Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA132733 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR066853.fastq.gz | Fastqsanger.gz | |||
| SRR066854.fastq.gz | Fastqsanger.gz | |||
| SRR066855.fastq.gz | Fastqsanger.gz | |||
| SRR066856.fastq.gz | Fastqsanger.gz | |||
| SRR066857.fastq.gz | Fastqsanger.gz |
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Project description:We use ChIP-seq to discover the genome-wide sites of acetylation of lysine 56 of the histone H3 (H3K56), which is a target of three histone modifying enzymes with known roles in diabetes and insulin resistance, in human adipocytes derived from mesenchymal stem cells. Surprisingly, we find that a very large fraction of genes show some level of acetylation on H3K56, but the highest levels of acetylation are associated with genes previously reported to be involved in type 2 diabetes. Using computational methods, we propose that the transcription factor E2F4 may be involved in recruiting histone modifying enzymes to these sites. We confirm this prediction by measuring the binding of E2F4 using ChIP-seq. We also examine the binding of two other proteins using ChIP-Seq: HSF-1 and C/EBPM-NM-1M-BM- . HSF-1 is a master regulator of stress responses, and is a target of the same histone modifiers as H3K56. We find a high degree of overlap between HSF-1 binding and H3K56 acetylation even in cells that are not stressed. By contrast, C/EBPM-NM-1M-BM- , which is not known to be modified by these enzymes, shows much less overlap with the sites of H3K56 acetylation. Our results represent the first mapping of the regulatory code of human adipocytes. Examination of H3K56 acetylation sites and E2F4,C/EBPM-NM-1 and HSF-1 binding sites in human adipocytes.
2011-05-31 | E-GEOD-24326 | biostudies-arrayexpress
Project description:We use ChIP-seq to discover the genome-wide sites of acetylation of lysine 56 of the histone H3 (H3K56), which is a target of three histone modifying enzymes with known roles in diabetes and insulin resistance, in human adipocytes derived from mesenchymal stem cells. Surprisingly, we find that a very large fraction of genes show some level of acetylation on H3K56, but the highest levels of acetylation are associated with genes previously reported to be involved in type 2 diabetes. Using computational methods, we propose that the transcription factor E2F4 may be involved in recruiting histone modifying enzymes to these sites. We confirm this prediction by measuring the binding of E2F4 using ChIP-seq. We also examine the binding of two other proteins using ChIP-Seq: HSF-1 and C/EBPα . HSF-1 is a master regulator of stress responses, and is a target of the same histone modifiers as H3K56. We find a high degree of overlap between HSF-1 binding and H3K56 acetylation even in cells that are not stressed. By contrast, C/EBPα , which is not known to be modified by these enzymes, shows much less overlap with the sites of H3K56 acetylation. Our results represent the first mapping of the regulatory code of human adipocytes.
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Project description:Genomic profiling of (1) histone H3K56 acetylation and (2) meiotic DSBs flanked by replication protein A (RPA). The major goal was to reveal the genome-wide distribution DSBs when the H3K56 residue was mutated to alanine (H3K56A).
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Project description:The conserved Notch pathway functions in diverse developmental and disease-related processes, requiring mechanisms to ensure appropriate target-selection and gene activation in each context. To investigate, we partitioned Drosophila chromatin into different states, based on histone modifications, establishing the preferred chromatin conditions for binding of CSL, the Notch pathway transcription factor. While most histone modifications were unchanged by CSL binding or Notch activation, rapid changes in H3K56 acetylation occurred at Notch regulated-enhancers. This modification required the histone acetyl-transferase CBP and was independent of transcription. Such rapid changes in H3K56 acetylation are a conserved indicator of enhancer activation, also occurring at mammalian Notch-regulated Hey1 and at Drosophila ecdysone-regulated genes. This core histone modification may therefore underpin the changes in chromatin accessibility needed to promote transcription following signaling activation. H3K56ac profile of control cells (KP) and of NICD overexpression cells (KN). In total 6 samples, with 2 input files (from 2 different conditions) and 2 replicates of H3K56ac ChIP samples of each condition.
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Project description:The conserved Notch pathway functions in diverse developmental and disease-related processes, requiring mechanisms to ensure appropriate target-selection and gene activation in each context. To investigate, we partitioned Drosophila chromatin into different states, based on histone modifications, establishing the preferred chromatin conditions for binding of CSL, the Notch pathway transcription factor. While most histone modifications were unchanged by CSL binding or Notch activation, rapid changes in H3K56 acetylation occurred at Notch regulated-enhancers. This modification extended over large regions, required the histone acetyl-transferase CBP and was independent of transcription. Such rapid changes in H3K56 acetylation are a conserved indicator of enhancer activation, also occurring at mammalian Notch-regulated Hey1 and at Drosophila ecdysone-regulated genes. This core histone modification may therefore underpin the changes in chromatin accessibility needed to promote transcription following signaling activation.
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