 | GSE134583 | GEO

Stag1 and Stag2 regulate cell fate decisions in hematopoiesis through non-redundant topological control [II]

Project description:Transcriptional regulators, including the cohesin complex member STAG2, are recurrently mutated in cancer. The role of STAG2 in gene regulation, hematopoiesis, and tumor suppression remains unresolved. We show Stag2 deletion in hematopoietic stem/progenitor cells (HSPC) results in altered hematopoietic function, increased self-renewal, and impaired differentiation. ChIP-sequencing revealed that while Stag2 and Stag1 can bind the same loci, a component of Stag2 binding sites are unoccupied by Stag1 even in Stag2-deficient HSPCs. While concurrent loss of Stag2 and Stag1 abrogated hematopoiesis, Stag2 loss alone decreased chromatin accessibility and transcription of lineage-specification genes, including Ebf1 and Pax5, leading to blunted HSPC commitment to the B-cell lineage. Our data illustrate a role for Stag2 in transformation and transcriptional dysregulation distinct from its shared role with Stag1 in chromosomal segregation.

2019-09-24 | GSE134997 | GEO

Cohesin Members Stag1 and Stag2 Display Distinct Roles in Chromatin Accessibility and Topological Control of HSC Self-Renewal and Differentiation [ChIP_LinNeg_Stag1Stag2CTCF]

Project description:Cohesin Members Stag1 and Stag2 Display Distinct Roles in Chromatin Accessibility and Topological Control of HSC Self-Renewal and Differentiation [ChIP_LinNeg_Stag1Stag2CTCF]

| PRJNA574136 | ENA

Cohesin Members Stag1 and Stag2 Display Distinct Roles in Chromatin Accessibility and Topological Control of HSC Self-Renewal and Differentiation [ATAC_LSK_GMP_CFUE_Stag2KOWT]

Project description:Cohesin Members Stag1 and Stag2 Display Distinct Roles in Chromatin Accessibility and Topological Control of HSC Self-Renewal and Differentiation [ATAC_LSK_GMP_CFUE_Stag2KOWT]

| PRJNA574134 | ENA

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