Histone methyltransferase SETDB1 selectively regulates cortical HTR3A interneuron development and anxiety-like behavior in mice [ChIP-seq]
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ABSTRACT:
PROVIDER: PRJNA826437 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18741431_1.fastq.gz | Fastqsanger.gz | |||
| SRR18741431_2.fastq.gz | Fastqsanger.gz | |||
| SRR18741432_1.fastq.gz | Fastqsanger.gz | |||
| SRR18741432_2.fastq.gz | Fastqsanger.gz | |||
| SRR18741433_1.fastq.gz | Fastqsanger.gz |
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Project description:Histone methyltransferase SETDB1 selectively regulates cortical HTR3A interneuron development and anxiety-like behavior in mice
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Project description:Histone methyltransferase SETDB1 is critically involved in brain development, but its role in regulating GABAergic interneurons remains unknown. Here, we used RNA-seq and ATAC-seq to study the gene expression and chromatin accessibility in ganglionic eminences (GE) at E15.5 from brain-specific Setdb1 conditional knockout mice (Setdb1-Nestin-cKO) and controls both in vitro and in vivo.
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Project description:SETDB1 functioning as a histone H3K9 specific methyltransferase, is critically involved in brain development. Here, we used H3K9me3 and H3K27me3 ChIPseq to study H3K9me3 redistribution and defined enhancer function of elements in genomes of NPCs from ganglionic eminences (GE) in brain-specific Setdb1 conditional knockout mice (Setdb1-Nestin-cKO) and controls at E15.5.
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Project description:GABAergic interneuron in the cortex comprise a very heterogenous group. and it is critical to identify discrete interneuron types to understand how their contributions to behavior can be modulated by external and internal cues. However, molecular difinition of these interneuron cell groups has been difficult. Comparative analysis of different interneuron subtypes can provide us new candidate marker genes which could target more specific interneu?on cell group. Here we identify oxytocin responsive novel class of interneuron through our comparative analysis. We employed the bacTRAP strategy, which uses BAC transgenic mice expressing EGFP-tagged ribosomal protein L10a in specific cell populations, to affinity purify polysome-bound mRNAs from Nek7, Dlx1, Cort, Htr3a, Oxtr expressing cortical interneurons. We show that Oxtr expressing cells are a subtype of somatostatin positive interneurons. Three independent TRAP replicates were collected and total RNA from the immunoprecipitates or flow-through (input) whole cortex lysates were amplified and hybridized. Data were normalized with the GCRMA algorithm and replicates were averaged across conditions. We recommend filtering data to remove probe sets with normalized expression values less than 50 in at least one condition. Because the Nek7 BAC labels non-neuronal cells, we recommend to delete astrocytes and oligodendrocytes genes from the list using GSE13379 data.
2014-10-07 | E-GEOD-56996 | biostudies-arrayexpress
Project description:GABAergic interneuron in the cortex comprise a very heterogenous group. and it is critical to identify discrete interneuron types to understand how their contributions to behavior can be modulated by external and internal cues. However, molecular difinition of these interneuron cell groups has been difficult. Comparative analysis of different interneuron subtypes can provide us new candidate marker genes which could target more specific interneuｒon cell group. Here we identify oxytocin responsive novel class of interneuron through our comparative analysis. We employed the bacTRAP strategy, which uses BAC transgenic mice expressing EGFP-tagged ribosomal protein L10a in specific cell populations, to affinity purify polysome-bound mRNAs from Nek7, Dlx1, Cort, Htr3a, Oxtr expressing cortical interneurons. We show that Oxtr expressing cells are a subtype of somatostatin positive interneurons.
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Project description:The early-life environment critically influences neurodevelopment and later psychological health. To elucidate neural and environmental elements that shape emotional behavior, we developed a rat model of individual differences in temperament and environmental reactivity. We selectively bred rats for high versus low behavioral response to novelty and found that high-reactive (bred high-responder, bHR) rats displayed greater risk-taking, impulsivity and aggression relative to low-reactive (bred low-responder, bLR) rats, which showed high levels of anxiety/depression-like behavior and certain stress vulnerability. The bHR/bLR traits are heritable, but prior work revealed bHR/bLR maternal style differences, with bLR dams showing more maternal attention than bHRs. The present study implemented a cross-fostering paradigm to examine the contribution of maternal behavior to the brain development and emotional behavior of bLR offspring. bLR offspring were reared by biological bLR mothers or fostered to a bLR or bHR mother and then evaluated to determine the effects on the developmental gene expression in the hippocampus and amygdala. Genome-wide expression profiling showed that cross-fostering bLR rats to bHR mothers shifted developmental gene expression in the amygdala (but not hippocampus). All samples were generated from Sprague-Dawley male rats selectively bred for high novelty response (HRs), low novelty response (LRs) or LRs that were crossfostered to either a LR dame or HR dame.
