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RNA sequencing analysis of gene expression in the mPFC of stressed DBA mice given vehicle of KDM5C inhibitor

ABSTRACT: RNA sequencing analysis of gene expression in the mPFC of stressed DBA mice given vehicle of KDM5C inhibitor

PROVIDER: PRJNA997271 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25385688.fastq.gz	Fastqsanger.gz
	SRR25385689.fastq.gz	Fastqsanger.gz
	SRR25385690.fastq.gz	Fastqsanger.gz
	SRR25385691.fastq.gz	Fastqsanger.gz
	SRR25385692.fastq.gz	Fastqsanger.gz

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Similar Datasets

RNA sequencing analysis of gene expression in the mPFC of stressed DBA mice given vehicle of KDM5C inhibitor

Project description:We performed high-throughput profiling of gene expression in the mPFC of stress-vulnerable DBA2/J mice subjected to subchronic and mild social defeat stress.DBA mice were subjected to 5-day of social defeat stress and then injected with KDM5C inhibitor (KDM5Ci) or vehicle. After behavioral tests, mice were euthanized for tissue collection. We then conducted the transcriptomics analysis. Our study provided insights into the understanding of the molecular mechanisms underlying stress susceptibility and provide the role of KDM5C in stress-induced behavioral changes.

2024-01-15 | GSE237941 | GEO

RNA sequencing analysis of IP (with GFP antibody) and Input samples of the mPFC of stressed DBA mice expressing GFP-L10a

Project description:We performed high-throughput profiling of gene expression in aPVT-projectors in the mPFC of DBA2/J mice subjected to subchronic and mild social defeat stress. DBA mice were subjected to 5-day of social defeat stress and then tested their social interaction and anhedonic state. After behavioral tests, mice were divided into five subtypes: SA, social interaction deficit, ANH: anhedonia, SA:ANH, both social dificit and anhedonia, RES, resilience and non-stressed (NS) control. Mice were euthanized for tissue collection. We then conducted the Immunoprecipitation and RNA-seq. Our study provided insights into the understanding of the molecular mechanisms underlying behavioral heterogeneity.

2024-01-15 | GSE238142 | GEO

RNA sequencing analysis of IP (with GFP antibody) and Input samples of the mPFC of stressed DBA mice expressing GFP-L10a

Project description:RNA sequencing analysis of IP (with GFP antibody) and Input samples of the mPFC of stressed DBA mice expressing GFP-L10a

| PRJNA998035 | ENA

NO001: Kdm5c controls promoter and enhancer activities

Project description:The functional organization of eukaryotic genomes correlates with specific patterns of histone methylations. Regulatory regions in genomes like enhancers and promoters differ in their extent of methylation of histone H3 at lysine-4 (H3K4), but it is largely unknown how the different methylation states are specified and controlled. Here, we show that the Kdm5c/Jarid1c/SMCX member of the Kdm5 family of H3K4 demethylases can be recruited to both enhancer and promoter elements in embryonic stem cells and neuronal progenitor cells via gene-specific transcription factors. Knockdown of Kdm5c deregulates transcription via local increases in H3K4me3. Our data show that restricting H3K4me3 modification at core promoters dampens transcription, but Kdm5c is required at enhancers for their full activity. Remarkably, an impaired enhancer function activates the intrinsic promoter activity of Kdm5c-bound distal elements. Our results demonstrate that the Kdm5c demethylase plays a crucial and dynamic role in the functional discrimination between enhancers and core promoters. RNA from four independent cultures from each sh Kdm5c #1, sh Kdm5c #2 and non-targeting shRNA polyclonal cell lines were hybridized in dye-swap against a common reference of RNA from IB10 ES cells.

2013-04-05 | E-GEOD-38862 | biostudies-arrayexpress

The Kdm5c histone demethylase controls enhancer and promoter function.

