Ontology highlight
ABSTRACT:
PROVIDER: PRJNA984473 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24948132_1.fastq.gz | Fastqsanger.gz | |||
| SRR24948132_2.fastq.gz | Fastqsanger.gz | |||
| SRR24948133_1.fastq.gz | Fastqsanger.gz | |||
| SRR24948133_2.fastq.gz | Fastqsanger.gz | |||
| SRR24948134_1.fastq.gz | Fastqsanger.gz |
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Project description:Histone modifiers are crucial for instructing multiple-stage cellular differentiation, yet the mechanisms underlying their temporal precision remain enigmatic. Here, we demonstrate that the H3K27 demethylase Kdm6b acts as an epigenetic regulator, coordinating stepwise motor neuron (MN) differentiation through sequential partnerships with stage-specific transcription factors (TFs). Genome-wide profiling reveals a progressive gain in Kdm6b occupancy, especially at distal regulatory elements, as differentiation proceeds. Kdm6b dynamically shapes chromatin landscapes by coordinating H3K27me3 removal with H3K27ac and H3K4me1 acquisition, thereby enabling timed gene activation from MN specification to maturation. Stage-specific inhibition of Kdm6b compromised the ordered expression of developmental genes. Mechanistically, Kdm6b interacts with temporal TFs over time to ensure precise transcriptional control and MN differentiation. Our work elucidates how a single epigenetic regulator achieves temporal fidelity in driving stepwise MN development, and exemplifies a mechanistic insight into epigenetic regulation in determining developmental timing, with broad implications for understanding neurodevelopment and related diseases.
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Project description:Behavioral deficits encompassing motor, cognitive, and psychological domains can emerge after removal of manganese (Mn) exposures in humans and other mammals. While epidemiological studies provide substantial evidence supporting latent persistent Mn neurotoxicity, reproducing such effects in cellular and non-mammalian model systems has slowed mechanistic understanding. Here we report in human induced pluripotent stem cell (hiPSC)-derived cortical cultures that chronic Mn exposure elicits clear latent and persistent neurotoxic effects in gene expression and functional outcomes. To identify persistent and latent effects, and investigate underlying mechanisms, single-cell RNA sequencing was employed in the hiPSC model to provide a comprehensive cell-type specific comparison of transcriptomic changes immediately at the termination versus after a prolonged cessation of chronic Mn exposures. Transcriptomic alterations revealed clear latency of effects after Mn cessation that were not detected immediately following the 40-day exposure. Identified alterations support the linkage between the latent and persistent effects of chronic Mn exposure and a broad range of neurodegenerative pathogenesis and provide insight into the cellular pathways involved.
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Project description:Acne is a common skin disease, closely involving bacterial infection, impaired lipid metabolism and host inflammatory response. Although microneedles (MNs) can deliver bacteriostats for acne treatment, the limited regulation of inflammatory microenvironment and lipid metabolism hinders the therapeutic effect on severe acne. Herein, we develop antimicrobial and anti-inflammatory peptides-laden MN (HMC-PEP MN) with a proteoglycan-mimetic peptide-grafted comb polymer as MN matrix, which effectively treats acne via regulation of both inflammatory microenvironment and lipid metabolism. Specifically, HMC-PEP MN inhibits the expression of pro-inflammatory factors by decreasing TREM2/M2 macrophage ratio in rabbit ear acne model. Integrative analyses of transcriptomic and metabolomic reveal that HMC-PEP MN effectively reduces sebaceous secretion, pro-inflammatory signal transduction, sustained proliferation and differentiation of keratinocytes via inhibition of the IGF1/IGF1R/PI3K/AKT/mTOR signaling pathway. The improved lipid metabolism of sebaceous glands is potential for inhibition of acne recurrence, which provides broad clinical application prospect.
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Project description:Sand biofilter for Mn removal Raw sequence reads
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Project description:Histone modifiers are crucial for instructing multiple-stage cellular differentiation, yet the mechanisms underlying their temporal precision remain enigmatic. Here, we demonstrate that the H3K27 demethylase Kdm6b acts as an epigenetic regulator, coordinating stepwise motor neuron (MN) differentiation through sequential partnerships with stage-specific transcription factors (TFs). Genome-wide profiling reveals a progressive gain in Kdm6b occupancy, especially at distal regulatory elements, as differentiation proceeds. Kdm6b dynamically shapes chromatin landscapes by coordinating H3K27me3 removal with H3K27ac and H3K4me1 acquisition, thereby enabling timed gene activation from MN specification to maturation. Stage-specific inhibition of Kdm6b compromised the ordered expression of developmental genes. Mechanistically, Kdm6b interacts with temporal TFs over time to ensure precise transcriptional control and MN differentiation. Our work elucidates how a single epigenetic regulator achieves temporal fidelity in driving stepwise MN development, and exemplifies a mechanistic insight into epigenetic regulation in determining developmental timing, with broad implications for understanding neurodevelopment and related diseases.dynamic epigenetic choreography to precisely regulate MN developmental programs from early MN fate specification, intermediate cell differentiation and growth to later maturation. The ordered expression of developmental genes was compromised by stage-specific Kdm6b inhibition. Our work resolves how a single epigenetic regulator achieves temporal precision in driving stepwise MN development, with broad implications for neurodevelopment and diseases.
