Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Temporal regulation of progenitor lineage progression and output by NFIs underlying human neocortical malformation

ABSTRACT: CUT&Tag-seq for NFIA, NFIB and NFIX in E10.5-E17.5 mouse cortical radial glial progenitors (RGPs)

ORGANISM(S): Mus musculus

PROVIDER: GSE229227 | GEO | 2026/09/18

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcriptomes of E16 neocortical tissue knockout from Nfia, Nfib and Nfix knockout mice

Project description:Transcriptomes of E16 neocortical tissue knockout from Nfia, Nfib and Nfix knockout mice

| PRJNA513290 | ENA

Common regulatory targets of NFIA, NFIX and NFIB during postnatal cerebellar development

Project description:Transcriptional regulation plays a central role in controlling neural stem and progenitor cell proliferation and differentiation during neurogenesis. For instance, transcription factors from the nuclear factor I (NFI) family have been shown to co-ordinate neural stem and progenitor cell differentiation within multiple regions of the embryonic nervous system, including the neocortex, hippocampus, spinal cord and cerebellum. Knockout of individual Nfi genes culminates in similar phenotypes, suggestive of common target genes for these transcription factors. However, whether or not the NFI family regulates common suites of genes remains poorly defined. Here, we use granule neuron precursors (GNPs) of the postnatal murine cerebellum as a model system to analyse regulatory targets of three members of the NFI family: NFIA, NFIB and NFIX. By integrating transcriptomic profiling (RNA-seq) of Nfia- and Nfix-deficient GNPs with epigenomic profiling (ChIP-seq against NFIA, NFIB and NFIX, and DNase I hypersensitivity assays), we reveal that these transcription factors share a large set of potential transcriptional targets, suggestive of complementary roles for these NFI family members in promoting neural development.

2020-03-12 | GSE146793 | GEO

Transcriptomes of Nfi deficient and wildtype mouse neocortical tissue at E16

Project description:Here, we generated transcriptomes of microdissected neocortex of Nfia knockout, Nfib knockout and wildtype littermate embryos at embryonic day 16.

2017-10-27 | GSE93604 | GEO

Common regulatory targets of NFIA, NFIX and NFIB during postnatal cerebellar development

Project description:Common regulatory targets of NFIA, NFIX and NFIB during postnatal cerebellar development

| PRJNA611985 | ENA

Region-specific DNA-binding properties of NFIA in the adult mouse brain

Project description:The goal of this study is to profile NFIA DNA-binding properties in the adult mouse brain. We performed chromatin immunoprecipitation of NFIA in the hippocampus and olfactory bulb of wildtype mice, and samples were subjected to sequencing. We find that NFIA preferentially binds DNA in the hippocampus but not in the olfactory bulb as evidenced by the distinct lack of NFIA binding peaks in the olfactory bulb. Mass spectrometry results suggested that NFIA has a significantly higher binding affinity for NFIB in the olfactory bulb, potentially blocking NFIA’s ability to bind DNA. Virally induced siRNAs against NFIB or scramble were injected into the olfactory bulb of adult wildtype mice to knock down NFIB. We performed chromatin immunoprecipitation of NFIA in the olfactory bulb injected with siRNA-NFIB or siRNA-scramble. Subsequent sequencing revealed an increase of NFIA binding in the olfactory bulb upon the depletion of NFIB as compared to the siRNA-scramble and wildtype controls.

2020-02-28 | GSE146064 | GEO

Dose-dependent NFI regulation of progenitor lifespan and output underlying human neocortical malformation.

Project description: Not available

| S-EPMC12776466 | biostudies-literature

NFI Transcription Factors Govern Stem Cell Chromatin Accessibility and Guard Against Irreversible Hair Loss [scRNA-seq]

Project description:Tissue homeostasis and regeneration rely upon resident stem cells (SCs), whose behavior is regulated through niche-dependent crosstalk. The mechanisms underlying SC maintenance are still unfolding. Here, using hair follicles (HFs) as model and spatiotemporal gene ablation in mice, we uncover transcription factors (TFs) NFIB and NFIX as guardians of the process. Complete NFI ablation causes SC depletion and hair loss which resembles irreversible alopecia in humans, who intriguingly also display reduced NFI. Through single cell transcriptomics, ATAC- and ChIP-seq profiling, we uncover a key role for NFIB/NFIX in governing chromatin accessibility of HFSC master TFs . When NFIB/NFIX are genetically removed, the stemness epigenetic landscape is lost, as enhancers driving HFSC identity are decommissioned and those of epidermal differentiation and wound-repair are de-repressed. Together, our findings expose NFIB/NFIX as crucial rheostats of tissue homeostasis, functioning to safeguard the SC epigenome from a breach in lineage confinement that otherwise triggers irreversible tissue degeneration.

2020-04-01 | GSE135143 | GEO

NFI Transcription Factors Govern Stem Cell Chromatin Accessibility and Guard Against Irreversible Hair Loss [bulk RNA-seq]

2020-04-01 | GSE135142 | GEO

NFI Transcription Factors Govern Stem Cell Chromatin Accessibility and Guard Against Irreversible Hair Loss [ChIP-seq]

2020-04-01 | GSE135145 | GEO

NFI Transcription Factors Govern Stem Cell Chromatin Accessibility and Guard Against Irreversible Hair Loss [ATAC-seq]

2020-04-01 | GSE135144 | GEO