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RDNA chromatin interactions in the MYC-driven Eμ-Myc transgenic mouse model of B-cell lymphoma [ChIP-seq UTF]

ABSTRACT: rDNA chromatin interactions in the MYC-driven Eμ-Myc transgenic mouse model of B-cell lymphoma [ChIP-seq UTF]

PROVIDER: PRJNA508322 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8279920_1.fastq.gz	Fastqsanger.gz
	SRR8279920_2.fastq.gz	Fastqsanger.gz
	SRR8279921_1.fastq.gz	Fastqsanger.gz
	SRR8279921_2.fastq.gz	Fastqsanger.gz
	SRR8279922_1.fastq.gz	Fastqsanger.gz

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rDNA chromatin interactions in the MYC-driven Eμ-Myc transgenic mouse model of B-cell lymphoma [4C-seq]

Project description:Long-range interactions of ribososomal DNA (rDNA) identified by 4C-seq in mouse wildtype, premalignant and malignant Eμ-Myc cells and tissue culture adapated Eμ-Myc-shUbtf and Eμ-Myc-LMP (empty vector) cells.

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rDNA chromatin interactions in the MYC-driven Eμ-Myc transgenic mouse model of B-cell lymphoma [RNA-seq]

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rDNA chromatin interactions in the MYC-driven Eμ-Myc transgenic mouse model of B-cell lymphoma [ChIP-seq]

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rDNA chromatin interactions in the MYC-driven Eμ-Myc transgenic mouse model of B-cell lymphoma [ChIP-seq UTF]

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rDNA chromatin interactions in the MYC-driven Eµ-Myc transgenic mouse model of B-cell lymphoma

Project description:rDNA chromatin interactions in the MYC-driven Eµ-Myc transgenic mouse model of B-cell lymphoma

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Gene expression and polysome profiling data of Eμ-Myc B-lymphoma cells

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Defining TFAP4 transcriptional regulation in pre-leukemic Eμ-MYC pre-B lymphoma cells

Project description:Defining TFAP4 transcriptional regulation in pre-leukemic Eμ-MYC pre-B lymphoma cells

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Effect of NEK2 deficiency on gene expression of CD19-selected spleen B cells of Eμ-myc mouse model

Project description:NEK2 overexpression in the B cell lineage affects B cell development. To determine whether deficiency of NEK2 inhibits B cell malignancies, we crossed Nek2 knockout mice with Eμ-myc transgenic mice, a well-established Myc-driven preclinical model for B cell malignancies. Three genotyping offsprings were obtained: Eμ-myc/Nek2+/+ (NEK2 wild type), Eμ-myc/Nek2+/- (NEK2 heterozygotes), and Eμ-myc/Nek2-/- (NEK2 homozygotes). Bulk RNA-seq was performed on CD19-selected spleen B cells to view the transcriptome differences.

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Defining TFAP4 transcriptional regulation in pre-leukemic Eμ-MYC pre-B lymphoma cells

Project description:Many lymphoid malignancies arise from deregulated c-MYC expression in cooperation with additional genetic lesions. While many of these cooperative genetic lesions have been discovered and their functions characterised, DNA sequence data of primary patient samples suggest that many more do exist. However, the nature of their contributions to c-MYC driven lymphomagenesis have not yet been investigated. We identified TFAP4 as a potent suppressor of c-MYC driven lymphoma development in a previous genome-wide CRISPR knockout screen in primary cells in vivo. CRISPR deletion of TFAP4 in Eµ-MYC transgenic haematopoietic stem and progenitor cells (HSPCs) and transplantation of these manipulated HSPCs into lethally irradiated animals significantly accelerated c-MYC-driven lymphoma development. Interestingly, TFAP4 deficient Eµ-MYC lymphomas all arose at the pre-B cell stage of B cell development. This observation prompted us to characterise the transcriptional profile of pre-B cells from pre-leukaemic mice transplanted with Eµ-MYC/Cas9 HSPCs that had been transduced with sgRNAs targeting TFAP4. This analysis revealed that TFAP4 deletion reduced expression of several master regulators of B cell differentiation, such as Spi1, SpiB and Pax5, which are direct target genes of both TFAP4 and MYC. We therefore conclude that loss of TFAP4 leads to a block in differentiation during early B cell development, thereby accelerating c-MYC-driven lymphoma development.

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Transgenic Eµ-myc mouse lymphoma array CGH data

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