Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA309462 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3112447.fastq.gz | Fastqsanger.gz | |||
| SRR3112448.fastq.gz | Fastqsanger.gz | |||
| SRR4046800.fastq.gz | Fastqsanger.gz | |||
| SRR4046791.fastq.gz | Fastqsanger.gz | |||
| SRR4046792.fastq.gz | Fastqsanger.gz |
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Project description:Genomic imprinting is an epigenetic regulation which leads to gene expression in a parent-of-origin specific manner. Previously we have demonstrated that AFF3, the central component of Super Elongation Complex-like 3 (SEC-L3), can specifically bind both the intergenic differentially methylated region (IG-DMR) and the enhancer within the imprinted Dlk1-Dio3 locus to regulate the expression of the Meg3 polycistron. However, the mechanism underlying how AFF3 can interact with distinct chromatin regulatory elements remains unknown. Here, we demonstrate that AFF3 is associated with the Krüppel-like zinc finger protein ZFP281. ZFP281 is required for the recruitment of AFF3 to the enhancer and regulates the allele-specific expression of the Meg3 polycistron in mouse embryonic stem (ES) cells at the transcriptional elongation level. Our genome-wide analyses further identify ZFP281 as a critical factor generally associating with AFF3 at enhancers and functioning together with AFF3 in regulating the expression of a subset of gene. Our study suggests that different zinc finger proteins can function as molecular switchers to regulate the context-dependent function of AFF3 and set a balanced chromatin state for maintaining the allele specific expression pattern of the imprinted Dlk1-Dio3 locus. PLEASE BE AWARE THAT THE SUBMITTER REQUESTED DELETION OF BIGWIG AND PEAK-CALL FILES POST-PUBLICATION. PLEASE CONTACT SUBMITTER FOR FURTHER INFORMATION.
2016-12-08 | GSE77115 | GEO
Project description:Genomic imprinting is a critical developmental process characteristic of parent-of-origin- specific gene expression. Here, we have identified the AFF family protein, Aff3, as a factor that functionally interacts with imprinted loci. Indeed, our genome-wide studies demonstrate that Aff3 specifically binds both imprinting control regions (ICRs) and enhancers within imprinted loci in an allele-specific manner. We have identified the molecular regulators involved in the recruitment of Aff3 to ICRs to impede transcription through the ICR, and provide a mechanism requiring Aff3 within the Super Elongation Complex-like 3 (SEC-L3) in the expression of an imprinted polycistronic transcript spanning the Dlk1-Dio3 locus. Our study also shows that DNA methylation at the ICR reinforces silencing of its related enhancers by controlling the binding and activity of Aff3 in an allele-specific manner. This study provides molecular details about the regulation of dosage-critical imprinted gene expression through Aff3âs function in transcriptional elongation control. ChIP-seq of Aff3 in different mES cells. ChIP-seq of Aff3, PolII, H3K9me3 in uniparental MEF cell lines. ChIP-seq of H3K27ac and PolII in mES cells after Aff3 shRNA and non-targeting shRNA. ChIP-seq of H3K27ac in wild type and Zfp57 knockout ES cells. Total RNA-seq and nascent RNA-seq of mES cells after Aff3 shRNA and non-targeting shRNA. Total RNA-seq of uniparental MEF cells after Aff3 shRNA and non-targeting shRNA.
2016-07-03 | E-GEOD-64489 | biostudies-arrayexpress
Project description:Genomic imprinting is a critical developmental process characteristic of parent-of-origin- specific gene expression. Here, we have identified the AFF family protein, Aff3, as a factor that functionally interacts with imprinted loci. Indeed, our genome-wide studies demonstrate that Aff3 specifically binds both imprinting control regions (ICRs) and enhancers within imprinted loci in an allele-specific manner. We have identified the molecular regulators involved in the recruitment of Aff3 to ICRs to impede transcription through the ICR, and provide a mechanism requiring Aff3 within the Super Elongation Complex-like 3 (SEC-L3) in the expression of an imprinted polycistronic transcript spanning the Dlk1-Dio3 locus. Our study also shows that DNA methylation at the ICR reinforces silencing of its related enhancers by controlling the binding and activity of Aff3 in an allele-specific manner. This study provides molecular details about the regulation of dosage-critical imprinted gene expression through Aff3’s function in transcriptional elongation control.
