KLF4 ChIP-seq at reprogramming 48 hours and Hic2, KLF4 ChIP-seq at reprogramming 48 hours with Hic2 overexpression
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ABSTRACT:
PROVIDER: PRJEB64539 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR11757982_1.fastq.gz | Fastqsanger.gz | |||
| ERR11757982_2.fastq.gz | Fastqsanger.gz | |||
| ERR11757983_1.fastq.gz | Fastqsanger.gz | |||
| ERR11757983_2.fastq.gz | Fastqsanger.gz | |||
| ERR11757984_1.fastq.gz | Fastqsanger.gz |
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Project description:Mouse embryonic fibroblasts (MEFs) with doxycycline (Dox)-inducible reprogramming cassette MKOS-ires-mOrange and a Nanog-GFP reporter were transduced with lentiviral Dox-inducible Ty1-BFP (blue fluoresce protein with Ty1 tag in the N-terminus) or Hic2-Ty1 (Hic2 with Ty1 tag in the C-terminus) expression vector with MOI 5. One day later reprogramming was initiated by the administration of Dox. 48 hours later, the cells for Hic2 ChIP-seq with anti-Ty1 antibody were crosslinked with 2mM of Disuccinimidyl Glutarate (DSG) for 45 min at room temperature (RT) under constant agitation, before being cross-linked with 1% formaldehyde solution for 10 min at room temperature. For KLF4 ChIP-seq, cells were only cross-linked with 1% formaldehyde solution for 10 min at room temperature. ChIP-seq library was generated with the NEBNext Ultra-II DNA Library Prep kit. Each library was uniquely barcoded using NEBNext Multiplex Oligos for Illumina. Samples were sequenced with the NextSeq High 40PE.
2024-04-26 | E-MTAB-13170 | biostudies-arrayexpress
Project description:Klf4 and Sox2 are among the core reprogramming factor, and have different function in reprogramming. Klf4 is supposed to trigger MET in the early stage of reprogramming ,Sox2 is well known plutipotent relative gene. Klf4 and Sox2 play important role in induced reprogramming. We performed this experiment to identify the targets regulated by Sox2 and Klf4 respectively.
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Project description:HIC2 is required for normal development of the heart. Loss of function mutants exhibit early embryonic lethality while heterozygous mutants have a partially penetrant ventricular septal defect. The aim of this study was to understand the function of HIC2 in early heart development by identifying potential transcriptional targets. We harvested whole hearts (which contain circulating erythrocytes) at embryonic day E9.5 and compared expression in a conditional loss of function mutant (Mesp1 Cre/+; Hic2 Fl/Fl) to controls (Hic2 Fl/Fl).
2017-06-17 | GSE100125 | GEO
Project description:The fetal hemoglobin (HBG) regulator BCL11A is repressed by HIC2 to regulate hemoglobin switching. HIC2 itself is under developmental control, highly expressed in fetal tissues and decreased in adult cells, but the mechanism of this developmental regulation is unclear. Here, we demonstrate that HIC2 is developmentally controlled by miRNAs, and loss of global miRNA biogenesis through DICER1 depletion leads to upregulation of HIC2 and HBG. We subsequently identify the adult-expressed let-7 miRNA family as a repressor of HIC2 expression. Ectopic expression of let-7 in fetal-type cells repressed HIC2 levels, while let-7 inhibition in adult erythroblasts upregulated HIC2 levels. Let-7 regulates BCL11A and HBG through induction of HIC2 and reduction of GATA1 binding at the BCL11A erythroid enhancer. Finally, HIC2 depletion rescues BCL11A-mediated repression of fetal hemoglobin in let-7 inhibited cells. Together these data demonstrate a key miRNA-mediated mechanism for developmental regulation of BCL11A expression and fetal hemoglobin repression in adult erythroid cells.
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Project description:The fetal hemoglobin (HBG) regulator BCL11A is repressed by HIC2 to regulate hemoglobin switching. HIC2 itself is under developmental control, highly expressed in fetal tissues and decreased in adult cells, but the mechanism of this developmental regulation is unclear. Here, we demonstrate that HIC2 is developmentally controlled by miRNAs, and loss of global miRNA biogenesis through DICER1 depletion leads to upregulation of HIC2 and HBG. We subsequently identify the adult-expressed let-7 miRNA family as a repressor of HIC2 expression. Ectopic expression of let-7 in fetal-type cells repressed HIC2 levels, while let-7 inhibition in adult erythroblasts upregulated HIC2 levels. Let-7 regulates BCL11A and HBG through induction of HIC2 and reduction of GATA1 binding at the BCL11A erythroid enhancer. Finally, HIC2 depletion rescues BCL11A-mediated repression of fetal hemoglobin in let-7 inhibited cells. Together these data demonstrate a key miRNA-mediated mechanism for developmental regulation of BCL11A expression and fetal hemoglobin repression in adult erythroid cells.
