Genome-wide maps of chromatin state in pluripotent and lineage-committed cells
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ABSTRACT:
PROVIDER: PRJNA735267 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14738400_1.fastq.gz | Fastqsanger.gz | |||
| SRR14738400_2.fastq.gz | Fastqsanger.gz | |||
| SRR14738392_1.fastq.gz | Fastqsanger.gz | |||
| SRR14738392_2.fastq.gz | Fastqsanger.gz | |||
| SRR14738393_1.fastq.gz | Fastqsanger.gz |
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Project description:Genome-wide maps of chromatin state (H3K4me3, H3K9me3, H3K27me3, H3K36me3, H4K20me3) in pluripotent and lineage-committed cells We report the application of single-molecule-based sequencing technology for high-throughput profiling of histone modifications in mammalian cells. By obtaining over four billion bases of sequence from chromatin immunoprecipitated DNA, we generated genome-wide chromatin-state maps of mouse embryonic stem cells, neural progenitor cells and embryonic fibroblasts. We find that lysine 4 and lysine 27 trimethylation effectively discriminates genes that are expressed, poised for expression, or stably repressed, and therefore reflect cell state and lineage potential. Lysine 36 trimethylation marks primary coding and non-coding transcripts, facilitating gene annotation. Trimethylation of lysine 9 and lysine 20 is detected at satellite, telomeric and active long-terminal repeats, and can spread into proximal unique sequences. Lysine 4 and lysine 9 trimethylation marks imprinting control regions. Finally, we show that chromatin state can be read in an allele-specific manner by using single nucleotide polymorphisms. This study provides a framework for the application of comprehensive chromatin profiling towards characterization of diverse mammalian cell populations. Histone H3 or H4 tri-methylation ChIP-Seq in singlicate from murine embryonic stem (ES) cells, ES-derived neural precursor cells, and embryonic fibroblasts.
2008-07-24 | E-GEOD-12241 | biostudies-arrayexpress
Project description:Genome-wide maps of chromatin state in pluripotent and lineage-committed cells.
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Project description:Genome-wide maps of chromatin state (H3K4me3, H3K9me3, H3K27me3, H3K36me3, H4K20me3) in pluripotent and lineage-committed cells We report the application of single-molecule-based sequencing technology for high-throughput profiling of histone modifications in mammalian cells. By obtaining over four billion bases of sequence from chromatin immunoprecipitated DNA, we generated genome-wide chromatin-state maps of mouse embryonic stem cells, neural progenitor cells and embryonic fibroblasts. We find that lysine 4 and lysine 27 trimethylation effectively discriminates genes that are expressed, poised for expression, or stably repressed, and therefore reflect cell state and lineage potential. Lysine 36 trimethylation marks primary coding and non-coding transcripts, facilitating gene annotation. Trimethylation of lysine 9 and lysine 20 is detected at satellite, telomeric and active long-terminal repeats, and can spread into proximal unique sequences. Lysine 4 and lysine 9 trimethylation marks imprinting control regions. Finally, we show that chromatin state can be read in an allele-specific manner by using single nucleotide polymorphisms. This study provides a framework for the application of comprehensive chromatin profiling towards characterization of diverse mammalian cell populations.
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Project description:We report the application of single-molecule-based sequencing technology for high-throughput profiling of histone modifications in mammalian cells. By obtaining over four billion bases of sequence from chromatin immunoprecipitated DNA, we generated genome-wide chromatin-state maps of mouse embryonic stem cells, neural progenitor cells and embryonic fibroblasts. We find that lysine 4 and lysine 27 trimethylation effectively discriminates genes that are expressed, poised for expression, or stably repressed, and therefore reflect cell state and lineage potential. Lysine 36 trimethylation marks primary coding and non-coding transcripts, facilitating gene annotation. Trimethylation of lysine 9 and lysine 20 is detected at satellite, telomeric and active long-terminal repeats, and can spread into proximal unique sequences. Lysine 4 and lysine 9 trimethylation marks imprinting control regions. Finally, we show that chromatin state can be read in an allele-specific manner by using single nucleotide polymorphisms. This study provides a framework for the application of comprehensive chromatin profiling towards characterization of diverse mammalian cell populations.
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Project description:Human embryonic stem cells share identical genomic sequences with other lineage-committed cells yet possess the remarkable properties of self-renewal and pluripotency. It has been proposed that epigenetic regulatory mechanisms, involving DNA methylation and various chromatin modifications, are at least partly responsible for the distinct cellular properties between different cell types. Previous studies focusing largely on gene promoters and CpG islands have identified close association between several chromatin modifications and DNA methylation, but revealed a relatively small degree of differences between pluripotent and lineage-committed cells. Here, we examine the association between 11 chromatin modifications and DNA methylation at high resolution throughout the genome in the human embryonic stem cells and primary fetal lung fibroblasts. We observe a new set of relationships between chromatin modifications and DNA methylation occurring outside of the promoter regions. We also find that epigenomic landscapes are drastically different between the ES cells and fibroblasts. In particular, over 40% of the human genome differs in their chromatin structure between the two cell types. Most of the changes come from a dramatic redistribution of the repressive H3K9me3 and H3K27me3 marks, which form large blocks that expand significantly in the fibroblasts relative to ES cells. Additionally, we identified numerous small and punctuated regions outside of promoters that are associated with many active chromatin modification marks, and show that chromatin dynamics at these potential regulatory sequences are associated with change in DNA methylation between the ES cells and fibroblasts. Our results provide new insights into epigenetic regulatory mechanisms underlying properties of pluripotency and cell fate commitment. ChIP-Seq Analysis of OCT4, KLF4, MYC, TAFII and P300 in hESC H1 cells. 36 cycles of sequencing was done on the Illumina Genome Analyzer or Analyzer II platforms.
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Project description:Human embryonic stem cells share identical genomic sequences with other lineage-committed cells yet possess the remarkable properties of self-renewal and pluripotency. It has been proposed that epigenetic regulatory mechanisms, involving DNA methylation and various chromatin modifications, are at least partly responsible for the distinct cellular properties between different cell types. Previous studies focusing largely on gene promoters and CpG islands have identified close association between several chromatin modifications and DNA methylation, but revealed a relatively small degree of differences between pluripotent and lineage-committed cells. Here, we examine the association between 11 chromatin modifications and DNA methylation at high resolution throughout the genome in the human embryonic stem cells and primary fetal lung fibroblasts. We observe a new set of relationships between chromatin modifications and DNA methylation occurring outside of the promoter regions. We also find that epigenomic landscapes are drastically different between the ES cells and fibroblasts. In particular, over 40% of the human genome differs in their chromatin structure between the two cell types. Most of the changes come from a dramatic redistribution of the repressive H3K9me3 and H3K27me3 marks, which form large blocks that expand significantly in the fibroblasts relative to ES cells. Additionally, we identified numerous small and punctuated regions outside of promoters that are associated with many active chromatin modification marks, and show that chromatin dynamics at these potential regulatory sequences are associated with change in DNA methylation between the ES cells and fibroblasts. Our results provide new insights into epigenetic regulatory mechanisms underlying properties of pluripotency and cell fate commitment.
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