MacroH2A1 ChIP-seq in G1/S phase and metaphase
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA979197 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24809413_1.fastq.gz | Fastqsanger.gz | |||
| SRR24809413_2.fastq.gz | Fastqsanger.gz | |||
| SRR24809414_1.fastq.gz | Fastqsanger.gz | |||
| SRR24809414_2.fastq.gz | Fastqsanger.gz | |||
| SRR24809415_1.fastq.gz | Fastqsanger.gz |
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Project description:The histone variant macroH2A forms large chromatin domains and serves as a transcriptional repression marker. It has been found that the overall quantity of macroH2A deposition on chromatin undergoes dynamic changes during the cell cycle. However, the genomic features relevant to these dynamic changes in macroH2A1 deposition during the cell cycle remain poorly understood. We combined ChIP‑seq and cell synchronization in mouse NIH-3T3 cells to examine the dynamic changes of macroH2A1 deposition on the genome between G1/S phase and metaphase. Interestingly, we observed that macroH2A1 deposition dynamically changes within the large macroH2A1 domain at G1/S phase and metaphase, which was associated with transcriptional activity. These dynamic changes occurring at gene bodies can specifically mark cell-cycle-specific genes. Taken together, we propose that macroH2A1 is a dynamic histone variant associated with cell-cycle-specific genes and plays a crucial role in cell-cycle-specific transcriptional repression.
2023-10-02 | GSE234016 | GEO
Project description:MacroH2A1 is a histone variant that is enriched on the inactive X chromosome (Xi) in mammals and is postulated to play an important, but unknown, role in the repression of gene expression. Here we show that although macroH2A1 marks repressed autosomal chromatin, it positively regulates transcription when located in the transcribed regions of many target genes. We used chromatin immunoprecipitation coupled with tiling microarrays (ChIP-chip) to determine the genomic localization of macroH2A1 in IMR90 human primary lung fibroblasts and MCF-7 breast cancer cells. The patterns of macroH2A1 deposition are largely similar across the autosomes of both cell lines. Our studies revealed a genomic localization pattern unique among histone variants, namely the occupation by macroH2A1 of large chromatin domains (>500 kb in some cases) that contain repressive chromatin marks (e.g., histone H3 lysine 27 trimethylation). The boundaries of macroH2A1-containing domains tend to occur in promoter proximal regions. Not all promoters, however, serve as macroH2A1 boundaries; many macroH2A1-containing chromatin domains invade the transcribed regions of genes whose products play key roles in development and cell-cell signaling. Surprisingly, the expression of many of these genes is positively regulated by macroH2A1. MacroH2A1 also plays a role in augmenting signal-regulated transcription, specifically for genes responsive to serum starvation. Collectively, our results document an unexpected role for macroH2A1 in the escape from heterochromatin-associated silencing and the enhancement of autosomal gene transcription. Two macroH2A1 ChIP-chip biological replicates from IMR90 human embryonic lung fibroblasts are included.
2010-06-20 | E-GEOD-18633 | biostudies-arrayexpress
Project description:MacroH2A1 ChIP-chip was performed on custom Nimblegen genomic tiling arrays, to understand the genomic binding patterns of this histone variant and its relationship to gene expression Keywords: ChIP-chip Two macroH2A biological replicates are included. An H3 ChIP-chip sample is included as a control
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Project description:MacroH2A1 ChIP-chip was performed on custom Nimblegen genomic tiling arrays, to understand the genomic binding patterns of this histone variant and its relationship to gene expression Keywords: ChIP-chip
2009-11-13 | GSE9607 | GEO
Project description:MacroH2A1 is a histone variant that is enriched on the inactive X chromosome (Xi) in mammals and is postulated to play an important, but unknown, role in the repression of gene expression. Here we show that although macroH2A1 marks repressed autosomal chromatin, it positively regulates transcription when located in the transcribed regions of many target genes. We used chromatin immunoprecipitation coupled with tiling microarrays (ChIP-chip) to determine the genomic localization of macroH2A1 in IMR90 human primary lung fibroblasts and MCF-7 breast cancer cells. The patterns of macroH2A1 deposition are largely similar across the autosomes of both cell lines. Our studies revealed a genomic localization pattern unique among histone variants, namely the occupation by macroH2A1 of large chromatin domains (>500 kb in some cases) that contain repressive chromatin marks (e.g., histone H3 lysine 27 trimethylation). The boundaries of macroH2A1-containing domains tend to occur in promoter proximal regions. Not all promoters, however, serve as macroH2A1 boundaries; many macroH2A1-containing chromatin domains invade the transcribed regions of genes whose products play key roles in development and cell-cell signaling. Surprisingly, the expression of many of these genes is positively regulated by macroH2A1. MacroH2A1 also plays a role in augmenting signal-regulated transcription, specifically for genes responsive to serum starvation. Collectively, our results document an unexpected role for macroH2A1 in the escape from heterochromatin-associated silencing and the enhancement of autosomal gene transcription.