2016-01-01 | GSE64489 | GEO
Project description:Although many long non-coding RNAs (lncRNAs) are controlled by genomic imprinting, their roles often remain unknown. The Dlk1-Dio3 imprinted domain expresses the lncRNA Meg3 (also called Gtl2) and multiple microRNAs and snoRNAs from the maternal chromosome. This locus constitutes an epigenetic model for pluripotency and development, particularly for neurogenesis. The domain’s Dlk1 (Delta-like-1) gene encodes a ligand that inhibits Notch1 signalling and regulates diverse developmental processes. Using a hybrid embryonic stem (ES) cell system, we find that Dlk1 becomes imprinted during neural differentiation and that this involves chromatin activation and transcriptional up-regulation on the paternal chromosome. On the maternal chromosome, the Dlk1 gene remains poised. This allelic protection against gene activation is controlled in cis by Meg3 expression and also involves the H3-lysine-27 methyltransferase Ezh2. Maternal Meg3 expression additionally protects against de novo DNA methylation at its promoter. Concordantly, we find that the lncRNA Meg3 is nuclear, accumulates onto the imprinted locus and overlaps in cis with Dlk1 in embryonic cells. Our data evoke an imprinting model in which a mono-allelic lncRNA prevents chromatin and gene activation in cis during development.
2018-04-10 | GSE99903 | GEO
Project description:Pluripotent stem cells are increasingly used for therapeutic models, including transplantation of neural progenitors derived from human embryonic stem cells (hESCs). Recently, long non-coding RNAs (lncRNAs), including Maternally Expressed Gene 3 (MEG3) that is derived from DLK1-DIO3 imprinted locus, were found to be expressed during neural developmental events. Their deregulations are associated with various neurological diseases. The DLK1-DIO3 imprinted locus encodes abundant non-coding RNAs (ncRNAs) that are regulated by differential methylation on the locus. The aim of our research is to study the correlation between the DLK1-DIO3 derived ncRNAs and the capacity of hESC neural lineage differentiation. We classified hESCs into MEG3-ON and MEG3-OFF based on the expression levels of MEG3 as well as its downstream miRNAs by qRT-PCR. Initial embryoid body (EB) formation was conducted to examine the three germ layer differentiation ability. cDNA microarray was used to analyze the gene expression profiles of hESCs. Directed neural lineage differentiation was performed, followed by analysis of neural lineage marker expression levels and neurite formation via qRT-PCR and immunocytochemistry methods to investigate the capacity of neural differentiation in MEG3-ON and MEG3-OFF hESCs To study the correlations between the DLK1-DIO3 derived ncRNAs and differentiation capacity of hESC toward neural lineage, we classified hESCs into MEG3-ON and MEG3-OFF based on the expression levels of MEG3 by qRT-PCR and validated the methylation patterns of DLK1-DIO3 locus by bisulfite-sequencing. Then we conducted transcriptome analysis of these two groups of hESCs by cDNA microarray. This set contained 12 microarray samples, including 4 MEG3-ON hESCs, 7 MEG3-OFF hESCs, and 1 embryoid body as the negative control of pluripotentcy for pluritest.
2014-11-05 | E-GEOD-58809 | biostudies-arrayexpress
Project description:The progression and transition between the naïve, formative, and primed pluripotent states are accompanied by a sharp activation of the de novo DNA methyltransferases and the reorganization of transcriptional and epigenetic landscapes. Here we identified Zinc Finger Protein 281 (ZFP281) as an essential factor in the formative-to-primed pluripotent state transition. Using a knockout mouse model and a knockin degron cell system, we revealed that transcription of Dnmt3a/3b depends on the activity of ZFP281 in embryonic stem cells, epiblast-like cells, and epiblast stem cells. Mechanically, chromatin-bound ZFP281 and DNA hydroxylase TET1 are decreased in the formative state but recovered in the primed state to compete with DNMT3A/3B for establishing the DNA methylation and gene expression programs of primed pluripotency. In addition, chromatin occupancy of ZFP281 and TET1 depend on the R-loop structures formed at the ZFP281 target gene promoters devoid of DNA methylation. Our study demonstrates a comprehensive role of ZFP281 in modulating DNA methylation and demethylation for the establishment and maintenance of primed pluripotency.
