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A comprehensive map coupling histone modifications with gene regulation in adult dopaminergic and serotonergic neurons [TRAP-Seq SER_Meth]

ABSTRACT: The adult brain is composed of hundreds of different neuronal subtypes, which retain their differentiated traits and identity throughout the lifespan of the organism. Nevertheless, in part due to technical limitations, the mechanisms governing this stability are not fully understood. Here, using a strategy that allows for ChIP-seq combined with RNA-seq in sparse neuronal populations in vivo, we present, to our knowledge, the first comparative analysis of permissive and repressive histone modifications in adult midbrain dopaminergic neurons, raphe nuclei serotonergic neurons and embryonic neural progenitors. Our results support a model wherein a sequential deposition of the repressive modifications H3K27me3 and H3K9me3 occur on developmental genes in a neuronal subtype specific manner. We furthermore show that aberrant gene expression during dopaminergic stress in a mouse model of Parkinson’s disease, or after methamphetamine injection, is characterized by the de-repression of genes with promoter regions that are dually marked by H3K4me3 and H3K27me3, whereas the induction of genes with promoter regions marked by any other combination of H3K27me3 and H3K9me3 occur less frequently. Our study provides to our knowledge the first genome-wide analysis of permissive/repressive histone modifications coupled to gene expression in these rare but clinically relevant neuronal subtypes. This strategy can be generalized for the identification and functional characterization of molecular determinants involved in the maintenance of gene expression in other classes of neurons.

ORGANISM(S): Mus musculus

PROVIDER: GSE108372 | GEO | 2018/01/25

REPOSITORIES: GEO

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A comprehensive map coupling histone modifications with gene regulation in adult dopaminergic and serotonergic neurons [TRAP-Seq mDA_Meth]

Project description:The adult brain is composed of hundreds of different neuronal subtypes, which retain their differentiated traits and identity throughout the lifespan of the organism. Nevertheless, in part due to technical limitations, the mechanisms governing this stability are not fully understood. Here, using a strategy that allows for ChIP-seq combined with RNA-seq in sparse neuronal populations in vivo, we present, to our knowledge, the first comparative analysis of permissive and repressive histone modifications in adult midbrain dopaminergic neurons, raphe nuclei serotonergic neurons and embryonic neural progenitors. Our results support a model wherein a sequential deposition of the repressive modifications H3K27me3 and H3K9me3 occur on developmental genes in a neuronal subtype specific manner. We furthermore show that aberrant gene expression during dopaminergic stress in a mouse model of Parkinson’s disease, or after methamphetamine injection, is characterized by the de-repression of genes with promoter regions that are dually marked by H3K4me3 and H3K27me3, whereas the induction of genes with promoter regions marked by any other combination of H3K27me3 and H3K9me3 occur less frequently. Our study provides to our knowledge the first genome-wide analysis of permissive/repressive histone modifications coupled to gene expression in these rare but clinically relevant neuronal subtypes. This strategy can be generalized for the identification and functional characterization of molecular determinants involved in the maintenance of gene expression in other classes of neurons.

2018-01-25 | GSE108371 | GEO

A comprehensive map coupling histone modifications with gene regulation in adult dopaminergic and serotonergic neurons [TRAP-Seq mDA_6-OHDA]

2018-01-25 | GSE108370 | GEO

A comprehensive map coupling histone modifications with gene regulation in adult dopaminergic and serotonergic neurons [scRNA-Seq]

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A comprehensive map coupling histone modifications with gene regulation in adult dopaminergic and serotonergic neurons [RNA-Seq]

2018-01-25 | GSE107655 | GEO

A comprehensive map coupling histone modifications with gene regulation in adult dopaminergic and serotonergic neurons [ChIP-Seq]

2018-01-25 | GSE107309 | GEO

Chip-seq from MEF cells H3K27me3

Project description:Genome wide chromatin maps have shown that spreading repressive histone modifications such as H3K9me3 and H4K20me3 are present on pericentromeric and telomeric repeats and on the inactive X chromosome where H3K27me3 or H3K9me3 alternately modify megabasepair sized domains. However, only a few regions along an autosome of which Homeobox gene clusters are notable examples, have been shown to display spreading of repressive histone modifications. Here we present a ChIP-Chip map of repressive and active histone modifications along mouse Chr.17 in embryonic, fibroblast cells. Our results show that the majority of H3K27me3 modifications form BLOCs rather than focal peaks. H3K27me3 BLOCs modify silent genes of all types and their flanking intergenic regions, indicating a negative correlation between H3K27me3 and transcription. However, non-transcribed gene-poor regions also lacked H3K27me3. We therefore performed a low resolution analysis of whole mouse Chr.17 which revealed that H3K27me3 specifically marks megabasepair sized domains that are enriched for genes, SINEs and active histone modifications. These genic H3K27me3 domains alternate with similar sized gene-poor domains that are deficient in active histone modifications, but enriched for LINE and LTR transposons as well as H3K9me3 and H4K20me3. Thus, a mouse autosome can be seen to contain alternating chromatin bands that predominantly separate genes from one retrotransposons class, which could offer unique chromatin compartments for the specific regulation of genes or the silencing of transposons. mapping of H3K27me3 histone modification in one MEF cell line (MEFF)