2016-10-19 | GSE88874 | GEO
Project description:Depression is a globally prevalent disabling mental illness with serious social hazards. Previous studies suggest that neuroinflammation plays an important role in the pathogenesis of depression, but the underlying mechanism remains elusive. Endogenous retrovirus (ERVs) is a type of transposable elements (TEs), consists around 8% of human genome but are mostly silenced in vivo. Repressive histone modifications H3K9me3 mediated by the methyltransferase SETDB1 plays a key role in maintaining silencing of ERVs. In this study, we constructed Setdb1-CK-cKO (KO) transgenic mice. Behavioral tests showed that the KO mice exhibited anxiety-depression-like behaviors compared to wild type (WT). Cortex snRNA-seq analysis revealed significant changes in astrocytes in addition to excitatory neurons, with the emergence of a new sub cluster of astrocytes in the KO whose transcriptional profile exhibited specific ERVs activation. We observed a large number of GFAP-positive cells in the KO cortex and striatum by Immunostaining, suggesting reactive astrogliosis. Transcriptomic analysis of astrocytes revealed significant upregulation of genes associated with inflammation in the KO cortex, including multiple chemokine genes. To investigate the potential molecular mechanism underlying "endogenous" neuroinflammation in KO mice, we focused on the purinergic receptor P2X7R, which has been reported to play an important role in mediating neuroinflammation and emotional behaviors. Most importantly, we found that the expression of P2rx7 was significantly upregulated in the KO neuron. We applied multiple epigenomic methods (RNA-seq, ATAC-seq, H3K9me3 ChIP-seq) to analyze in detail the molecular mechanism by which SETDB1 regulates the P2rx7 gene expression, and identified a novel enhancer fragment, mE1. We further constructed a SETDB1 knockout human 293T cell line and examined chromatin accessibility by ATAC-seq. We found a regulatory fragment hE1 with enhancer activity, which was present at a similar location in the human P2RX7 locus, suggesting that this mechanism is conserved between human and mouse. Knockout of P2X7R effectively ameliorated neuroinflammation and partially alleviated neuronal dysfunction as well as behaviors in Setdb1-CK-cKO mice.
2026-04-04 | GSE290414 | GEO
Project description:Depression is a globally prevalent disabling mental illness with serious social hazards. Previous studies suggest that neuroinflammation plays an important role in the pathogenesis of depression, but the underlying mechanism remains elusive. Endogenous retrovirus (ERVs) is a type of transposable elements (TEs), consists around 8% of human genome but are mostly silenced in vivo. Repressive histone modifications H3K9me3 mediated by the methyltransferase SETDB1 plays a key role in maintaining silencing of ERVs. In this study, we constructed Setdb1-CK-cKO (KO) transgenic mice. Behavioral tests showed that the KO mice exhibited anxiety-depression-like behaviors compared to wild type (WT). Cortex snRNA-seq analysis revealed significant changes in astrocytes in addition to excitatory neurons, with the emergence of a new sub cluster of astrocytes in the KO whose transcriptional profile exhibited specific ERVs activation. We observed a large number of GFAP-positive cells in the KO cortex and striatum by Immunostaining, suggesting reactive astrogliosis. Transcriptomic analysis of astrocytes revealed significant upregulation of genes associated with inflammation in the KO cortex, including multiple chemokine genes. To investigate the potential molecular mechanism underlying "endogenous" neuroinflammation in KO mice, we focused on the purinergic receptor P2X7R, which has been reported to play an important role in mediating neuroinflammation and emotional behaviors. Most importantly, we found that the expression of P2rx7 was significantly upregulated in the KO neuron. We applied multiple epigenomic methods (RNA-seq, ATAC-seq, H3K9me3 ChIP-seq) to analyze in detail the molecular mechanism by which SETDB1 regulates the P2rx7 gene expression, and identified a novel enhancer fragment, mE1. We further constructed a SETDB1 knockout human 293T cell line and examined chromatin accessibility by ATAC-seq. We found a regulatory fragment hE1 with enhancer activity, which was present at a similar location in the human P2RX7 locus, suggesting that this mechanism is conserved between human and mouse. Knockout of P2X7R effectively ameliorated neuroinflammation and partially alleviated neuronal dysfunction as well as behaviors in Setdb1-CK-cKO mice.
