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Expression data from wild type versus HDAC knock out mouse embryonic stem cells

ABSTRACT: Histone deacetylase 1 (HDAC1) is an enzyme that promotes deacetylation of acetylated lysine residues in histones and other proteins. Histone acetylation is often associated with gene activation and expression. Los of HDAC1 leads to severe problems in development and proliferation. Moreover, it seems to be the major histone deacetylase in mouse embryonic stem cells. We used microarrays to identify putative HDAC1 target genes. Keywords: Fold change anaylsis between wild type nad HDAC KO ES cells

ORGANISM(S): Mus musculus

PROVIDER: GSE5583 | GEO | 2006/09/19

SECONDARY ACCESSION(S): PRJNA95449

REPOSITORIES: GEO

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Transcription profiling of embryonic stem cells from wild type and histone deacetylase 1 (HDAC1) knock out mice to identify putative HDAC1 target genes.

Project description:Histone deacetylase 1 (HDAC1) is an enzyme that promotes deacetylation of acetylated lysine residues in histones and other proteins. Histone acetylation is often associated with gene activation and expression. Los of HDAC1 leads to severe problems in development and proliferation. Moreover, it seems to be the major histone deacetylase in mouse embryonic stem cells. We used microarrays to identify putative HDAC1 target genes. Experiment Overall Design: Wild type and HDAC1 mouse embryonic stem cell, originating from same litter, were used for RNA extraction and hybridization on Affymetrix microarrays.

2007-11-13 | E-GEOD-5583 | biostudies-arrayexpress

Genome-wide anaylsis of histone acetylation during mouse ESC differentiation [ChIP-seq]

Project description:Using acetylated histone H3 ChIP-seq, we reveal that the histone H3 acetylation level is gradually increased on the neural gene loci while decreased on the neural-inhibitory gene loci during mouse ESC neural differentiation. By overlapping with the targets of HDAC1 ChIP-seq, we identify Nodal as a target gene repressed by histone deacetylation. Thus, our study reveals an intrinsic mechanism that epigenetic histone deacetylation ensures neural fate commitment by restricting Nodal signaling. Examination of HDAC1 in differentiated day 2 cells and acetylated histone H3 in day 2, day 4 and day 6 cells.

2015-02-19 | E-GEOD-66025 | biostudies-arrayexpress

Genome-wide anaylsis of histone acetylation during mouse ESC differentiation [ChIP-seq]

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Rpd3L HDAC links H3K4me3 to transcriptional repression memory

Project description:Transcriptional memory is critical for the faster reactivation of necessary genes upon environmental changes and requires that the genes were previously in an active state. However, whether transcriptional repression also displays “memory” of the prior transcriptionally inactive state remains unknown. In this study, we show that transcriptional repression of approximately 540 genes in yeast occurs much more rapidly if the genes have been previously repressed during carbon source shifts. This novel transcriptional response has been termed transcriptional repression memory(TREM). Interestingly, Rpd3L histone deacetylase (HDAC), targeted to active promoters induces TREM. Mutants for Rpd3L exhibit increased acetylation at active promoters and delay TREM and RNA PolII dissociation significantly. Surprisingly, the interaction between H3K4me3 and Rpd3L via the Pho23 PHD finger is sufficient to induce histone deacetylation and TREM by Rpd3L. Therefore, we propose that an active mark, H3K4me3 enriched at promoters, instructs Rpd3L HDAC to induce histone deacetylation and TREM.

2018-10-23 | E-MTAB-6551 | biostudies-arrayexpress

Expression profiling of histone deacetylase (HDAC) family member genes in human synovial sarcoma cells

Project description:We applied RNA sequencing to generate gene expression profiles for human synovial sarcoma SYO-1 and Yamato-SS cells. We particularly focused on eleven histone deacetylase (HDAC) family genes, and found that HDAC1 and -2 are consistently expressed at relatively higher levels in both two cell lines.