2008-12-22 | E-GEOD-12721 | biostudies-arrayexpress

Chip-chip from MEF cells with H3ac, H4ac, H4K20me1, H3K27me3, H3K9me3, H4K20me3, H3K4me2, H3K4me3 and H3K9ac

Project description:Genome wide chromatin maps have shown that spreading repressive histone modifications such as H3K9me3 and H4K20me3 are present on pericentromeric and telomeric repeats and on the inactive X chromosome where H3K27me3 or H3K9me3 alternately modify megabasepair sized domains. However, only a few regions along an autosome of which Homeobox gene clusters are notable examples, have been shown to display spreading of repressive histone modifications. Here we present a ChIP-Chip map of repressive and active histone modifications along mouse Chr.17 in embryonic, fibroblast cells. Our results show that the majority of H3K27me3 modifications form BLOCs rather than focal peaks. H3K27me3 BLOCs modify silent genes of all types and their flanking intergenic regions, indicating a negative correlation between H3K27me3 and transcription. However, non-transcribed gene-poor regions also lacked H3K27me3. We therefore performed a low resolution analysis of whole mouse Chr.17 which revealed that H3K27me3 specifically marks megabasepair sized domains that are enriched for genes, SINEs and active histone modifications. These genic H3K27me3 domains alternate with similar sized gene-poor domains that are deficient in active histone modifications, but enriched for LINE and LTR transposons as well as H3K9me3 and H4K20me3. Thus, a mouse autosome can be seen to contain alternating chromatin bands that predominantly separate genes from one retrotransposons class, which could offer unique chromatin compartments for the specific regulation of genes or the silencing of transposons. Keywords: Chip-chip, chromosome 17 wide unbiased mapping unbiased mapping of several histone modifications on chromosome 17 in two independent MEF cell lines

2008-11-23 | E-GEOD-11335 | biostudies-arrayexpress

RNA-chip from MEF cells

Project description:Genome wide chromatin maps have shown that spreading repressive histone modifications such as H3K9me3 and H4K20me3 are present on pericentromeric and telomeric repeats and on the inactive X chromosome where H3K27me3 or H3K9me3 alternately modify megabasepair sized domains. However, only a few regions along an autosome of which Homeobox gene clusters are notable examples, have been shown to display spreading of repressive histone modifications. Here we present a ChIP-Chip map of repressive and active histone modifications along mouse Chr.17 in embryonic, fibroblast cells. Our results show that the majority of H3K27me3 modifications form BLOCs rather than focal peaks. H3K27me3 BLOCs modify silent genes of all types and their flanking intergenic regions, indicating a negative correlation between H3K27me3 and transcription. However, non-transcribed gene-poor regions also lacked H3K27me3. We therefore performed a low resolution analysis of whole mouse Chr.17 which revealed that H3K27me3 specifically marks megabasepair sized domains that are enriched for genes, SINEs and active histone modifications. These genic H3K27me3 domains alternate with similar sized gene-poor domains that are deficient in active histone modifications, but enriched for LINE and LTR transposons as well as H3K9me3 and H4K20me3. Thus, a mouse autosome can be seen to contain alternating chromatin bands that predominantly separate genes from one retrotransposons class, which could offer unique chromatin compartments for the specific regulation of genes or the silencing of transposons. Keywords: RNA-chip, chromosome 17 wide expression mapping mouse chromosome 17 wide expression mapping of transcribed genes by hybridization of ds cDNA in two independent MEF cell lines

2008-11-23 | E-GEOD-11337 | biostudies-arrayexpress

Genome-wide mapping of histone marks at single-nucleosome resolution

Project description:Histone post-translational modifications (PTM) encode much of genome's regulatory information. However, regular chromatin immunoprecipitation followed by sequencing (ChIP-seq) protocols trace histone PTM to genomic regions spanning several nucleosomes, making it difficult to study how different histone PTM combine within individual nucleosomes to regulate the genome. Here, we devised computational and statistical methods to map H3K4me3, H3K27Ac, H3K9me3, and H3K27me3 to individual nucleosomes using MNase digestion of chromatin coupled with ChIP-seq. A significant number of nucleosomes were marked by two or more of histone marks. Nucleosomes marked simultaneously by H3K4me3 and H3K27me3 were prevalent among bivalent domains compared to the genomic background whereas nucleosomes having the repressive marks H3K27me3 and H3K9me3 were enriched at the transcription staring site of highly active genes only if they were also co-localized with the activating mark H3K27Ac. Inclusion of alternatively spliced exons on the final mRNA is correlated with nucleosomes marked by H3K4me3, H3K27Ac, and H3K27me3, but is largely unaffected by nucleosomes marked by H3K9me3. Together, these findings reveal that combinatorial patterns of histone PTM within individual nucleosomes are fundamental to encode regulatory information.

2018-09-14 | GSE73004 | GEO

Chip-seq from MEF cells H3K27me3

2008-12-22 | GSE12721 | GEO

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