Transcriptome analysis of Meg3 KD and IG-DMR maternal deletion in ESC, pMN, and MN
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PROVIDER: PRJNA470618 | ENA |
REPOSITORIES: ENA
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Project description:Analysis of gene expression at three time-points upon Meg3 KD and IG-DMR maternal deletion during motor neuron differentiation
2018-11-01 | GSE114228 | GEO
Project description:We report the DNA-methylation profiling of 10 regions selected from the DLK1-DIO3 domain on chromosome 14q32 in BM/PB samples from patients with acute promyelocytic leukaemia (APL), other subclasses of acute myeloid leukaemia and healthy donors, using high-throughput amplicon bisulfite sequencing with Roche 454 technology. We identify monoallelic-hypermethylation in APL only at the differentially methylated region (DMR) located upstream from the MEG3 gene (MEG3-DMR), whereas no changes in the DNA methylation profile were detected at the imprinting control region of the domain (IG-DMR) among the samples analysed. We show that the expression profile of 6 miRNAs clustered downstream from the MEG3-DMR correlates with the methylation profile at both DMRs. We demonstrate that miRNAs expression negatively correlates with DNA-methylation at the IG-DMR and MEG3 gene-body, whereas the correlation was positive for the CpGs located in the promoter of MEG3, including the binding sites for the insulator CTCF. We propose a loss of imprinting at the CTCF binding sites in patients with APL. These results are consistent with the previously reported DLK1-DIO3 miRNAs overexpression in APL, indicating a possible involvement of these ncRNAs in the pathogenesis of the disease. Investigation of the epigenetic regulation of the miRNAs clustered in 14q32 by next-generation sequencing
2014-02-13 | E-GEOD-42543 | biostudies-arrayexpress
Project description:We report the DNA-methylation profiling of 10 regions selected from the DLK1-DIO3 domain on chromosome 14q32 in BM/PB samples from patients with acute promyelocytic leukaemia (APL), other subclasses of acute myeloid leukaemia and healthy donors, using high-throughput amplicon bisulfite sequencing with Roche 454 technology. We identify monoallelic-hypermethylation in APL only at the differentially methylated region (DMR) located upstream from the MEG3 gene (MEG3-DMR), whereas no changes in the DNA methylation profile were detected at the imprinting control region of the domain (IG-DMR) among the samples analysed. We show that the expression profile of 6 miRNAs clustered downstream from the MEG3-DMR correlates with the methylation profile at both DMRs. We demonstrate that miRNAs expression negatively correlates with DNA-methylation at the IG-DMR and MEG3 gene-body, whereas the correlation was positive for the CpGs located in the promoter of MEG3, including the binding sites for the insulator CTCF. We propose a loss of imprinting at the CTCF binding sites in patients with APL. These results are consistent with the previously reported DLK1-DIO3 miRNAs overexpression in APL, indicating a possible involvement of these ncRNAs in the pathogenesis of the disease.
2014-02-13 | GSE42543 | GEO
Project description:Imprinting at the Dlk1-Dio3 cluster is controlled by the IG-DMR, an imprinting control region differentially methylated between maternal and paternal chromosomes. The maternal IG-DMR is essential for imprinting control, functioning as a cis enhancer element. Meanwhile, DNA methylation at the paternal IG-DMR is thought to prevent enhancer activity. To explore whether suppression of enhancer activity at the methylated IG-DMR requires the transcriptional repressor TRIM28, we analyzed Trim28chatwo embryos and performed epistatic experiments with IG-DMR deletion mutants. We found that while TRIM28 regulates the enhancer properties of the paternal IG-DMR, it also controls imprinting through other mechanisms. Additionally, we found that the paternal IG-DMR, previously deemed dispensable for imprinting, is required in certain tissues, demonstrating that imprinting is regulated in a tissue-specific manner. Using ChRO-seq to analyze nascent transcription, we show that different tissues have a distinctive regulatory landscape at the Dlk1-Dio3 cluster, providing insight into potential mechanisms of tissue-specific imprinting control. ChRO-seq identified 30 novel transcribed regulatory elements, including a candidate regulatory region that depends on the paternal IG-DMR. Together, our findings challenge the model that Dlk1-Dio3 imprinting is regulated through a single mechanism and demonstrate that different tissues use distinct strategies for imprinting control.