2024-02-05 | GSE216196 | GEO
Project description:The fetal hemoglobin (HBG) regulator BCL11A is repressed by HIC2 to regulate hemoglobin switching. HIC2 itself is under developmental control, highly expressed in fetal tissues and decreased in adult cells, but the mechanism of this developmental regulation is unclear. Here, we demonstrate that HIC2 is developmentally controlled by miRNAs, and loss of global miRNA biogenesis through DICER1 depletion leads to upregulation of HIC2 and HBG. We subsequently identify the adult-expressed let-7 miRNA family as a repressor of HIC2 expression. Ectopic expression of let-7 in fetal-type cells repressed HIC2 levels, while let-7 inhibition in adult erythroblasts upregulated HIC2 levels. Let-7 regulates BCL11A and HBG through induction of HIC2 and reduction of GATA1 binding at the BCL11A erythroid enhancer. Finally, HIC2 depletion rescues BCL11A-mediated repression of fetal hemoglobin in let-7 inhibited cells. Together these data demonstrate a key miRNA-mediated mechanism for developmental regulation of BCL11A expression and fetal hemoglobin repression in adult erythroid cells.
2024-02-05 | GSE216195 | GEO
Project description:The fetal hemoglobin (HBG) regulator BCL11A is repressed by HIC2 to regulate hemoglobin switching. HIC2 itself is under developmental control, highly expressed in fetal tissues and decreased in adult cells, but the mechanism of this developmental regulation is unclear. Here, we demonstrate that HIC2 is developmentally controlled by miRNAs, and loss of global miRNA biogenesis through DICER1 depletion leads to upregulation of HIC2 and HBG. We subsequently identify the adult-expressed let-7 miRNA family as a repressor of HIC2 expression. Ectopic expression of let-7 in fetal-type cells repressed HIC2 levels, while let-7 inhibition in adult erythroblasts upregulated HIC2 levels. Let-7 regulates BCL11A and HBG through induction of HIC2 and reduction of GATA1 binding at the BCL11A erythroid enhancer. Finally, HIC2 depletion rescues BCL11A-mediated repression of fetal hemoglobin in let-7 inhibited cells. Together these data demonstrate a key miRNA-mediated mechanism for developmental regulation of BCL11A expression and fetal hemoglobin repression in adult erythroid cells.
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Project description:To further understand the mechanism of reprogramming, the mouse embryonic fibroblast cells were infected with Oct4, Klf4, c-Myc and Sox2 with special sequence. 1) Oct4 and Klf4 containing retrovirus was delivered on day 0. 2) Oct4, Klf4 and c-Myc were delivered on Day 1.5. 3) c-Myc and Sox-2 were deivered on Day 3. 4) Sox2 were delivered on Day 4.5. 5) Vitamin C containging medium were used from Day 6. The gene expression of Day 0 (MEF), Day 1.5, Day 3, Day 4.5 and Day 6 were analyzed with micro array to indentify the possible underlying mechanism. Especially the factors related to MET/EMT, cell cycle and epigenetic were focused. MEF cells were subjected for reprogramming with special protoocl: 1) Oct4 and Klf4 containing retrovirus were delivered on day 0. 2) Oct4, Klf4 and c-Myc were delivered on Day 1.5. 3) c-Myc and Sox-2 were deivered on Day 3. 4) Sox2 were delivered on Day 4.5. 5) Vitamin C containging medium were used from Day 6. RNA on Day 0 (MEF), Day 1.5, Day 3, Day 4.5 and Day 6 were collected for analysis.
2012-07-11 | E-GEOD-39260 | biostudies-arrayexpress
Project description:Rationale: 22q11 deletion syndrome arises from recombination between low copy repeats on chromosome 22. Typical deletions result in hemizygosity for TBX1 associated with congenital cardiovascular disease. Deletions distal to the typically deleted region result in a similar cardiac phenotype but lack extra-cardiac features of the syndrome suggesting that a second haploinsufficient gene maps to this interval. Objective: The transcription factor HIC2 is lost in most distal deletions as well as a minority of typical deletions. We used mouse models to test the hypothesis that HIC2 hemizygosity causes congenital heart disease. Methods and Results: We created a genetrap mouse allele of Hic2. The genetrap reporter was expressed in the heart throughout the key stages of cardiac morphogenesis. Homozygosity for the genetrap allele was embryonic lethal before embryonic day E10.5 while the heterozygous condition exhibited a partially penetrant late lethality. One third of heterozygous embryos had a cardiac phenotype. Magnetic resonance imaging demonstrated a ventricular septal defect with overriding aorta. Conditional targeting indicated a requirement for Hic2 within the Nkx2.5+ and Mesp1+ cardiovascular progenitor lineages but not in the Wnt1+ neural crest or Mef2c+ second heart field lineages. Microarray analysis revealed increased expression of BMP10. Conclusions: Our results demonstrate a novel role for Hic2 in cardiac development. Hic2 is the first gene within the distal 22q11 interval to have a demonstrated haploinsufficient cardiac phenotype in mice. Together our data suggests HIC2 haploinsufficiency likely contributes to the cardiac defects seen in distal 22q11 deletion syndrome. The aim of this microarray experiment was to compare gene expression changes in the E13.5 mouse heart in a conditional knockout of Hic2 (Mesp1Cre/+; Hic2FL/FL) against control. All samples represent pools of isolated hearts from E13.5 mouse embryos. 3 replicates of each genotype were assayed. The genotypes are: 'WT' (Hic2FL/FL) 'KO' (Mesp1Cre/+; Hic2 FL/FL)
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