Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA257297 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1534810.fastq.gz | Fastqsanger.gz | |||
| SRR1534811.fastq.gz | Fastqsanger.gz | |||
| SRR1534812.fastq.gz | Fastqsanger.gz | |||
| SRR1534805.fastq.gz | Fastqsanger.gz | |||
| SRR1534806.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 13 |
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Project description:Retinal pigment epithelial cells are critical for eye function and loss of cell function is linked to age-related blindness. Relatively little is known about the transcriptional regulatory networks in these cells. The datasets presented here are ChIP-seq experiments for RNA polymerase II , transcription factors and histone modifications in human retinal pigment epithelial cells.
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Project description:Whole genome profiling of histone methylation (H3K4me3, H3K27me3 and RNA Pol II) in Ciliary derived stem/progenitor cells and differentiated cells. In the present study we focus on the cellular differentiation that involves loss of pluripotency and gain of lineage and cell type-specific characteristics and we show developments from adult ciliary derived stem/progenitor cells to differentiated retinal neurons/glial cells of human cadaveric eyes in vitro. Ciliary pigment epithelial cells isolated from human cadaveric eye balls were cultured in the presence of mitogens like Epidermal Growth Factor (EGF) and Fibroblast Growth Factors (FGF) to generate neurospheres (Stem/progenitor population). The generated neurospheres were plated on laminin and poly-D-lysine-coated cover slips in the presence of the Brain derived neurotrophic factor (BDNF), Retinoic acid (RA) and 10% FBS for the differentiation (Retinal neuron/glial cells). Global Methylation patterns of histone H3K4me3, RNA Pol II and H3K27me3 were analysed in the present study. This work would provide an outline of epigenetic modifications in ciliary derived stem/progenitor cells and the progeny that underwent differentiation into retinal neurons/glial cells and present that specific histone methylations are involved in gene expression reprogramming during the process of differentiation.
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Project description:Instructive mechanisms are present for induction of DNA methylation, as shown by methylation of specific CpG islands (CGIs) by specific inducers and in specific cancers. However, instructive factors involved are poorly understood, except for involvement of low transcription and trimethylation of histone H3 lysine 27 (H3K27me3). Here, we used methylated DNA immunoprecipitation (MeDIP) combined with a CGI oligonucleotide microarray analysis, and identified 5510 and 521 genes with promoter CGIs resistant and susceptible, respectively, to DNA methylation in prostate cancer cell lines. Expression analysis revealed that the susceptible genes had low transcription in a normal prostatic epithelial cell line. Chromatin immunoprecipitation with microarray hybridization (CHiP-chip) analysis of RNA polymerase II (Pol II) and histone modifications showed that, even among the genes with low transcription, the presence of Pol II was associated with marked resistance to DNA methylation (OR = 0.22; 95% CI = 0.12-0.38), and H3K27me3 was associated with increased susceptibility (OR = 11.20; 95% CI = 7.14-17.55). The same was true in normal human mammary epithelial cells for 5430 and 733 genes resistant and susceptible, respectively, to DNA methylation in breast cancer cell lines. These results showed that the presence of Pol II, active or stalled, and H3K27me3 can predict the epigenetic fate of promoter CGIs independently of transcription levels. To analyze DNA methylation status in normal and cancer cells, MeDIP-CGI oligonucleotide microarray analysis was performed. To analyze expression and histone modification status in normal cells, GeneChip analysis and ChIP-oligonucleotide microarray analysis were performed.
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Project description:Heterochromatin comprises tightly compacted repetitive regions of eukaryotic chromosomes. The inheritance of heterochromatin through mitosis requires RNA interference (RNAi), which guides histone modification 1 during the DNA replication phase of the cell cycle2. Here, we show that the alternating arrangement of origins of replication and non-coding RNA in pericentromeric heterochromatin results in competition between transcription and replication. Co-transcriptional RNAi releases RNA polymerase II (PolII), allowing completion of DNA replication by the leading strand DNA polymerase, and associated histone modifying enzymes3 which spread heterochromatin with the replication fork. In the absence of RNAi, stalled forks are repaired by homologous recombination without histone modification. RNA PolII ChIP from wild type and dcr1-deleted samples in exponentially growing and HU-arrested cultures.
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