2023-12-14 | GSE227093 | GEO
Project description:The progression and transition between the naïve, formative, and primed pluripotent states are accompanied by a sharp activation of the de novo DNA methyltransferases and the reorganization of transcriptional and epigenetic landscapes. Here we identified Zinc Finger Protein 281 (ZFP281) as an essential factor in the formative-to-primed pluripotent state transition. Using a knockout mouse model and a knockin degron cell system, we revealed that transcription of Dnmt3a/3b depends on the activity of ZFP281 in embryonic stem cells, epiblast-like cells, and epiblast stem cells. Mechanically, chromatin-bound ZFP281 and DNA hydroxylase TET1 are decreased in the formative state but recovered in the primed state to compete with DNMT3A/3B for establishing the DNA methylation and gene expression programs of primed pluripotency. In addition, chromatin occupancy of ZFP281 and TET1 depend on the R-loop structures formed at the ZFP281 target gene promoters devoid of DNA methylation. Our study demonstrates a comprehensive role of ZFP281 in modulating DNA methylation and demethylation for the establishment and maintenance of primed pluripotency.
2023-12-14 | GSE247461 | GEO
Project description:The progression and transition between the naïve, formative, and primed pluripotent states are accompanied by a sharp activation of the de novo DNA methyltransferases and the reorganization of transcriptional and epigenetic landscapes. Here we identified Zinc Finger Protein 281 (ZFP281) as an essential factor in the formative-to-primed pluripotent state transition. Using a knockout mouse model and a knockin degron cell system, we revealed that transcription of Dnmt3a/3b depends on the activity of ZFP281 in embryonic stem cells, epiblast-like cells, and epiblast stem cells. Mechanically, chromatin-bound ZFP281 and DNA hydroxylase TET1 are decreased in the formative state but recovered in the primed state to compete with DNMT3A/3B for establishing the DNA methylation and gene expression programs of primed pluripotency. In addition, chromatin occupancy of ZFP281 and TET1 depend on the R-loop structures formed at the ZFP281 target gene promoters devoid of DNA methylation. Our study demonstrates a comprehensive role of ZFP281 in modulating DNA methylation and demethylation for the establishment and maintenance of primed pluripotency.
2023-12-14 | GSE226041 | GEO
Project description:The progression and transition between the naïve, formative, and primed pluripotent states are accompanied by a sharp activation of the de novo DNA methyltransferases and the reorganization of transcriptional and epigenetic landscapes. Here we identified Zinc Finger Protein 281 (ZFP281) as an essential factor in the formative-to-primed pluripotent state transition. Using a knockout mouse model and a knockin degron cell system, we revealed that transcription of Dnmt3a/3b depends on the activity of ZFP281 in embryonic stem cells, epiblast-like cells, and epiblast stem cells. Mechanically, chromatin-bound ZFP281 and DNA hydroxylase TET1 are decreased in the formative state but recovered in the primed state to compete with DNMT3A/3B for establishing the DNA methylation and gene expression programs of primed pluripotency. In addition, chromatin occupancy of ZFP281 and TET1 depend on the R-loop structures formed at the ZFP281 target gene promoters devoid of DNA methylation. Our study demonstrates a comprehensive role of ZFP281 in modulating DNA methylation and demethylation for the establishment and maintenance of primed pluripotency.
2023-12-14 | GSE226040 | GEO
Project description:Pluripotent stem cells are increasingly used for therapeutic models, including transplantation of neural progenitors derived from human embryonic stem cells (hESCs). Recently, long non-coding RNAs (lncRNAs), including Maternally Expressed Gene 3 (MEG3) that is derived from DLK1-DIO3 imprinted locus, were found to be expressed during neural developmental events. Their deregulations are associated with various neurological diseases. The DLK1-DIO3 imprinted locus encodes abundant non-coding RNAs (ncRNAs) that are regulated by differential methylation on the locus. The aim of our research is to study the correlation between the DLK1-DIO3 derived ncRNAs and the capacity of hESC neural lineage differentiation. We classified hESCs into MEG3-ON and MEG3-OFF based on the expression levels of MEG3 as well as its downstream miRNAs by qRT-PCR. Initial embryoid body (EB) formation was conducted to examine the three germ layer differentiation ability. cDNA microarray was used to analyze the gene expression profiles of hESCs. Directed neural lineage differentiation was performed, followed by analysis of neural lineage marker expression levels and neurite formation via qRT-PCR and immunocytochemistry methods to investigate the capacity of neural differentiation in MEG3-ON and MEG3-OFF hESCs
2014-11-05 | GSE58809 | GEO