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Tet2 deficiency altered hematopoietic stem and progenitor cells ageing process

ABSTRACT: Tet2 deficiency altered hematopoietic stem and progenitor cells ageing process

PROVIDER: PRJNA761674 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15810428_1.fastq.gz	Fastqsanger.gz
	SRR15810428_2.fastq.gz	Fastqsanger.gz
	SRR15810429_1.fastq.gz	Fastqsanger.gz
	SRR15810429_2.fastq.gz	Fastqsanger.gz
	SRR15810430_1.fastq.gz	Fastqsanger.gz

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Tet2 deficiency altered hematopoietic stem and progenitor cells ageing process

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Project description:Loss of function TET2 mutations are frequently seen in myelodysplastic syndrome (MDS) patients. Previous studies have demonstrated that TET2 deficiency enhances maintenance of MDS hematopoietic stem and progenitor cells (HSPCs). Nonetheless, the pathogenic role of TET2 in MDS progression remains elusive. Here, we demonstrate Tet2 knockout (KO) markedly accelerated malignant transformation in Nup98-HoxD13 (NHD13) transgenic mice and promotes leukemogenesis of HoxA9 transduction/transplant mice. Consistently, low TET2 level cooperating with high HOXA9 level predicts poor outcome of MDS patients. Notably, Tet2 KO conferred a clonal advantage to the HSPCs of NHD13 mice. Whole-exome sequencing revealed that Tet2 KO facilitates accumulation of mutations at genes associated with leukemogenesis, including Arih2, whose loss of function promotes MDS cells proliferation. Using 5-hydroxymethylcytosine immunoprecipitation coupled with high-throughput sequencing analysis, we found while Tet2 deletion decreased overall 5hmC levels, it also increased 5hmC distribution at certain mutation loci such as Arih2. Vitamin C treatment, which mimics Tet2/Tet3 restoration, blocked disease progression in Tet2-deficient NHD13 mice. Collectively, our findings demonstrate that TET2 activity governs occurrence of secondary mutations in MDS HSPCs, providing a rationale for enhancing TETs function to block MDS-malignant transformation.

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