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Identifying functional enhancers regulating Cebpa expression and adipocyte differentiation (mRNA-Seq)

ABSTRACT: Identifying functional enhancers regulating Cebpa expression and adipocyte differentiation (mRNA-Seq)

PROVIDER: PRJNA923019 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23054527.fastq.gz	Fastqsanger.gz
	SRR23054528.fastq.gz	Fastqsanger.gz
	SRR23054529.fastq.gz	Fastqsanger.gz
	SRR23054530.fastq.gz	Fastqsanger.gz
	SRR23054531.fastq.gz	Fastqsanger.gz

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Cebpa in adipocyte differentiation

Project description:Cebpa in adipocyte differentiation

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Identifying functional enhancers regulating Cebpa expression and adipocyte differentiation (mRNA-Seq)

Project description:To explore the effect of enhancer repression on adipocyte differentiation in a transcriptome-wide manner, we infected cells with 1 mL lentiviruses medium containing dCas9-KRAB-En2-sgRNAs (Experimental group) or dCas9-KRAB (Control group) at the multiplicity of infection (MOI) of 100 for 12 h. We performed transcriptional profiling by RNA sequencing (RNA-seq) for dCas9-KRAB-En2 and dCas9-KRAB cells at day 7 of differentiation.

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Project description:Cebpa is a critical transcription factor gene for adipocyte differentiation and adipose tissue development. However, mechanisms controlling Cebpa expression during adipogenic differentiation remain largely unknown. Here, we generated the high-resolution chromatin interaction maps of Cebpa in 3T3-L1 preadipocytes (3T3-L1) and 3T3-L1 adipocytes (3T3-L1-AD) using circularized chromosome conformation capture coupled with next-generation sequencing (4C-seq), and characterized differences in their chromatin interactomes and chromatin status of the interaction sites during adipogenic differentiation. We performed a 4C-seq experiment on inguinal white adipose tissue (iWAT) to evaluate whether chromatin interaction between Cebpa-L1-AD-En2 and Cebpa promoters in 3T3-L1 adipocytes also exists in mouse adipose tissue.

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The p30 isoform of CEBPA uncovers a silent enhancer to drive the expression of the tumor promoting factor CD73 in CEBPA mutant AML

Project description:The key myeloid transcription factor (TF) CEBPA is frequently mutated in acute myeloid leukemia (AML), but the molecular ramifications of this leukemic driver mutation remain elusive. To investigate CEBPA mutant AML, we compared gene expression changes in human CEBPA mutant AML and in the corresponding CebpaLp30 mouse model, and identified a conserved cross-species transcriptional program. ChIP-seq revealed aberrantly activated enhancers, exclusively occupied by the leukemia-associated CEBPA-p30 isoform. One leukemic-enhancer upstream of Nt5e, encoding CD73, was physically and functionally linked to this conserved AML gene, and could be activated by CEBPA. Targeting of CD73-adenosine signaling increased AML survival in transplanted mice. Our data indicate a first-in-class link between a TF cancer driver mutation and a druggable, direct transcriptional target.

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CEBPA Dysfunction Intiates CSF3R Mutant Acute Myeloid Leukemia Through Disruption of Myeloid Lineage Enhancers (Microarray)

Project description:Acute Myeloid Leukemia (AML) develops due to the acquisition of mutations from multiple functional classes. Here, we demonstrate that activating mutations in the granulocyte colony stimulating factor receptor (CSF3R), cooperate with loss of function mutations in the transcription factor CEBPA to promote acute leukemia development. Terminal myeloid differentiation in response to granulocyte colony-stimulating factor signaling requires wild type CEBPA and is blocked by mutations in CEBPA. Inhibition of the histone demethylase LSD1, restores differentiation and in combination with JAK/STAT blockade, produces significant disease response in vivo. Mutant CEBPA blocks myeloid differentiation by preventing the activation of differentiation-associated enhancers. As enhancer activation precedes promoter activation, CEBPA mutations must occur prior to CSF3R mutations to effectively block differentiation and promote leukemia formation in vivo. This study demonstrates that order-dependent oncogene interaction is a fundamental process in AML. Dissecting this process is critical for understanding disease evolution to enable the development of effective therapeutics.

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