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Project description:The histone variant macroH2A1 and the poly(ADP-ribose) polymerase PARP-1 both regulate gene transcription by modulating chromatin structure and function. Of the two macroH2A1 splice variants, macroH2A1.1 and macroH2A1.2, the former is often suppressed in cancer and has the unique ability to interact with poly(ADP-ribose). Using ChIP-seq in primary lung fibroblasts, we demonstrate that macroH2A1 is incorporated into either of two spatially and functionally distinct types of chromatin; the first is marked by H3 K27 trimethylation, while the second contains a set of nine histone acetylations. MacroH2A1-regulated genes are involved in cancer progression are specifically found in macroH2A1-containing acetylated chromatin. Through the recruitment of PARP-1, macroH2A1.1 promotes the acetylation of H2B K12 and K120 which plays a key role in the regulation of macroH2A1 target genes in primary cells. The macroH2A1/PARP-1 pathway regulating H2B K12 and K120 acetylation is disrupted in cancer cells, in part, explaining macroH2A1M-bM-^@M-^Ys role in cancer suppression. Two biological replicates of the macroH2A1 ChIP and two corresponding input samples were sequenced
2014-09-15 | E-GEOD-54845 | biostudies-arrayexpress
Project description:The histone variant macroH2A1 and the poly(ADP-ribose) polymerase PARP-1 both regulate gene transcription by modulating chromatin structure and function. Of the two macroH2A1 splice variants, macroH2A1.1 and macroH2A1.2, the former is often suppressed in cancer and has the unique ability to interact with poly(ADP-ribose). Using ChIP-seq in primary lung fibroblasts, we demonstrate that macroH2A1 is incorporated into either of two spatially and functionally distinct types of chromatin; the first is marked by H3 K27 trimethylation, while the second contains a set of nine histone acetylations. MacroH2A1-regulated genes are involved in cancer progression are specifically found in macroH2A1-containing acetylated chromatin. Through the recruitment of PARP-1, macroH2A1.1 promotes the acetylation of H2B K12 and K120 which plays a key role in the regulation of macroH2A1 target genes in primary cells. The macroH2A1/PARP-1 pathway regulating H2B K12 and K120 acetylation is disrupted in cancer cells, in part, explaining macroH2A1’s role in cancer suppression.
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Project description:Whole transcriptome expression analysis of HFF cells on Affymetrix Human Tiling 1.0 array set. Cells were synchronised by serum starvation and transcriptome-wide expression in G1 phase. Expression data were processed with MAT (Johnson et al., "Model-based analysis of tiling-arrays for ChIP-chip." Proc Natl Acad Sci USA, 103:12457-62, 2006.).
2012-12-18 | GSE36155 | GEO
Project description:Oncogene induced senescence (OIS) is a tumor suppressive mechanism typified by stable proliferative arrest, a persistent DNA damage response and the senescent-associated secretory phenotype (SASP). MacroH2A1, a tumor suppressive histone variant, is upregulated during OIS. Using ChIP-seq, we found that macroH2A1 undergoes dramatic relocalization during OIS. SASP genes are enriched in macroH2A1-containing chromatin and macroH2A1 is a critical component of the positive feedback loop that maintains SASP expression. Endoplasmic reticulum (ER) stress, a feature of OIS that requires macroH2A1, leads to ATM activation. ER stress triggers a negative feedback loop reducing SASP expression by causing the ATM-dependent removal of macroH2A1 from SASP genes. MacroH2A1 represents a critical control point in the regulation of SASP expression during OIS by We demonstrate that SASP gene expression is regulated by the combined actions of a positive feedback loop that requires macroH2A1 and a negative feedback loop where ER stress leads to ATM activation critical for the removal of macroH2A1 from SASP genes and consequently their repression.
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