Phf23 regulates embryonic neurogenesis by increasing the level of H3K27ac of Tcf4 [CUT&Tag]
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PROVIDER: PRJNA1163697 | ENA |
REPOSITORIES: ENA
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Project description:Epigenetic regulation is an important cell fate modality that is ubiquitous in neural development and plays an important role in both the fate determination and differentiation of neural stem cells (NSCs). The epigenetic regulator Phf23 is widely expressed in different human tissues and is involved in various biological processes, but its functional role in development has rarely been reported. Here, we found that Phf23 is an important epigenetic regulator that maintains embryonic neurogenesis in mice, and its absence leads to inhibition of the acetylation level of H3K27ac through the function of Hdac2, resulting in the blockage of embryonic NSCs differentiation at embryonic day 13.5 (E13.5). Tcf4, a transcription factor closely associated with neurogenesis, is a key downstream target gene of Phf23 in regulating embryonic neurogenesis, which may provide insights into the neuromodulatory network of the brain and the diagnosis and treatment of clinically relevant diseases.
2025-06-30 | GSE277736 | GEO
Project description:Epigenetic regulation is an important cell fate modality that is ubiquitous in neural development and plays an important role in both the fate determination and differentiation of neural stem cells (NSCs). The epigenetic regulator Phf23 is widely expressed in different human tissues and is involved in various biological processes, but its functional role in development has rarely been reported. Here, we found that Phf23 is an important epigenetic regulator that maintains embryonic neurogenesis in mice, and its absence leads to inhibition of the acetylation level of H3K27ac through the function of Hdac2, resulting in the blockage of embryonic NSCs differentiation at embryonic day 13.5 (E13.5). Tcf4, a transcription factor closely associated with neurogenesis, is a key downstream target gene of Phf23 in regulating embryonic neurogenesis, which may provide insights into the neuromodulatory network of the brain and the diagnosis and treatment of clinically relevant diseases.
2025-06-30 | GSE277737 | GEO
Project description:Phf23 regulates embryonic neurogenesis by increasing the level of H3K27ac of Tcf4 [RNA-seq]
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Project description:HAND2, MEIS2 and TCF4 are master transcription factors (TFs) in neuroblastoma and create an interconnected core regulatory circuitry (CRC) by directly occupying each other's and their own super-enhancers (SEs), which leads to high levels of each TF expression inside the CRC. Additionally, CRC TFs cooperatively co-occupy the same SE components, which promotes the expression of genes involved in cell identity and cell-type-specific activities. Super-enhancer-mediated CRC enriched at key oncogenes in neuroblastoma. In the present study, CUT&Tag (Cleavage Under Targets and Tagmentation) analysis was performed to explore the target of HAND2, MEIS2 and TCF4 in NB cells.
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Project description:Mutations of TCF4, which encodes a basic helix-loop-helix transcription factor, cause Pitt-Hopkins syndrome (PTHS) via multiple genetic mechanisms. TCF4 is a complex locus expressing multiple transcripts by alternative splicing and use of multiple promoters. We report a three-generation family segregating mild intellectual disability with an apparently balanced chromosomal translocation t(14;18)(q23.3;q21.2) that we characterized as a complex unbalanced karyotype 46,XY,der(14)del(14)(q23.3q23.3)t(14;18)(q23.3;q21.2)del(18)(q21.2q21.2) del(18)(q21.2q21.2)inv(18)(q21.2q21.2),der(18)t(14 ;18)(q23.3;q21.2) disrupting TCF4. Using whole genome sequencing, transcriptome sequencing, qRT-PCR and nCounter analysis, we characterized the breakpoint junctions from derivative chromosomes and gene expression at the TCF4 locus. Our analyses revealed that family members segregating mild intellectual disability with the complex chromosome aberration had normal expression of genes along chromosomes 14 or 18 and no marked changes in expression of genes other than TCF4. Affected individuals had 12-33 fold higher mRNA levels of TCF4 than did unaffected controls or individuals with PTHS. Increased levels of TCF4 transcript variants originating distal to the translocation breakpoint, not the fusion transcript generated by the derivative chromosome, contributed to this increased. Although validation in additional patients is required, our findings suggest that the dysmorphic features and severe intellectual disability characteristic of PTHS is partially rescued by overexpression of short TCF4 transcripts encoding a nuclear localization signal, a transcription activation domain, and the basic helix-loop-helix domain. Examination of TCF4 Isoform expression comparison between mutant and control skin fibroblast tissues
2016-05-31 | E-GEOD-77742 | biostudies-arrayexpress
Project description:In order to study the molecular mechanisms involving TCF4 in keratinocytes under different inflammatory responses, control and TCF4 knock down keratinocytes were stimulated with inflammatory cytokines and conducted RNA-seq to profile the gene expression.
2024-06-05 | GSE260642 | GEO
Project description:Haplo-insufficiency of TCF4 induced by mutations or microdeletion of TCF4 gene causes Pitt-Hopkins Diseases. Recent gene association studies revealed that mutations of TCF4 is significantly associated with schizophrenia. But the role of TCF4 in developing neocortex is not known. The goal of this study is to identify TCF4 itranscriptional regulatory pathways in developing neocortex by analyzing transcriptomes of dorsal telencephalons of TCF4knockout, TCF4Heterozygote and WT littermates and comparing differential expressed genes between these genotypes.
2019-02-06 | GSE79663 | GEO
Project description:Common genetic variants in and around the gene encoding transcription factor 4 (TCF4) are associated with an increased risk of schizophrenia whereas rare variants have been found in patients with intellectual disability (ID), developmental disorders and autism spectrum disorder (ASD). Haploinsufficiency of TCF4 also causes Pitt Hopkins syndrome (PTHS); a condition characterized by developmental delay, ID and autonomic dysfunction. To understand the role of TCF4 in these disorders, we have used chromatin immunoprecipitation and next generation sequencing (ChIP-seq) to identify the genomic binding sites for TCF4. In this study we identify 10,604 binding sites assigned to 5,437 genes. De novo motif enrichment found that approximately 77% of the TCF4 binding sites contained at least one E-box (5’-CAtcTG). Furthermore, the majority of TCF4 binding sites overlapped with H3K27ac histone mark for active enhancers. Enrichment analysis on the set of TCF4 targets identified numerous, highly significant functional clusters for pathways including nervous system development, ion transport and signal transduction and co-expression modules for genes associated with synaptic function and brain development. Importantly, we found that genes harboring de novo mutations in schizophrenia (P < 5.3 x 10-7), ASD (P < 2.5 x 10-4) and ID (P < 7.6 x 10-3) were also enriched among TCF4 targets. These data demonstrate that TCF4 binding sites are found in a large number of neuronal genes that include genetic risk factors for common neurodevelopmental disorders.
2017-12-08 | GSE96915 | GEO
Project description:H3K27ac CUT&Tag analysis of Sox17-Erg and Etv2 reprogramming of cardiac fibroblasts into endothelial cells
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