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Acute loss of TET function results in aggressive myeloid cancer in mice

ABSTRACT: Acute loss of TET function results in aggressive myeloid cancer in mice

PROVIDER: PRJNA294512 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR2229290.fastq.gz	Fastqsanger.gz
	SRR2229300_1.fastq.gz	Fastqsanger.gz
	SRR2229300_2.fastq.gz	Fastqsanger.gz
	SRR2229310_1.fastq.gz	Fastqsanger.gz
	SRR2229310_2.fastq.gz	Fastqsanger.gz

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Acute loss of TET function results in aggressive myeloid cancer in mice [RNA-Seq]

Project description:TET-family dioxygenases oxidize 5-methylcytosine (5mC) in DNA, and exert tumor suppressor activity in many types of cancers. Even in the absence of TET coding region mutations, TET loss-of-function is strongly associated with cancer. We show that acute elimination of TET function induces the rapid development of an aggressive, fully-penetrant and cell-autonomous myeloid leukemia in mice, pointing to a causative role for TET-loss-of-function in this myeloid malignancy. Phenotypic and transcriptional profiling showed aberrant differentiation of hematopoietic stem/ progenitor cells, impaired erythroid and lymphoid differentiation and strong skewing to the myeloid lineage, with only a mild relation to changes in DNA modification. We also observed progressive accumulation of DNA damage and strong impairment of DNA break repair, suggesting a key role for TET proteins in maintaining genomic integrity.

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Acute loss of TET function results in aggressive myeloid cancer in mice [WGBS]

Project description:To evaluate the DNA methylation in LSK cells from the bone marrow of wildtype or Tet2/3 DKO mice. In order to address the impact of the loss of Tet2/3 proteins in DNA methylation in LSK cells, we compared by WGBS the methylome of wild and, Tet2/3 DKO LSK cells in bone marrow.

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Acute loss of TET function results in aggressive myeloid cancer in mice.

Project description:TET-family dioxygenases oxidize 5-methylcytosine (5mC) in DNA, and exert tumour suppressor activity in many types of cancers. Even in the absence of TET coding region mutations, TET loss-of-function is strongly associated with cancer. Here we show that acute elimination of TET function induces the rapid development of an aggressive, fully-penetrant and cell-autonomous myeloid leukaemia in mice, pointing to a causative role for TET loss-of-function in this myeloid malignancy. Phenotypic and transcriptional profiling shows aberrant differentiation of haematopoietic stem/progenitor cells, impaired erythroid and lymphoid differentiation and strong skewing to the myeloid lineage, with only a mild relation to changes in DNA modification. We also observe progressive accumulation of phospho-H2AX and strong impairment of DNA damage repair pathways, suggesting a key role for TET proteins in maintaining genome integrity.

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Acute loss of TET function results in aggressive myeloid cancer in mice

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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Project description:This SuperSeries is composed of the SubSeries listed below.

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Inducible disruption of Tet genes results in myeloid malignancy, readthrough transcription, and a heterochromatin-to-euchromatin switch [WGBS]

Project description:The three mammalian TET dioxygenases oxidize the methyl group of 5-methylcytosine (5mC) in DNA, and the oxidised methylcytosines are essential intermediates in all known pathways of DNA demethylation. To define the in vivo consequences of complete TET deficiency, we inducibly deleted all three Tet genes in the mouse genome. Tet1/2/3 inducible TKO (iTKO) mice succumbed to acute myeloid leukaemia by 4-5 weeks. Single-cell RNA sequencing of Tet iTKO bone marrow cells revealed the appearance of new myeloid cell populations characterised by a striking increase in expression of all members of the stefin/cystatin gene cluster on mouse chromosome 16. In patients with acute myeloid leukaemia, high stefin/cystatin gene expression correlates with poor clinical outcomes. Increased expression of the clustered stefin/cystatin genes was associated with a heterochromatin-to-euchromatin compartment switch with readthrough transcription downstream of the clustered stefin/cystatin genes as well as other highly expressed genes but only minor changes in DNA methylation. Our data highlight new roles for TET enzymes that are distinct from their established function in DNA demethylation, and instead involve increased transcriptional readthrough and changes in three-dimensional genome organisation.

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Project description:Acute loss of TET function results in aggressive myeloid cancer in mice [WGBS]

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