DNA methylation of neural differentiation from human adipose derived stem cells
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ABSTRACT:
PROVIDER: PRJNA607743 | ENA |
REPOSITORIES: ENA
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Project description:This study investigates the molecular mechanisms by which the DNA/RNA-binding protein HNRNPU regulates gene expression during early human neural development. Pathogenic variants in HNRNPU cause a severe neurodevelopmental disorder, but the underlying mechanisms remain poorly understood. To explore the role of HNRNPU in transcriptional and epigenetic regulation, we used human induced pluripotent stem cell (hiPSC)-derived neuroepithelial stem cells (NES) and differentiating neural cells as model systems. We performed formaldehyde crosslinking and ribonucleoprotein immunoprecipitation followed by RNA sequencing (fRIP-seq) to identify RNA targets bound by HNRNPU, whole-genome bisulfite sequencing (WGBS) to assess the impact of HNRNPU silencing on DNA methylation landscapes, and CUT&RUN profiling to map chromatin marks at regulatory regions. Together, these datasets provide a comprehensive view of HNRNPU’s interactions with RNA, and its influence on the epigenetic state of key developmental genes. The data can be used to study RNA–protein interactions, DNA methylation dynamics, and chromatin regulation during neural differentiation. Mass spectrometry data was deposited to PRIDE under accession number PXD061718.
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Project description:Neural crest cells (NCCs) originate from the neural tube during early embryogenesis, and they are a pivotal cell population involved in vertebrate development. NCCs are mainly divided into cranial NCCs (cNCCs) and trunk NCCs (tNCCs), which subsequently differentiate into diverse tissues and organs. Proper differentiation and fate determination into NCCs are essential for normal development and survival of individuals, and abnormal differentiation of NCCs can lead to various diseases such as cardiac disorders and tumors. Epigenetic mechanisms, including histone modification and DNA methylation, are crucial for regulating NCC differentiation. However, the specific mechanisms of DNA methylation underlying the differentiation of cNCCs and tNCCs remain poorly understood. This study aimed to address this knowledge gap by comparing the differentiation mechanisms of cranial and trunk NCCs derived from human induced pluripotent stem cells. Through integrated analysis of the transcriptome and DNA methylome data, we found that along with differentiation, DNA demethylation upstream of the transcription start sites of myocyte enhancer factor 2C (MEF2C) in cNCCs and thyroid hormone receptor alpha-2 (THRA2) in tNCCs led to increased expression of these genes. Furthermore, MEF2C and THRA2 were found to potentially regulate NCC markers. Our findings contribute to a detailed understanding of regulatory mechanisms of DNA methylation in normal NCC differentiation and may provide insights into the pathogenesis of NCC-related diseases such as neuroblastoma.
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Project description:Tissue and their component cells have unique DNA methylation profiles comprising DNA methylation patterns of tissue-dependent and differentially methylated regions (T-DMRs). T-DMRs are found throughout the genome and influence tissue-specific gene expression. DNA methylation profile of T-DMRs underlies the network of tissue- and developmental stage-specific transcription factors and their targets. The adult brain consists of various kinds of cells that sequentially appear as neurons, astrocytes, and oligodendrocytes from late gestation through the neonatal period. Distinctive neural progenitor cells (NPCs) that exhibit different differentiation poteintials to neurons to glial cells are generated during mid-to-late gestation. To explore DNA methylation profiles of mouse NPCs, we compared neurospheres derived from telencephalons at embryonic day 11.5 (E11.5NSph) and 14.5 (E14.5NSph) by T-DMR profiling with restriction tag-mediated amplification (D-REAM) combined with Affymetrix GeneChip Mouse Promoter 1.0R Array. We used HpyCH4IV, a methylation-sensitive restriction enzyme that recognizes ACGT residues. Because these are uniformly distributed across the genome, it enables less biased analysis. By comparing D-REAM data between E11.5NSph and E14.5NSph, we identified genes with T-DMRs including those involved in neural develpment and/or associated with neurological disorders in humans. The present study elucidates the underlying dynamics of the DNA methylation profile of T-DMRs during neural development, including insights into developmental stage-specific hypomethylation of T-DMRs around TSSs.
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Project description:Human induced pluripotent stem cells (hiPSCs) are useful as a tool for reproducing neural development in vitro. However, each hiPSC line has a different ability to differentiate into specific lineages, as known as differentiation propensity, resulting in reduced reproducibility and increased time and cost requirements for research use. To overcome this issue, we searched for predictive signatures of neural differentiation propensity of hiPSCs using DNA methylation which is the main modulator of cellular properties. We obtained 32 lines of hiPSC and its comprehensive DNA methylation data by Infinium MethylationEPIC beadchip. To assess the neural differentiation efficiency of these hiPSCs, we measured the percentage of PAX6-positive cells on day 7 of neural stem cell induction by the dual-SMAD inhibition protocol. Using DNA methylation data of undifferentiated hiPSCs and their measured differentiation efficiency into neural stem cells as the set of data, and HSIC Lasso, a machine learning-based nonlinear feature selection method, we attemted to identify neural differentiation associated differentially methylated sites. Epigenome-wide unsupervised clustering could not distinguish between hiPSCs with varying differentiation efficiency. On the other hand, HSIC Lasso identified 62 probes that can explain the neural differentiation efficiency of hiPSCs. Selected features by HSIC Lasso were particularly enriched within the 3 Mbp on chromosome 5, harboring the IRX2, C5orf38, and IRX1 genes. Within this region, DNA methylation rates were correlated with neural differentiation efficiency particular to female hiPSCs and negatively correlated with gene expression of the IRX1/2 genes. In addition, forced expression of the IRX1/2 genes impaired the neural differentiation ability of hiPSCs. We have shown for the first time that DNA methylation state on the IRX1/2 genes of hiPSCs is predictive biomarker of their ability for neural differentiation. The predictive markers for neural differentiation efficiency identified in this study can be useful for selection of suitable undifferetiated hiPSCs prior to differentiation induction.
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