Project description:Here, we show that the Kdm5c/Smcx member of the Jarid1 family of H3K4 demethylases is recruited to both enhancer and core promoter elements in ES and neuronal progenitor cells (NPC). Knockdown of Kdm5c deregulates transcription via a local increase in H3K4me3. While at core promoters the function of Kdm5c is to restrict transcription, loss of Kdm5c impairs enhancer function. Remarkably, an impaired enhancer function activates promoter activity from Kdm5c-bound intergenic regions. Our results demonstrate that the Kdm5c demethylase plays a crucial role in the functional identity and discrimination of enhancers and core promoters. We speculate that this is related to recruitment of H3K4me3 binders like the TFIID and NURF complexes6-8. Providing functional identity to genomic regions through balancing enzymes that deposit and remove histone modifications may prove to be a general epigenetic mechanism for the functional indexing of eukaryotic genomes. Examination of the KDM5C binding sites in mouse embryonic stem cells and in neuronal progenitor cells. Effect of KDM5C knock down on H3K4me3 and H3K4me1 levels and gene expression.

2013-04-01 | E-GEOD-34975 | biostudies-arrayexpress

NO001: Kdm5c controls promoter and enhancer activities

Project description:RNA from four independent cultures from each sh Kdm5c #1, sh Kdm5c #2 and non-targeting shRNA polyclonal cell lines were hybridized in dye-swap against a common reference of RNA from IB10 ES cells

2013-04-05 | E-MTAB-1177 | biostudies-arrayexpress

VTA and NAC labeled ribosome from mPFC

Project description:Projection-dependent ribosome profling from mouse mPFC. Ribosome from NAC- and VTA- projecting mPFC cells were immunoprecipited using GFP-trap (Chromotech). Translating mRNA was isolated and analyzed

2017-09-15 | GSE101185 | GEO

The Histone Demethylase KDM5C Functions as a Tumor Suppressor in AML by Repression of B ivalently M arked Immature Genes

Project description:To uncover novel epigenetic regulators in AML, we performed an in vivo short hairpin RNA (shRNA) screen in the context of Cebpa mutant AML. This led to the identification of the Histone 3 Lysine 4 (H3K4) demethylase, KDM5C, as a novel tumor suppressor in AML. KDM5C potentially functions as a transcriptional repressor via its demethylase activity at promoters, and dysregulation could therefore have widespread consequences. Here, we found that reduced Kdm5c/KDM5C expression is associated with accelerated growth in both human and murine AML cell lines. In vivo, Kdm5c knockdown in a Cebpa mutant AML mouse model resulted in a more aggressive, immature and short-latency phenotype. Mechanistically, we show that knockdown of Kdm5c increased H3K4me3 globally. This translated into the up-regulation of a group of bivalently marked immature genes, resulting in a de-differentiation phenotype which could be reversed by modulating levels of pro-differentiation factors. Finally, we demonstrated that low levels of KDM5C were associated with a decrease in long-term disease-free survival, specifically in female patients. This emphasizes the clinical relevance of our findings and identifies KDM5C as a novel female-biased tumor suppressor in AML.

2023-03-10 | PXD016568 | Pride

COMPARATIVE PROTEOMICS ANALYSIS OF THE IRIDOCORNEAL REGION OF DBA/2J AND DBA/2J-Gpnmb+/SjJ MICE

Project description:In this study, we performed a comparative proteomics analysis of the iridocorneal region in DBA/2J and Gpnmb+ mice to gain deeper insight into the molecular mechanisms underlying IOP elevation following iris pigment dispersion/

2026-02-09 | PXD064786 | Pride

A genetically defined mPFC-thalamic circuit underlies pain chronicity

Project description:Chronic pain is a major health care problem with great social and economic consequences. Although the medial prefrontal cortex (mPFC) and the thalamus have been implicated in regulating pain, whether and how these regions may involve in pain chronification process have remained largely unknown. Here, we show that Foxp2+ neurons in mPFC, which are corticothalamic (CT) neurons representing the major mPFC output to thalamus, are deactivated in chronic inflammatory pain. Interestingly, prolonged, but not short-term, inactivation of the Foxp2+ neurons in mPFC increases the sensitivity to noxious stimulations. Conversely, chemogenetic activation of this neuronal cluster induces robust antinociceptive effects in both naïve mice and mice with chronic inflammatory pain. Furthermore, we found that the mPFC Foxp2+ neurons project to several thalamic relay nuclei and that activation of the mPFC to the parataenial nucleus of thalamus (PTN) circuit relieves pain. Finally, RNA-seq of the mPFC Foxp2+ neurons revealed that many genes related to neuronal activity are dysregulated in mice with chronic inflammatory pain. Collectively, our studies revealed that Foxp2+ neurons in mPFC that project to thalamus play a critical role in somatosensory processing and pain chronification.

2023-09-16 | GSE243136 | GEO

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