2026-04-04 | GSE275354 | GEO
Project description:Depression is a globally prevalent disabling mental illness with serious social hazards. Previous studies suggest that neuroinflammation plays an important role in the pathogenesis of depression, but the underlying mechanism remains elusive. Endogenous retrovirus (ERVs) is a type of transposable elements (TEs), consists around 8% of human genome but are mostly silenced in vivo. Repressive histone modifications H3K9me3 mediated by the methyltransferase SETDB1 plays a key role in maintaining silencing of ERVs. In this study, we constructed Setdb1-CK-cKO (KO) transgenic mice. Behavioral tests showed that the KO mice exhibited anxiety-depression-like behaviors compared to wild type (WT). Cortex snRNA-seq analysis revealed significant changes in astrocytes in addition to excitatory neurons, with the emergence of a new sub cluster of astrocytes in the KO whose transcriptional profile exhibited specific ERVs activation. We observed a large number of GFAP-positive cells in the KO cortex and striatum by Immunostaining, suggesting reactive astrogliosis. Transcriptomic analysis of astrocytes revealed significant upregulation of genes associated with inflammation in the KO cortex, including multiple chemokine genes. To investigate the potential molecular mechanism underlying "endogenous" neuroinflammation in KO mice, we focused on the purinergic receptor P2X7R, which has been reported to play an important role in mediating neuroinflammation and emotional behaviors. Most importantly, we found that the expression of P2rx7 was significantly upregulated in the KO neuron. We applied multiple epigenomic methods (RNA-seq, ATAC-seq, H3K9me3 ChIP-seq) to analyze in detail the molecular mechanism by which SETDB1 regulates the P2rx7 gene expression, and identified a novel enhancer fragment, mE1. We further constructed a SETDB1 knockout human 293T cell line and examined chromatin accessibility by ATAC-seq. We found a regulatory fragment hE1 with enhancer activity, which was present at a similar location in the human P2RX7 locus, suggesting that this mechanism is conserved between human and mouse. Knockout of P2X7R effectively ameliorated neuroinflammation and partially alleviated neuronal dysfunction as well as behaviors in Setdb1-CK-cKO mice.
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Project description:Depression is a globally prevalent disabling mental illness with serious social hazards. Previous studies suggest that neuroinflammation plays an important role in the pathogenesis of depression, but the underlying mechanism remains elusive. Endogenous retrovirus (ERVs) is a type of transposable elements (TEs), consists around 8% of human genome but are mostly silenced in vivo. Repressive histone modifications H3K9me3 mediated by the methyltransferase SETDB1 plays a key role in maintaining silencing of ERVs. In this study, we constructed Setdb1-CK-cKO (KO) transgenic mice. Behavioral tests showed that the KO mice exhibited anxiety-depression-like behaviors compared to wild type (WT). Cortex snRNA-seq analysis revealed significant changes in astrocytes in addition to excitatory neurons, with the emergence of a new sub cluster of astrocytes in the KO whose transcriptional profile exhibited specific ERVs activation. We observed a large number of GFAP-positive cells in the KO cortex and striatum by Immunostaining, suggesting reactive astrogliosis. Transcriptomic analysis of astrocytes revealed significant upregulation of genes associated with inflammation in the KO cortex, including multiple chemokine genes. To investigate the potential molecular mechanism underlying "endogenous" neuroinflammation in KO mice, we focused on the purinergic receptor P2X7R, which has been reported to play an important role in mediating neuroinflammation and emotional behaviors. Most importantly, we found that the expression of P2rx7 was significantly upregulated in the KO neuron. We applied multiple epigenomic methods (RNA-seq, ATAC-seq, H3K9me3 ChIP-seq) to analyze in detail the molecular mechanism by which SETDB1 regulates the P2rx7 gene expression, and identified a novel enhancer fragment, mE1. We further constructed a SETDB1 knockout human 293T cell line and examined chromatin accessibility by ATAC-seq. We found a regulatory fragment hE1 with enhancer activity, which was present at a similar location in the human P2RX7 locus, suggesting that this mechanism is conserved between human and mouse. Knockout of P2X7R effectively ameliorated neuroinflammation and partially alleviated neuronal dysfunction as well as behaviors in Setdb1-CK-cKO mice.
2026-04-04 | GSE275352 | GEO