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Integrated analysis of transcriptional and chromatin alteration in Jak2V617F and Asxl1-/-Jak2V617F BM c-kit+ cells

ABSTRACT: Integrated analysis of transcriptional and chromatin alteration in Jak2V617F and Asxl1-/-Jak2V617F BM c-kit+ cells

PROVIDER: PRJNA751476 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15322700_1.fastq.gz	Fastqsanger.gz
	SRR15322700_2.fastq.gz	Fastqsanger.gz
	SRR15322701_1.fastq.gz	Fastqsanger.gz
	SRR15322701_2.fastq.gz	Fastqsanger.gz
	SRR15322702_1.fastq.gz	Fastqsanger.gz

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Integrated analysis of transcriptional and chromatin alteration in Jak2V617F and Asxl1-/-Jak2V617F BM c-kit+ cells

Project description:We performed bulk RNA-seq, transposase-accessible chromatin using sequencing (ATAC-Seq) and chromatin immunoprecipitation (ChIP)-seq on Asxl1-/-Jak2VF and Jak2VF BM c-kit+ cells to elucidate the transcriptional and associated epigenetic alterations after Asxl1 deletion. GSEA showed that the upregulated genes in Asxl1-/-Jak2VF were significantly associated with bona fide PcG target genes, as identified by the overlap between H3K27me3 and H2AK119ub1 ChIP-seq experiments . Integrated analysis of RNA-seq and ATAC-seq data showed that there existed a significant increase of chromatin accessibility associated with upregulated genes, and these sites with gained accessibility were enriched with increased levels of H3K4me1 and H3K27ac, histone marks of active enhancers in Asxl1-/-Jak2VF BM c-kit+ cells. Moreover, PcG target gene Egr1 was upregulated in BM c-kit+ cells compared with other three genotypes and considered as key gene for disease phenotypes.

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Project description:Recent studies have shown that both TET2 mutation and JAK2V617F mutation are frequent in myeloproliferative neoplasms patients. The pathophysiological roles of each mutation have been elucidated in murine models, but the cooperative effect of the two mutations has not been elucidated yet. In this study, we examined the function of the cooperative effect of loss-of-TET2 function and JAK2V617F mutation in murine hematopoiesis. In this study, we utilized wild type (WT) mice, TET2 knock down (TET2KD) mice, JAK2V617F transgenic mice, double mutant mice. We transplanted 4 types of E14.5 fetal liver cells (WT, TET2KD, JAK2V617F, double mutant) into lethally irradiated mice. At 10-16 weeks post-transplantation, LSK cells from the BM of the recipients were collected, and gene expression analysis was performed. (WT,5 mice at 16 weeks; TET2KD, 5 mice at 10 weeks; JAK2V617F, 5 mice at 16 weeks; double mutant, 5 mice at 13 weeks)

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Project description:The JAK2V617F mutation has been reported in about 40-60% of Essential Thrombocythemia (ET) patients. However, little is known about specific molecular abnormalities of the hematopoietic stem cell compartment of ET according to JAK2 mutation. Therefore, we compared the gene expression profiles of bone marrow (BM) CD34+ cells from 16 patients with and without the JAK2V617F mutation to identify differentially expressed genes. Keywords: cell type comparison Sample name and JAK2V617F mutation: - BM CD34+ cells from healthy subject (CTR) - ET JAK2V617F-positive: ET 1, ET 4, ET 6, ET 7, ET 8, ET 10, ET 12, ET 15 - ET JAK2V617F-negative: ET 2, ET 3, ET 5, ET 9, ET 11, ET 13, ET 14, ET 16

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Interleukin-1 contributes to clonal expansion and progression of bone marrow fibrosis in JAK2V617F-induced myeloproliferative neoplasm

Project description:The somatic JAK2V617F mutation is found in a majority of patients with myeloproliferative neoplasms (MPN). Chronic inflammation is often associated with MPN, but the role of inflammation in the pathogenesis of MPN remains elusive. Expression of interleukin-1 (IL-1), a key regulator of inflammation, is found elevated in MPN. Here, we show that increased IL-1β enhances myeloid cell expansion and promotes the development of bone marrow (BM) fibrosis in heterozygous Jak2V617F mouse model of MPN. Genetic deletion of IL-1 receptor 1 (IL-1R1) preferentially inhibited the expansion of Jak2 mutant hematopoietic stem/progenitor cells. Furthermore, IL-1R1 deletion or blockade with anti-IL-1R1 antibody significantly reduced leukocytosis and splenomegaly, and markedly inhibited BM fibrosis in homozygous Jak2V617F mutant mice. Collectively, our results suggest that IL-1 signaling plays an important role in progression to BM fibrosis in MPN, and targeting of IL-1R1 could be a useful strategy for the treatment of myelofibrosis.

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