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DNA methylation - PRDM8 reveals aberrant DNA methylation in aging syndromes and is relevant for hematopoietic and neuronal differentiation.

ABSTRACT: DNA methylation - PRDM8 reveals aberrant DNA methylation in aging syndromes and is relevant for hematopoietic and neuronal differentiation.

PROVIDER: PRJNA592138 | ENA |

REPOSITORIES: ENA

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DNA methylation - PRDM8 reveals aberrant DNA methylation in aging syndromes and is relevant for hematopoietic and neuronal differentiation.

Project description:Dyskeratosis congenita (DKC) and idiopathic aplastic anemia (AA) are bone marrow failure syndromes that share characteristics of premature aging with severe telomere attrition. In this study, we analyzed blood samples of 62 AA and 13 DKC patients to demonstrate that their epigenetic age predictions are overall increased, albeit not directly correlated with telomere length. Aberrant DNA methylation was observed in the gene PRDM8 in DKC and AA as well as in other diseases with premature aging phenotype, such as Down syndrome, Werner syndrome and Hutchinson-Gilford-Progeria syndrome. To gain further insight into the functional relevance of PRDM8 we generated induced pluripotent stem cells (iPSCs) with heterozygous and homozygous knockout. Loss of PRDM8 impaired hematopoietic and neuronal differentiation of iPSCs, but it did not impact on epigenetic age. Taken together, aberrant DNA methylation in PRDM8 provides a biomarker for bone marrow failure syndromes, which may contribute to the hematopoietic and neuronal phenotypes of premature aging syndromes.

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PRDM8 reveals aberrant DNA methylation in aging syndromes and is relevant for hematopoietic and neuronal differentiation.

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Gene expression - PRDM8 reveals aberrant DNA methylation in aging syndromes and is relevant for hematopoietic and neuronal differentiation.

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Gene expression - PRDM8 reveals aberrant DNA methylation in aging syndromes and is relevant for hematopoietic and neuronal differentiation.

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Project description:Many pediatric malignancies are embryonal in nature, and one hypothesis for the origin of embryonal tumors is that they arise from a defect in differentiation, either by an inability to terminally differentiate or a reversion to a pluripotent state. There is emerging evidence that epigenetic regulation plays an important role in the transition from embryonic stem cell to a more committed cell fate, utilizing both de novo DNA methylation and poised M-bM-^@M-^XbivalentM-bM-^@M-^Y chromatin domains (H3K27me3 and H3K4me3) to abolish pluripotency and gain lineage- and cell-type-specific characteristics as a cell differentiates. Thus inappropriate epigenetic silencing by aberrant DNA methylation of bivalent genes required for differentiation could lead to the uncontrolled cell growth observed in cancer. Our broad hypothesis is that aberrant DNA methylation in cancer is targeted to a non-random subset of critical pathways used in normal development. This dysregulation of the normal epigenetic program used in development promotes cellular proliferation and provides a mechanism to block differentiation in pediatric cancers, such as rhabdomyosarcoma. Examination of DNA methylation in fourteen human rhabdomyosarcoma patient samples using RRBS. In addition, RRBS was used to examine DNA methylation in one human rhabdomyosarcoma cell line (RD) forced to terminally differentiate by expression of the forced heterodimer MyoD~E12 (MDE). Lastly, RRBS was used to examine DNA methylation changes during normal differentiation in one primary human normal myoblast cell line

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