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Histone chaperon ASF1B recruits distinct epigenetic factors in regulation of histone variant H3.3 during the fetal and adult erythropoiesis [ChIP-seq]

ABSTRACT: To identify the role of ASF1B in regulation of histone modification during murine erythropoiesis, H3K27ac and H3.3 ChIP-seq was performed in the WT and ASF1B KO E14.5 fetal liver and bone marrow cells. ASF1B was found bind to the promoter and potential enhancer region. Loss of ASF1B impaired H3.3 and H3K27ac enrichments during development.

ORGANISM(S): Mus musculus

PROVIDER: GSE214527 | GEO | 2026/05/15

REPOSITORIES: GEO

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Histone chaperon ASF1B recruits distinct epigenetic factors in regulation of histone variant H3.3 during the fetal and adult erythropoiesis.

Project description:To gain insight into ASF1B function during erythropoiesis, RNA-seq was performed in CD71/Ter119 Fluorescence-Activated Cell Sorting (FACS) cells of WT and ASF1B KO E14.5 fetal liver(S0-S5) and bone marrow(E1-E4). Notably, depletion of ASF1B in E14.5 E4/E5 fetal liver cells significantly reduced the expression of genes associated with erythroid differentiation. In contrast, depletion of ASF1B in E4 bone marrow cells significantly reduced the expression of genes enriched in chromatin assembly.

2026-05-15 | GSE215076 | GEO

Histone chaperon ASF1B recruits distinct epigenetic factors in regulation of histone variant H3.3 during the fetal and adult erythropoiesis II

Project description:To gain insight into ASF1A, ASF1B and HIRA function during erythropoiesis, RNA-seq was performed in murine erythroleukemia (MEL) cells, human umbilical cord-derived progenitor erythroid 2 (HUDEP2) cells and human CD34+ erythroid progenitor cells. Notably, depletion of ASF1A, ASF1B and HIRA with/without DMSO induction significantly reduced the expression of genes associated with erythroid differentiation. Meanwhile, depletion of ASF1A and ASF1B in HUDEP2 cells as well as depletion of ASF1B in CD34+ cells significantly reduced the expression of genes associated with erythroid differentiation.

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Histone chaperon ASF1B recruits distinct epigenetic factors in regulation of histone variant H3.3 during the fetal and adult erythropoiesis [ATAC-seq]

Project description:To determine ASF1B function in chromatin accessbility, ATAC Seq was performed in both WT and ASF1B KO mouse liver. Loss of ASF1B caused generally decresed of chrmoatin accessbility on the promoters.

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Histone chaperon ASF1B recruits distinct epigenetic factors in regulation of histone variant H3.3 during the fetal and adult erythropoiesis

Project description:This SuperSeries is composed of the SubSeries listed below.

2026-05-15 | GSE214528 | GEO

Histone chaperone ASF1B promotes human β-cell proliferation via recruitment of histone H3.3.

Project description: Not available

| S-EPMC5176155 | biostudies-literature

Genome-wide incorporation dynamics reveal distinct categories of turnover for the histone variant H3.3

Project description:We developed a system to study the DNA replication-independent turnover nucleosomes containing the histone variant H3.3 in mammalian cells. By measuring the genome-wide incorporation of H3.3 at different time points following epitope-tagged H3.3 expression, we find three categories of H3.3-nucleosome turnover in vivo: rapid turnover, intermediate turnover and, specifically at telomeres, slow turnover. Our data indicate that H3.3-containing nucleosomes at enhancers and promoters undergo a rapid turnover that is associated with active histone modification marks including H3K4me1, H3K4me3, H3K9ac, H3K27ac and the histone variant H2A.Z. The rate of turnover is negatively correlated with H3K27me3 at regulatory regions and with H3K36me3 at gene bodies. Examination of incorporation dynamics of histone variant H3.3

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Genome-wide RNA-sequencing of human islets 48 hour after transduction with adenoviruses expressing either GFP (control), or histone chaperone ASF1B.

