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Transcriptome changes caused by Phf6 deletion in Committed leukemic cells from the retroviral-HoxA9 AML mouse model [RNA-seq Committed leukemic cell]

ABSTRACT: Transcriptome changes caused by Phf6 deletion in Committed leukemic cells from the retroviral-HoxA9 AML mouse model [RNA-seq Committed leukemic cell]

PROVIDER: PRJNA1047181 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27007426_1.fastq.gz	Fastqsanger.gz
	SRR27007426_2.fastq.gz	Fastqsanger.gz
	SRR27007427_1.fastq.gz	Fastqsanger.gz
	SRR27007427_2.fastq.gz	Fastqsanger.gz
	SRR27007428_1.fastq.gz	Fastqsanger.gz

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Transcriptome changes caused by Phf6 deletion in Committed leukemic cells from the retroviral-HoxA9 AML mouse model [RNA-seq Committed leukemic cell]

Project description:Hematopoietic conditional knockout (cKO) of Phf6 in a mouse retroviral-HoxA9 AML model led to increased transplantability. We performed bulk RNA-Seq on the 'committed' population (c-Kit+, Ly6C+) sort purified from primary recipients of HoxA9-transduced Ctrl (Vav-Cre/+, Phf6 +/Y marrow transduced with HoxA9) and cKO cells (Vav-Cre/+, Phf6 flox/Y marrow transduced with HoxA9) 8 weeks after transplantation. Our results reveal that Phf6 deletion has minimal effects on the transcriptome of the committed population (see separately deposited series for effects on the transcriptome of leukemia initiating [LIC-e] cells).

2023-12-15 | GSE249109 | GEO

Chromatin accessibility changes caused by Phf6 deletion in Leukemia-initiating cells from the retroviral-HoxA9 AML mouse model [ATAC-Seq LICe]

Project description:Hematopoietic conditional knockout (cKO) of Phf6 in a mouse retroviral-HoxA9 AML model led to increased transplantability and accumulation of a c-Kit+ Ly6C- population that we termed the 'Leukemia Initiating Cell-Enriched' (LIC-e) population. We performed bulk ATAC-Seq on the LIC-e population sort purified 4 days after transduction of Ctrl (Vav-Cre/+, Phf6 +/Y) or cKO (Vav-Cre/+, Phf6 flox/Y) marrow retrovirally transduced with HoxA9.

2023-12-15 | GSE249110 | GEO

Evaluation of the NUP98-HOXA9 role as oncogenic transcription factor

Project description:To study the oncogenic mechanism triggered by the leukemic fusion protein NUP98-HOXA9, we cloned the cDNA of NUP98-HOXA9 into a retroviral vector (pMSCV-IRES-GFP) and efficiently transduced the HEK293FT human cell line. We performed a ChIP-seq analysis to identify the DNA binding sites of NUP98-HOXA9. These results allowed us to demonstrate that NUP98-HOXA9 regulates the expression of genes involved in the development of Acute Myeloid Leukemia by directly interacting with their enhancer regions. We further investigated the functional contribution to the DNA binding profile of the two moieties that compose the fusion protein. We cloned the coding region of HOXA9 wt and NUP98 wt in the same retroviral vector, established two new cellular models, 293FT-HOXA9 and 293FT-NUP98, and performed separate ChIP-seq analyses. We demonstrated that both moieties contribute importantly to the regulation of the target genes.

2016-12-31 | GSE62586 | GEO

Transcriptome changes caused by Phf6 deletion in Leukemia-initiating cells from the retroviral-HoxA9 AML mouse model [RNA-seq LICe]

Project description:Transcriptome changes caused by Phf6 deletion in Leukemia-initiating cells from the retroviral-HoxA9 AML mouse model [RNA-seq LICe]

| PRJNA1047178 | ENA

HOXA9 Reprograms the Enhancer Landscape During Leukemic Transformation

Project description:HOXA9 Reprograms the Enhancer Landscape During Leukemic Transformation

| PRJNA401435 | ENA

Chromatin accessibility changes caused by Phf6 deletion in Leukemia-initiating cells from the retroviral-HoxA9 AML mouse model [ATAC-Seq LICe]

Project description:Chromatin accessibility changes caused by Phf6 deletion in Leukemia-initiating cells from the retroviral-HoxA9 AML mouse model [ATAC-Seq LICe]

| PRJNA1047180 | ENA

Leukemic hematopoietic stem cell FLA2

Project description:Sca1+Lineage-cKit+ fetal liver (FL) and bone marrow (BM) cells were sorted and infected with Hoxa9+Meis retroviral particles, which provided fully leukemic complement to hematopoietic cells. These cells were injected into mice and leukemia onset was monitored in vivo. Leukemic stem cell (L-HSC) frequencies of these primary leukemias were evaluated using limiting dilution stem cell transfer in secondary recipients. The L-HSC frequency is near absolute for the FLA2 leukemia (around 1 L-HSC per 1.4 total leukemic bone marrow cells), whereas the other leukemias (FLB1, FLB2 and BM-derived leukemias) generated within the same experiment have a wide range of L-HSC frequencies. Keywords: other

2012-06-04 | GSE7235 | GEO

PHF6 suppresses self-renewal of leukemic stem cells in AML

Project description:PHF6 suppresses self-renewal of leukemic stem cells in AML

| PRJNA1128120 | ENA

Development of NUP98-HOXA9 gene expression signatures

Project description:To explore the molecular mechanisms induced by the leukemic fusion protein NUP98-HOXA9, we performed gene expression analysis of human hematopoietic progenitors and primary samples of patients that express NUP98-HOXA9. By combining these data with ChIP-seq results, we observed that the fusion protein is able to both activate and repress the expression of its target genes.

2016-12-31 | GSE62585 | GEO

Phf6-null hematopoietic stem cells have enhanced self-renewal capacity and oncogenic potentials

Project description:Plant homeodomain finger gene 6 (PHF6) encodes a 365-amino-acid protein containing two plant homology domain fingers. Germline mutations of human PHF6 cause Börjeson–Forssman–Lehmann syndrome, a congenital neurodevelopmental disorder. Loss-of-function mutations of PHF6 are detected in patients with acute leukemia, mainly of T cell lineage and in a small proportion of myeloid lineage. The functions of PHF6 in physiological hematopoiesis and leukemogenesis remain incompletely defined. To address this question, we generated a conditional Phf6 knockout mouse model and investigated the impact of Phf6 loss on the hematopoietic system. We found that Phf6 knockout mice at 8-week age had reduced numbers of CD4+ and CD8+ T cells in the peripheral blood compared to the wild-type littermates. There were decreased granulocyte-monocytic progenitors but increased Lin-c-Kit+Sca-1+ (LSK) cells in the marrow of young Phf6 knockout mice. Functional studies including competitive repopulation unit and serial transplantation assays revealed an enhanced reconstitution and self-renewal capacity in Phf6 knockout hematopoietic stem cells (HSCs). Aged Phf6 knockout mice had myelodysplasia-like presentations including decreased platelet counts, megakaryocyte dysplasia, and enlarged spleen related to extramedullary hematopoiesis. Moreover, we found that Phf6 loss lowered the threshold of NOTCH1-induced leukemic transformation at least partially through increased leukemia-initiating cells. Transcriptome analysis on the restrictive rare HSC subpopulations revealed upregulated cell cycling and oncogenic functions, with alteration of expression of key genes in those pathways. In summary, our studies demonstrate the in vivo crucial roles of Phf6 in physiological and malignant hematopoiesis.

2019-08-21 | GSE129465 | GEO

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