2019-02-06 | GSE126152 | GEO

Pharmacological HDAC inhibition attenuates cardiac hypertrophy and histone acetylation of target genes

Project description:Cardiac hypertrophy is characterized by an increase in heart size and profound gene expression changes. Pharmacological histone deacetylase (HDAC) inhibitors attenuate pathological cardiac remodeling and hypertrophic gene expression. Published literature has linked enzymes that mediates histone acetylation to pathogenesis, however, the role of histone acetylation to define hypertrophic gene regulatory events are not well understood. We used chromatin immunoprecipitation (ChIP) coupled with massive parallel sequencing (seq) to comprehensively examine genome-wide histone acetylation changes in a pre-clinical model of pathological cardiac hypertrophy by transverse aortic constricted (TAC). We examined the gene targets conferred by the prototypical HDAC inhibitor Trichostatin A (TSA). TSA induces genome-wide histone acetylation and deacetylation in the heart. Alterations to histone acetylation were found on genes involved in cardiac morphology such as cardiac contraction, collagen deposition, inflammation and extracellular matrix. Gene set enrichment analysis identified NF-kappa B (NFKB), as a transcription factor positively correlated with TAC and negatively correlated with TSA by ChIP-seq. Histone acetylation on the promoters of NKFB target genes was increased, consistent with gene activation. In contrast, the promoters of these genes were deacetylated by TSA in hypertrophic animals and reduced expression of NFKB target genes. Our results suggest a potential mechanism for TSA mediated cardioprotection conferred by histone deacetylation of target genes implicating the importance of inflammation. ChIP-seq profiles for histone acetylation in left ventricles of mice that develop cardiac hypertrophy and treated with HDAC inhibitors were generated by deep sequencing, using Illumina GAIIx.

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Gene expression profiles of prostate cancer cell line with or without HDAC inihbitors

Project description:Histone deacetylase (HDAC) inibitors suppress cell proliferation of prostate cancer, but the detailed mechanisms are unknown. Moreover, HDAC includes 18 family members, namely HDAC1-11 and SIRT1-7, and differences of effects on prostate cancer proliferation among these enzymes are also unknown. Thus, we clarified differences of gene expression between prostate cancer cell line (LNCaP) treated with pan-HDAC inhibitors (TSA and OBP-801) or selective HDAC inhibitor (NCC-149, HDAC8-specific inhibitor)using cDNA microarray. LNCaP treated with TSA (1Î¼M), NCC149 (2Î¼M), OBP-801 (200nM) or DMSO for 24hrs, RNA was extracted from cells, and cDNA array was performed.

2015-11-04 | E-GEOD-74418 | biostudies-arrayexpress

Relative quantification of acetylated histone peptides in HAP1 cells after treatment with MS-275

Project description:In a previous exploratory mass spectrometry experiment, we unravelled multiple histone and non-histone deacetylation targets of class I HDACs following acetyl-enrichment. Here, using targeted mass spectrometry without prior acetyl-enrichment, we validated selected histone targets in HAP1 cells treated for various time points with the HDAC1, HDAC2 and HDAC3 specific inhibitor MS-275. We confirmed significantly increased signals upon MS-275 treatment for 20 out of 21 selected acetylated peptides of histones H2A.V, H2B type 1-K/1-F, H3.3 and H4. The abundance of most of the selected acetylated peptides was increased already upon 6 hours of MS-275 treatment, and further increased after 24 hours. In summary, this validation experiment demonstrates the reliability of previous targeted approach and gives an additional insight in the the dynamics of acetylation increases following catalytic inactivation of HDAC1, HDAC2 and HDAC3.

2022-08-16 | PXD030272 | panorama

The Smc3 deacetylase Hos1 closes the cohesin acetylation cycle

Project description:Cohesion between sister chromatids is mediated by the chromosomal cohesin complex. In budding yeast, cohesin is loaded onto chromosomes during the G1 phase of the cell cycle. During S-phase, the replication fork-associated acetyltransferase Eco1 acetylates the cohesin subunit Smc3 to promote establishment of sister chromatid cohesion. At the time of anaphase, Smc3 loses its acetylation again, but the Smc3 deacetylase and possible importance of Smc3 deacetylation are unknown. Here, we show that the class I histone deacetylase family member Hos1 is responsible for Smc3 deacetylation. Cohesin is protected from deacetylation while bound to chromosomes, but is deacetylated as soon as it dissociates from chromosomes following separase cleavage at anaphase onset. Non-acetylated Smc3 is required as a substrate for cohesion establishment in the following cell cycle. Our results complete the description of the Smc3 acetylation cycle and provide unexpected insight into the importance of de novo Smc3 acetylation for cohesion establishment.

2010-06-10 | GSE22257 | GEO

Gene expression profiles of prostate cancer cell line with or without HDAC inihbitors

2015-11-04 | GSE74418 | GEO

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