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2016-09-10 | GSE86611 | GEO

The histone H3 variant H3.3 regulates gene body DNA methylation [ChIP-seq]

Project description:Gene bodies of vertebrates and flowering plants are occupied by histone variant H3.3 and DNA methylation. The origin and significance of these profiles remain largely unknown. The profiles of enrichments in DNA methylation and H3.3 over gene bodies are correlated and both depend similarly on gene transcription levels. This suggests a mechanistic link between H3.3 and gene body methylation. We engineered H3.3 knockdown in Arabidopsis and observed transcription reduction that predominantly affected genes responsive to environmental cues. When H3.3 levels were reduced, gene bodies showed a loss of DNA methylation correlated with transcription levels. To study the origin of changes in DNA methylation profiles when H3.3 levels are reduced, we examined genome wide distributions of several histone H3 marks, H2A.Z, linker histone H1 and nucleosome densities. We observed that in absence of H3.3, H1 distribution increased in gene bodies. This depends on levels of gene transcription. We propose that H3.3 prevents recruitment of H1, which in turn promotes chromatin folding and antagonizes access to DNA methyltransferases responsible for gene body methylation. Thus, gene body methylation is likely shaped by H3.3 dynamics in relation with transcriptional activity.

2017-04-24 | GSE96834 | GEO

The histone H3 variant H3.3 regulates gene body DNA methylation [BiSulfite-seq]

Project description:Gene bodies of vertebrates and flowering plants are occupied by histone variant H3.3 and DNA methylation. The origin and significance of these profiles remain largely unknown. The profiles of enrichments in DNA methylation and H3.3 over gene bodies are correlated and both depend similarly on gene transcription levels. This suggests a mechanistic link between H3.3 and gene body methylation. We engineered H3.3 knockdown in Arabidopsis and observed transcription reduction that predominantly affected genes responsive to environmental cues. When H3.3 levels were reduced, gene bodies showed a loss of DNA methylation correlated with transcription levels. To study the origin of changes in DNA methylation profiles when H3.3 levels are reduced, we examined genome wide distributions of several histone H3 marks, H2A.Z, linker histone H1 and nucleosome densities. We observed that in absence of H3.3, H1 distribution increased in gene bodies. This depends on levels of gene transcription.We propose that H3.3 prevents recruitment of H1, which in turn promotes chromatin folding and antagonizes access to DNA methyltransferases responsible for gene body methylation. Thus, gene body methylation is likely shaped by H3.3 dynamics in relation with transcriptional activity.

2017-04-24 | GSE95175 | GEO

The histone H3 variant H3.3 regulates gene body DNA methylation in Arabidopsis thaliana

Project description:Gene bodies of vertebrates and flowering plants are occupied by histone variant H3.3 and DNA methylation. The origin and significance of these profiles remain largely unknown. The profiles of enrichments in DNA methylation and H3.3 over gene bodies are correlated and both depend similarly on gene transcription levels. This suggests a mechanistic link between H3.3 and gene body methylation. We engineered H3.3 knockdown in Arabidopsis and observed transcription reduction that predominantly affected genes responsive to environmental cues. When H3.3 levels were reduced, gene bodies showed a loss of DNA methylation correlated with transcription levels. To study the origin of changes in DNA methylation profiles when H3.3 levels are reduced, we examined genome-wide distributions of several histone H3 marks, H2A.Z, linker histone H1 and nucleosome densities. We observed that in absence of H3.3, H1 distribution increased in gene bodies. This depends on levels of gene transcription. We propose that H3.3 prevents recruitment of H1, which in turn promotes chromatin folding and antagonizes access to DNA methyltransferases responsible for gene body methylation. Thus, gene body methylation is likely shaped by H3.3 dynamics in relation with transcriptional activity.

2017-04-25 | GSE97252 | GEO

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