2019-02-28 | GSE119882 | GEO
Project description:In this experiment we sought to identify region with differential PRC2, JARID2, and H3K27me3 occupancy in human induced pluripotent stem cell lines with silenced or expressed MEG3 locus to indirectly determine the effect of this ncRNA on PRC2 function. 8 hIPSC lines, 5 MEG3+ and 3 MEG3-; ChIP-seq for EZH2, JARID2, and H3K27me3. Some done in replicates.
2013-12-25 | E-GEOD-48516 | biostudies-arrayexpress
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:The imprinted Dlk1-Dio3 domain comprises the developmental genes Dlk1 and Rtl1, which are silenced on the maternal chromosome in different cell types. On this parental chromosome, the domain’s imprinting control region activates a polycistron that produces the lncRNA Meg3 and many miRNAs (Mirg) and C/D-box snoRNAs (Rian). Although Meg3 lncRNA is nuclear and associates with the maternal chromosome, it is unknown whether it controls gene repression in cis. We created mouse embryonic stem cells (mESCs) that carry an ectopic poly(A) signal, reducing RNA levels along the polycistron, and generated Rian-/- mESCs as well. Upon ESC differentiation, we found that Meg3 lncRNA (but not Rian) is required for Dlk1 repression on the maternal chromosome. Biallelic Meg3 expression acquired through CRISPR-mediated demethylation of the paternal Meg3 promoter led to biallelic Dlk1 repression, and to loss of Rtl1 expression. lncRNA expression also correlated with DNA hypomethylation and CTCF binding at the 5’-side of Meg3. Using Capture Hi-C, we found that this creates a Topologically Associating Domain (TAD) organization that brings Meg3 close to Dlk1 on the maternal chromosome. The requirement of Meg3 for gene repression and TAD structure may explain how aberrant MEG3 expression at the human DLK1-DIO3 locus associates with imprinting disorders.
2024-03-28 | GSE207166 | GEO
Project description:MEG3 was known as a growth suppressor in tumor cells by activating p53. Besides, MEG3 could regulate transforming growth factor-β (TGF-β) signaling pathway, which is the key regulator of skeletal myogenesis and can enhance the proliferation of myogenic cells. Previous study also showed MEG3 was highly expressed in the paraxial mesoderm and probably regulated muscle development. To investigate the potential function of MEG3 in muscle development, we detected the expression levels of protein-coding genes after MEG3 over-expression or knockdown in C2C12 cell line using microarrays.
2018-09-28 | GSE73524 | GEO
Project description:Meg3 is a long non-coding RNA. It's target genes are unknown. The mouse pancreatic beta cell line MIN6-4N was used to assess the expression of genes upon stable Meg3 overexpression Stable cell lines were isolated that have integated pcDNA3.1 or pcDNA3.1-mMeg3.The cells were processed for RNA isolation. The level of Meg3 expression was assessed by RT-PCR. RNA preps were used for microarray analysis.
2015-05-21 | E-GEOD-57716 | biostudies-arrayexpress
Project description:This experiment was designed to detect differences in PRC2 occupancy in a human induced pluripotent cell line (MRC5) naturally deficient in MEG3 RNA after lentiviral overexpression of MEG3. MRC5 were transduced with lentiviruses for the overexpression of MEG3 lncRNA or GFP as a control. ChIP-seq was performed with EZH2 and JARID2 antibodies.
2013-12-25 | E-GEOD-48515 | biostudies-arrayexpress