2025-09-24 | GSE305767 | GEO
Project description:Meningiomas are mostly benign brain tumors, with a potential for becoming atypical or malignant. Based on comprehensive genomic, transcriptomic and epigenomic analyses of meningiomas, we compared benign tumors to atypical ones. We show that the vast majority of primary (de novo) atypical meningiomas display loss of NF2, which co-occurs either with genomic instability or recurrent mutations in SMARCB1. These tumors harbor increased H3K27me3 repressive signal and a hypermethylated phenotype, mainly occupying the polycomb repressive complex 2 (PRC2) binding sites in human embryonic stem cells (hESCs), thereby phenocopying a more primitive cellular state. Consistent with this observation, and based on differential gene expression analysis as well as correlation of mRNA:miRNA regulatory networks, atypical meningiomas exhibit up-regulation of EZH2, the catalytic subunit of the PRC2 complex, well as the E2F2 and FOXM1 transcriptional networks that promote proliferation through activation of the cell cycle pathways. In addition, based on H3K27ac ChIP-seq analysis, we show atypical tumors to display an activated super-enhancer near the meningeal identity transcription factor ZIC1, leading to its transcriptional upregulation. The H3k27ac ChIP-seq data for 15 benign meningiomas and 2 dura samples listed below were created by Dr. Justin Cotney in Dr. James Noonan’s lab at Yale and previously published in a paper by our group with Drs. Cotney and Noonan as co-authors (Clark et al. Science, 2013). Sample IDs: MN-297, MN-288, MN-292, MN-163, MN-1037, MN-105, MN-201, MN-249, MN-191, MN-1066, MN-169, MN-291, MN-24, MN-79, MN-1044, CONTROL1, CONTROL2. In this study, we used these benign meningioma H3k27ac ChIP-seq data as controls and compared them to the newly created ChIP-seq data. Sample IDs: MN-54, MN-97 and MN-171. This GEO entry contains ChIP-seq results for both data sets.
2016-12-20 | GSE91372 | GEO
Project description:The most common genetic mutation found in familial and sporadic amyotrophic lateral sclerosis (ALS), as well as fronto-temporal dementia (FTD), is a repeat expansion in the C9orf72 gene. C9orf72 is highly expressed in human myeloid cells, and although neuroinflammation and microglial pathology are widely found in ALS/FTD, the underlying mechanisms are poorly understood. Here, using human induced pluripotent stem cell-derived microglia-like cells (hiPSC-MG) harbouring C9orf72 mutation (mC9-MG) together with gene-corrected isogenic controls (isoC9-MG) and C9ORF72 knock-out hiPSC-MG (C9KO-MG), we show that reduced C9ORF72 protein is associated with impaired phagocytosis and an exaggerated inflammatory response upon stimulation with lipopolysaccharide, driven by sustained activation of NLRP3 inflammasome and NF-kB signalling. Analysis of the hiPSC-MG C9ORF72 interactome revealed an association of C9ORF72 with key regulators of autophagy, a process involved in the homeostatic regulation of the innate immune response. We found impaired initiation of autophagy in C9KO-MG and mC9-MG. Furthermore, through motor neuron-microglial (MN-MG) co-culture studies, we identified that autophagy deficit in mC9-MG led to increased vulnerability of C9 MNs to excitotoxic stimulus. Pharmacological activation of autophagy ameliorated the sustained activation of NLRP3 inflammasome and NF-B signalling, reversed the phagocytic deficit found in mC9-MG and also reduced MN death in MN-MG co-cultures. We validated these findings in blood-derived macrophages from people with C9orf72 mutation. Our results reveal an important role for C9ORF72 in regulating microglial immune homeostasis and identify dysregulation in human myeloid cells as a contributor to neurodegeneration in ALS/FTD
2023-03-02 | PXD032320 | Pride