This SuperSeries is composed of the SubSeries listed below.
Single-cell transcriptomics reveals a new dynamical function of transcription factors during embryonic hematopoiesis.
Specimen part, Disease, Cell line, Treatment
View SamplesHistone acetylation and other modifications of the chromatin are important regulators of gene expression and, consequently, may contribute to drug-induced behaviors and neuroplasticity. Previous studies have shown that a reduction on histone deacetylase (HDAC) activity results on the enhancement of some psychostimulant-induced behaviors. In the present study, we extend those seminal findings by showing that the administration of the HDAC inhibitor sodium butyrate enhances morphine-induced locomotor sensitization and conditioned place preference. In contrast, this compound has no effects on the development of morphine tolerance and dependence. Similar effects were observed for cocaine and ethanol-induced behaviors. These behavioral changes were accompanied by a selective boosting of a component of the transcriptional program activated by chronic morphine administration that included circadian clock genes and other genes relevant in addictive behavior. Our results support an specific role for histone acetylation and the epigenetic modulation of transcription at a reduced number of biologically relevant loci on non-homeostatic, long lasting, drug-induced behavioral plasticity. To further investigate the molecular bases of sodium butyrate action on long-lasting behavioral responses to morphine, we screened for potential substrates of their interaction by performing a genome-wide comparison of the striatal transcriptome after chronic administration of morphine in the absence or presence of sodium butyrate.
Selective boosting of transcriptional and behavioral responses to drugs of abuse by histone deacetylase inhibition.
Sex, Age, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Genomic landscape of transcriptional and epigenetic dysregulation in early onset polyglutamine disease.
Sex, Age, Specimen part
View SamplesTranscriptional dysregulation is an important early feature of polyglutamine diseases. One of its proposed causes is defective neuronal histone acetylation, but important aspects of this hypothesis, such as the precise genomic topography of acetylation deficits
Genomic landscape of transcriptional and epigenetic dysregulation in early onset polyglutamine disease.
Sex, Age, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Genomic targets, and histone acetylation and gene expression profiling of neural HDAC inhibition.
Sex, Age, Specimen part, Treatment
View SamplesHistone deacetylase inhibitors (HDACis) have been shown to potentiate hippocampal-dependent memory and synaptic plasticity and to ameliorate cognitive deficits and degeneration in animal models for different neuropsychiatric conditions. However, the impact of these drugs on hippocampal histone acetylation and gene expression profiles at the genomic level, and the molecular mechanisms that underlie their specificity and beneficial effects in neural tissue, remains obscure. Here, we mapped four relevant histone marks (H3K4me3, AcH3K9,14, AcH4K12 and pan-AcH2B) in hippocampal chromatin and investigated at the whole-genome level the impact of HDAC inhibition on acetylation profiles and basal and activity-driven gene expression. HDAC inhibition caused a dramatic histone hyperacetylation that was largely restricted to active loci pre-marked with H3K4me3 and AcH3K9,14. In addition, the comparison of Chromatin immunoprecipitation sequencing and gene expression profiles indicated that Trichostatin A-induced histone hyperacetylation, like histone hypoacetylation induced by histone acetyltransferase deficiency, had a modest impact on hippocampal gene expression and did not affect the transient transcriptional response to novelty exposure. However, HDAC inhibition caused the rapid induction of a homeostatic gene program related to chromatin deacetylation. These results illuminate both the relationship between hippocampal gene expression and histone acetylation and the mechanism of action of these important neuropsychiatric drugs.
Genomic targets, and histone acetylation and gene expression profiling of neural HDAC inhibition.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
The Scc2-Scc4 complex acts in sister chromatid cohesion and transcriptional regulation by maintaining nucleosome-free regions.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Budding yeast Wapl controls sister chromatid cohesion maintenance and chromosome condensation.
No sample metadata fields
View SamplesThe Scc2/Scc4 complex binds to broad nucleosome-free regions in the promoters of highly expressed genes. The cohesin loader is recruited to these sites by the RSC chromatin remodeling complex
The Scc2-Scc4 complex acts in sister chromatid cohesion and transcriptional regulation by maintaining nucleosome-free regions.
No sample metadata fields
View SamplesCohesin acetylation by Eco1 during DNA replication establishes sister chromatid cohesion. We show that acetylation makes cohesin resistant to Wapl activity from S-phase until mitosis. Wapl turns out to be a key regulator of cohesin dynamics on chromosomes by controling cohesin maintenance following its establishment in S-phase and its role in chromosome condensation.
Budding yeast Wapl controls sister chromatid cohesion maintenance and chromosome condensation.
No sample metadata fields
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